University roles and responsibilities
- Senior Lecturer in Cardiac Electrophysiology
Affiliations and memberships
- Honorary Director of Translational Research, Ashford and St Peters NHS Trust
- Honorary Assistant Professor, University of Pittsburgh
- Representative of the Physiological Society, University of Surrey
- Honorary Teaching Fellow, Department of Physiology, Royal Free and University College Medical School (2008-2010)
- Professional Development Spine Tutor/Facilitator, Academic Centre for Medical Education, Medical Education, University College London (2002-2008)
My research concerns the characterisation of intracellular and intercellular signalling pathways, primarily in cardiac and smooth muscle, in relation to normal and pathological excitation-contraction coupling. In particular, I am interested in evaluating these signalling pathways to explain the fundamental processes regulating: excitation and conduction of electrical signals; generation of contractile force; regulation of cell growth. I have translated these fundamental studies to characterise the basic intracellular and intercellular changes that underlie pathological situations associated with the heart (e.g. arrhythmias, heart failure, hypertrophic muscle growth) and smooth muscle organs (e.g. pulmonary hypertension, atherosclerosis, overactive bladder). My work involves investigative laboratory experimentation with well-characterised animal models of normal function and human pathological conditions, as well as collaboration with clinicians to extend this work to the use of tissues obtained from patients with clinically characterised pathological conditions.
My particular expertise, for which I have international recognition, is concerned with the role of intracellular phosphatises and kinases to regulate the activity of several key stages concerned with electrical signal transmission, contractile regulation and tissue growth and development. I have pioneered studies that have characterised the role of the intracellular Ca2+-dependent phosphatase, calcineurin, in these fundamental physiological pathways/
These explore the role of serine-threonine protein phosphatase 3, calcineurin, its intracellular targets and the contribution it has to the normal and pathological function of cardiac and visceral smooth muscle organs. In particular I am investigating:
- The regulation of gap junction and ion channel function in myocardium, including tissue from patients with atrial fibrillation and animal models of left ventricular hypertrophy. This is motivated to understand the cell and tissue basis of cardiac arrhythmias.
- Regulation by intracellular phosphatases of myocardial and visceral organ hypertrophy and characterisation of consequent changes to the key intracellular regulatory pathways associated with pathologies such as cardiac arrhythmias, myocardial failure, benign lower urinary tract disorders and initiation of visceral pain.
- Protocols to devise and validating more accurate methods to measure the electrical properties of cells (e.g. with impedance and dielectrophoresis methodologies) to generate more reliable experimental models to evaluate the action of the above phosphatises and kinases.
- Investigation of the role of the above intracellular signalling pathways to control chronobiological rhythms and their association with atrial fibrillation.
- Prof CH Fry on regulation of the biophysical properties of cardiac and smooth muscle, including novel methods to measure gap junction properties in multicellular tissues, as well as control of epithelial transmitter release and downstream modulation of smooth muscle function.
- Dr Michaele Mahmoudi.on biomarkers in cardiac pathologies.
- Prof M Hughes and Dr F Labeed, FEPS, Biochemical engineering division; Faculty of Engineering and Physical Sciences, University of Surrey on the development of techniques to measure the biophysical properties of muscle cells.
- Cardiologists/cardiac surgeons at St George's Hospital, Ashford & St Peters and The Royal Surrey County Hospital NHS trusts to characterise abnormal functional properties of myocardium with well-characterised cardiac pathologies.1. I am the lead on the investigative component on the HASTE foundation funded grant in collaboration with Royal Surrey.2. Honorary director of translational research, Ashford and St Peters NHS Trust.
- Prof R La Ragione, School of Veterinary Medicine, University of Surrey. Prof La Ragione is a collaborator in my currently funded BHF grant.
- Dr Richard Heads at King's College London concerning the role of calcineurin in fibroblast dysfunction during cardiac inflammation.
- I have recently expanded the atrial fibrillation project (HASTE) and initiated collaborations with Prof David Paterson, Oxford University and Dr Andrew James, University of Bristol.
- Dr Van Der Veen (University of Surrey) Dr Sam Boatang (University of Reading) on role of clock genes in cardiac arrhythmias.
- Dr A Aiello, Centre for Cardiovascular Sciences, University of La Plata, Buenos Aires, Argentina. Dr Aiello's expertise is in Na loading transporters in the heart. This was facilitated by:
- Santander Staff Award (£2K) to visit and conduct research at University of La Plata, Argentina (2012 and 2014)
- Santander PhD students award (£5K) for a PhD student from La Plata University (2012)
- Awarded a Santander scholarship certificate for an outstanding performance and dedication in the field of study - FHMS - (March 2013).
- Dr Perrino, Department of Physiology and Cell Biology, University of Nevada Reno, USA. Dr Perrino is an experienced biochemist in manufacturing constitutively active calcineurin isoforms.
- Prof P Lampe, Fred Hutchinson, Cancer Research Centre, Seattle, USA. Prof Lampe is an expert in gap junctions biochemistry and phosphorylation.
- Patch-clamp technique
- Intracellular microelectrode or extracellular monophasic action potential recording simultaneously with isometric muscle contractions
- Tissue impedance measurement
- Multi-electrode array system
- Recording isometric muscle contractions in cardiac and smooth muscle preparations
- Measurement of isolated cardiomyocyte mechanics
- Immunofluorescence with laser scanning confocal microscopy
- Real-time intracellular Ca2+ imaging by epifluorescence microscopy, cell shortening by video-scanning methods
- Protein phosphatase activity assays
- Subcellular tissue fractionation
- SDS-PAGE and western blotting
- Mouse genotyping
- Baculovirus protein expression system.
- Single cardiac and vascular smooth muscle cells isolation techniques
- Primary and cell-line tissue culture
- Proliferation assay
- 2013-2015 (£128,000; PI: R Jabr, Co-I: CH Fry). Title: Investigation of the role of calcineurin in persistent electrophysiological myocardial changes following regression from left ventricular hypertrophy. Funded by British Heart Foundation
- 2013-2014 (£8,000; Co-PI: R Jabr). Title: MicroRNAs as potential biomarkers in coronary artery calcification. Biomedical & Health Research Pump-Priming Funds grant, University of Surrey, 2011-2015 (£638,000) HASTE Foundation. Title: Improving detection and characterising the fundamental basis of atrial fibrillation. I am the Lead on the investigative research component (Dr E Leatham is lead on the clinical component and Prof CH Fry the manager of both components)
- 2008-2010 (£147,280; PI: R Jabr, Co-I: CH Fry). Title: The role of calcineurin in regulating action potential propagation in normal and hypertrophied myocardium through connexin43 dephosphorylation. Funded by British Heart Foundation
- 2009-2012 (€300,000; PI: CH Fry; Co-I, R Jabr). Title: Combatting Incontinence: InComb-EU Framework 7.
- 1999-2000 (£80,000- PI R Jabr). Title: Contractile and electrophysiological properties of cardiac ventricular myocytes in spontaneously hypertensive rats before and during development of hypertension, 1999. Funded by Kuwait University.
Invited research lectures
- 2012 Centre for Cardiovascular investigation; Faculty of Medicine; University of La Plata. Title: The differential role of calcineurin isoforms in the cardiovascular system.
- 2011 Physiological Society Meeting, Oxford, July, 2011 Title: Inter-relationship between conduction velocity, intracellular Ca2+ and gap junction resistance in ventricular myocardium
- 2011 University of Surrey, FHMS, research day, 'Hot topics in cardiovascular research'. Title: Cellular mechanisms for cardiac arrhythmogenesis.
- 2010 Pfizer, sandwich, UK. Title: Role of calcineurin in overactive bladder.
- 2010 The FP7 mid-term meeting, UK. Title: Use of the dielectrophoresis technique for selective cell sorting of bladder urothelial cells.
- 2009 The European Society of Cardiology, Munich, Germany. Title: Calcineurin nuclear import.
- 2009 The Marie Curie- Nuclear Receptors Biology Meeting, UK. Title: Role of nuclear calcineurin in the heart.
- 2008 UK Gap Junction meeting, University of Surrey, UK. Title: Calcineurin slows conduction velocity during rapid pacing in guinea pig papillary muscle.
Postgraduate research supervision
I currently supervise three PhD students at University of Surrey. I'm also a co-supervisor for one PhD student in Biochemical Engineering division; Faculty of Engineering & Physical Sciences, and one PhD student in Dept of Biochemistry & Physiology, University of Surrey.
2010-present Line manager for three postdoctoral fellows. Two financed from HASTE project and one from currently funded BHF project grant.
Completed postgraduate research projects I have supervised
Postgraduate research students
- 2009-2013 Supervised three MSc Toxicology students
- 2009-2012 Supervised MSc Erasmus students (University of Milan)
- 2009-2011 Mentor for PhD/MD/MSc students in Clinical Medicine Division at The Postgraduate Medical School, University of Surrey
- 2007-2008 Co-supervised MD/PhD student at NHLI, Imperial College London
- 2009-2010 Line managed postdoctoral fellow, funded by BHF project grant
- 2000-2008 Trained/co-supervised several postdoctoral fellows at UCL/King's College London and Imperial College London (NHLI)
Module organiser for BMS1032 Physiology 1 module (15 credits; Level 4)
Module organiser for BMS2038 Physiology 2 module (15 credits; Level 5)
Undergrad Physiology teaching:Cardiovascular system; Renal physiology; body fluids and electrolytes; acid-base balance; female reproductive system and pregnancy; Physiology practicals.
- Receptors and intracellular signalling pathways for undergraduate/ postgraduate modules including: L5 BMS2035, MSc Toxicology, MSc Nutrition Medicine, MSc Health and Clinical Sciences
- Cardiovascular toxicity for MSc Toxicology.
anisotropy in left ventricular hypertrophy are associated with topographical changes to gap-junction coupling and
intracellular conductance by measuring these variables in the same preparations.
Methods and Results?Left ventricular papillary muscles were excised from aortic-banded or sham-operated guinea-pig
hearts. With intracellular stimulating and recording microelectrodes, CV was measured in 3 dimensions with simultaneous
conductance mapping with subthreshold stimuli and correlated with quantitative histomorphometry of myocardial
architecture and connexin 43 distribution. In hypertrophied myocardium, CV in the longitudinal axis was smaller and
transverse velocity was greater compared with control; associated with similar differences of intracellular conductance,
consistent with more cell contacts per cell (5.7±0.2 versus 8.1±0.5; control versus hypertrophy), and more intercalated
disks mediating side-to-side coupling (8.2±0.2 versus 10.2±0.4 per cell). Intercalated disk morphology and connexin 43
immunolabelling were not different in hypertrophy. Hypertrophied preparations showed local submillimeter (H250 ¼m)
regions with slow conduction and low intracellular conductance, which, although not affecting CV on the millimeter
scale, were consistent with discontinuities from increased microscopical connective tissue content.
Conclusions?With myocardial hypertrophy, altered longitudinal and transverse CV, and greater nonuniformity of CV anisotropy
correspond to changes of intracellular conductance. These are associated with alteration of myocardial architecture, specifically
the topography of cell?cell coupling and gap-junction connectivity.
and protection in cardiomyocytes.
Methods: iNOS expression was studied in isolated neonatal rat ventricular myocyte cultures in response to bacterial lipopolysaccharide
(LPS) or following transfection with constitutively active calcineurin or Src and in hearts isolated from wild-type or calcineruin A² knockout
mice. Cell injury in response to simulated ischemia?reperfusion was studied following overexpression of active calcineurin. Regulation of
the iNOS gene promoter by calcineurin was studied using promoter-luciferase reporter and chromatin immunoprecipitation assays.
Results: Overexpression of constitutively active Src co-operated with [Ca2+]c elevation to induce iNOS expression, and LPS-induced iNOS
expression was abrogated by pharmacological inhibition of calcineurin or tyrosine kinase. LPS also induced tyrosine kinase-dependent but
calcineurin-independent phosphorylation of Src Tyr418. LPS induced myocardial iNOS expression in wild-type but not calcineurin A²
knockout mice. Overexpression of constitutively active calcinuerin in isolated cardiomyocytes caused deposphorylation and nuclear
accumulation of the c1 isoform of nuclear factor of activated T-cells (NFATc1), induced strong iNOS expression, and induced NOSdependent
protection against simulated ischemia?reperfusion prior to cardiomyocyte hypertrophy. Co-transfection of a mouse iNOS
promoter-luciferase reporter in combination with active calcineurin and wild-type or dominant negative Src confirmed that constitutive
activation of calcineurin was sufficient for transactivation. Chromatin immunoprecipitation confirmed calcineurin-dependent in vivo binding
of NFATc1 to consensus sites within the iNOS promoter.
Conclusions: These results support a cardioprotective role for calcineurin mediated by NFAT-dependent induction of iNOS expression and
co-operativity between calcineurin and Src.
regulates the proliferation of many cell types through activation
of the nuclear factor of activated T cells (NFAT). Two main
isoforms of the calcineurin catalytic subunit [calcineurin A (CnA)
and CnA ] have been identified, although their expression and function
are largely unknown in smooth muscle. Western blot analysis and
confocal imaging were performed in freshly isolated and cultured rat
aortic myocytes to identify these CnA isoforms and elucidate the
effect of PDGF on their cellular distribution and interaction with
NFAT isoforms. CnA and CnA isoforms displayed differential
cellular distribution, with CnA being evenly distributed between the
nucleus and cytosol and CnA being restricted to the cytosol. In
contrast with the rat brain, we found no evidence for particulate/
membrane localization of calcineurin. PDGF caused significant nuclear
translocation of CnA and induced smooth muscle cell proliferation,
with both effects being abrogated by the calcineurin inhibitor
cyclosporin A, the novel NFAT inhibitors A-285222 and inhibitor of
NFAT-calcineurin association-6, and the adenylyl cyclase activator
forskolin. PDGF also caused cyclosporin A-sensitive translocation of
NFATc3, with no apparent effect on either CnA or NFATc1 distribution.
Moreover, 87% of nuclear CnA was found to colocalize with
NFATc3, consistent with the finding that CnA bound more avidly than
CnA to a glutathione S-transferase-NFATc3 fusion protein. Based on
their differential distribution in aortic muscle, our results suggest that
CnA and CnA are likely to have different cellular functions. However,
CnA appears to be specifically activated by PDGF, and we postulate
that calcineurin-dependent nuclear translocation of NFATc3 is involved
in smooth muscle proliferation induced by this mitogen.
Raised [Ca2+]i decreased Gj, reduced Cx43 phosphorylation at S365 and increased it at S368; these changes were reversed by calcineurin inhibitors. Cx43-S368 phosphorylation was reversed by the protein kinase C inhibitor chelerythrine. Raised [Ca2+]i also decreased I1 phosphorylation, also prevented by calcineurin inhibitors, to increase activity of the Ca2+-independent phosphatase, PPI. The PP1 inhibitor, tautomycin, prevented Cx43-365 dephosphorylation, Cx43-S368 phosphorylation and Gj reduction in raised [Ca2+]i. PP2A had no role. Conduction velocity was reduced by raised [Ca2+]i and reversed by calcineurin inhibitors. Reduced action potential conduction and Gj in raised [Ca2+] are regulated by calcineurin-dependent Cx43-S365 phosphorylation, leading to Cx43-S368 dephosphorylation. The calcineurin action is indirect, via I1 dephosphorylation and subsequent activation of PP1.
contractile function, histological structure and expression of
proteins related to tissue protection and apoptosis.
Material and Methods
In vitro preparations of bladder wall and ex vivo perfused pig
bladders were heated from 37 to 42°C, 46 and 50°C for
15 min. Isolated preparations were heated by radiant energy
and perfused bladders were heated by altering perfusate
temperature. Spontaneous contractions or pressure variations
were recorded, as well as responses to the muscarinic agonist
carbachol or motor nerve excitation in vitro during heating.
Tissue histology in control and after heating was analysed
using haematoxylin and eosin staining and 40-6-diamidino-2-
phenylindole (DAPI) nuclear labelling. The effects of heating
on protein expression levels of (i) heat shock proteins HSP27-
pSer82 and inducible-HSP70 and (ii) caspase-3 and its
downstream DNA-repair substrate poly-[ADP-ribose]
polymerase (PARP) were measured.
Heating to 42°C reduced spontaneous contractions or
pressure variations by ~70%; effects were fully reversible.
There were no effects on carbachol or nerve-mediated
responses. Tissue histology was unaffected by heating, and
expression of heat shock proteins as well as caspase-3 and
PARP were also unaltered. A TRPV1 antagonist had no
effect on the reduction of spontaneous activity. Heating to
46°C had a similar effect on spontaneous activity and also
reduced the carbachol contracture. Urothelial structure was
damaged, caspase-3 levels were increased and inducible-
HSP70 levels declined. At 50°C evoked contractions were
abolished, the urothelium was absent and heat shock
proteins and PARP expression was reduced with raised
Heating to 42°C caused a profound, reversible and
reproducible attenuation of spontaneous activity, with no
tissue damage and no initiation of apoptosis pathways.
Higher temperatures caused tissue damage and activation of
apoptotic mechanisms. Mild heating offers a novel approach
to reducing bladder spontaneous activity.
Background and Purpose.
To characterise the molecular mechanisms that determine variability of atropine?resistance of nerve?mediated contractions in human and guinea?pig detrusor smooth muscle
Atropine?resistance of nerve?mediated contractions, and the role of P2X1 receptors, was measured in isolated preparations from guinea?pigs and also humans with or without overactive bladder syndrome, from which the mucosa was removed. Nerve?mediated ATP release was measured directly with amperometric ATP?sensitive electrodes. Ecto?ATPase activity of guinea?pig and human detrusor samples was measured in vitro by measuring the concentration?dependent rate of ATP breakdown. The transcription of ecto?ATPase subtypes in human samples was measured by qPCR.
Atropine resistance was greatest in guinea?pig detrusor, absent in human tissue from normally?functioning bladders and intermediate in human overactive bladder. Greater atropine resistance correlated with reduction of contractions by the ATP?diphospho?hydrolase apyrase, directly implicating ATP in their generation. E?NTPDase?1 was the most abundantly transcribed ecto?ATPase of those tested and transcription was reduced in tissue from human overactive, compared to normal, bladders. E?NTPDase?1 enzymatic activity was inversely related to the magnitude of atropine resistance. Nerve?mediated ATP release was continually measured and varied with stimulation frequency over the range 1?16 Hz.
Conclusion and Implications
Atropine?resistance in nerve?mediated detrusor contractions is due to ATP release and its magnitude is inversely related to E?NTPDase?1 activity. ATP is released under different stimulation conditions compared to acetylcholine that implies different routes for their release
1 Gray RP, Dhillon P, Jacques A, Walker JM, Jabr RI, Marston S, Peters NS, McKenna W, Fry CH (2014). Electromechanical properties of isolated myocardium from patients with hypertrophic obstructive cardiomyopathy. Circulation (Arrhythmias and Electrophysiology) - under revision.
2 Fry CH, Gray RP, Dhillon PS, Jabr RI, Patel PM, Peters NS (2014). Relationship between intracellular conductance, action potential conduction, gap junction topology and tissue architecture in guinea-pig left ventricular hypertrophy. Circulation (Arrhythmias and Electrophysiology) - under revision
3 Dhillon PS, Chowdhury RA, Patel PM, Jabr R, Momin AU, Vecht J, Gray R, Shipolini A, Fry CH, Peters NS. (2014) Relationship between connexin expression and gap-junction resistivity in human atrial myocardium. Circulation (Arrhythmias and Electrophysiology):1: 7: 321-329.
4 Fry CH and Jabr RI. (2014) T-type Ca2+ channels and the urinary and male genital tracts. Pflügers Archives - European Journal of Physiology: 466: 781-789.
5 Paul MA, Mesquita RF, Jabr R, Marber MS, Brain SD, Mahadeo VB, Heads RJ (2014). Protein kinase-C epsilon regulates cardiac fibroblast phenotype by transcriptional co-operation with calcineurin via TLR4 and COX-2. Molecular and Cellular Biology; 34: 574-594
6 Dhillon PD, Gray R, Kojodjojo P, Jabr R, Chowdhury R, Fry CH, Peters NS (2013). The relationship between gap junction conductance and conduction velocity in mammalian myocardium. Circulation Electrophysiology and Arrhythmias: 6: 1208-1214.
7 Fahmi A, Smart N, Punn A, Jabr R, Marber M, Heads R (2013). p42/p44-MAPK and PI3K are Sufficient for IL-6 Family Cytokines/gp130 to Signal to Hypertrophy and Survival in Cardiomyocytes in the Absence of JAK/STAT Activation. Cell Signalling: 25: 898-909.
8 Fry CH, Salvage SC, Manazza A, Dupont E, Labeed FH, Hughes MP, Jabr RI (2012). Cytoplasm resistivity of mammalian atrial myocardium determined by dielectrophoresis and impedance methods. Biophysical Journal: 103: 2287-2294.
9 Fry CH, Young JS, Jabr RI, McCarthy C, Ikeda Y, Kanai AJ (2012). Modulation of spontaneous activity in the overactive bladder - the role of P2Y agonists. American Journal of Physiology, Renal Physiology: 302: F1447-1454.
10 Wyndaele JJ, Gammie A, Bruschini H, De Wachter S, Fry CH, Jabr RI, Kirschner-Hermanns R, Madersbacher H (2011). Bladder compliance what does it represent: can we measure it, and is it clinically relevant? Neurourology and Urodynamics: 30: 714-722.
11 Fry CH, Sadananda P, Wood DN, Thiruchelvam N, Jabr RI, Clayton R (2011). Modeling the urinary tract - computational, physical, and biological methods. Neurourology and Urodynamics: 30: 692-699.
12 Fry CH, Jabr RI. (2010) The action potential and nervous conduction. Surgery Feb.
13 Cook AR, Bardswell SC, Pretheshan S, Dighe K, Kanaganayagam GS, Jabr RI, Merkle S, Marber MS, Engelhardt S, Avkiran M (2009). Paradoxical resistance to myocardial ischemia and age-related cardiomyopathy in NHE1 transgenic mice: a role for ER stress? Journal of Molecular and Cellular Cardiology; 46: 225-233.
14. Jabr RI, Gorog DA, Tanno M, Fisher SG, Cao XB, Bellahcene M, Dighe K, Kabir AM, Quinlan RA, Kato K, Gaestel M, Marber MS, Heads RJ (2009). MAPKAPK-2 modulates p38-MAPK localisation and small heat shock protein phosphorylation, but does not mediate the injury associated with p38-MAPK activation during myocardial ischemia. Cell Stress and Chaperons; 14: 477-489.
15. Jabr RI, Wilson AJ, Riddervold MH, Jenkins AH, Perrino BA, Clapp LH (2007). Nuclear translocation of calcineurin Aß but not Aα by platelet-derived growth factor in rat aortic smooth muscle. American Journal of Physiology, Cell Physiology 2007: 292: C2213-2225.
16. Obasanjo-Blackshire K, Mesquita RS, Jabr RI, Molkentin J, Marber MS, Xia Y and Heads RJ (2006). Calcineurin regulates NFAT-dependent iNOS expression and protection of cardiomyocytes: co-operation with Src tyrosine kinase. Cardiovascular Research: 71: 672-683.
17. Clapp LC, Jabr RI (2003). The BK channel: protective or detrimental in genetic hypertension? Circulation Research 2003: 93: 893-895.
18. Jabr RI, Wilson AJ, Clapp LH (2000). Calcium modulation of vascular smooth muscle ATP-sensitive K+ channels: Role of protein phosphatase-2B. Circulation Research: 87: 1019-1025.
19. Jabr RI, Yamazaki J, Hume JR (2000). Lysophosphatidylcholine triggers intracellular calcium release and activation of non-selective cation channels in renal arterial smooth muscle cells. Pflügers Archives; 439: 495-500.
20. Jabr RI, Toland H, Gelband CH, Wang XX, Hume JR (1997). Prominent role of sarcoplasmic reticulum Ca2+ stores in canine hypoxic pulmonary vasoconstriction. British Journal of Pharmacology: 122: 21-30.
21. Aiello ER, Jabr RI, Cole WC (1995). Arrhythmias and delayed recovery of cardiac action potential during reperfusion after ischemia: Role of oxygen radical-induced no-reflow phenomenon. Circulation Research: 77: 153-162.
22. Jabr RI, Cole WC (1995). Oxygen-derived free radical stress activates non-selective cation current in guinea-pig ventricular myocytes: Role of sulfhydryl groups. Circulation Research: 76: 812-824.
23. Jabr RI, Cole WC (1993). Alterations in electrical activity and membrane ionic currents induced by intracellular exposure of guinea-pig ventricular myocytes to oxy-radical stress. Circulation Research: 72: 1229-1244.
24. Jabr RI, Braveny P, Juggi JS (1988). Recovery of the conduction system from ischemic arrest and cardioplegia in perfused rat heart. Canadian Journal of Cardiology: 4: 90-96
Abstracts-Presented in national and international conferences:
2013Qasem AH, Fry CH, Mahmoudi M, Jabr RI. Assessment of Gap Junction Communication between Human Umbilical Vein Endothelial Cells and Monocytes In Response To Tumour Necrosis Factor (TNF-α). Presented in 1) British Society for Cardiovascular Research & Atherosclerosis Society (London, June 2013); and 2) International Unions of Physiological Society (IUPS) Congress, Birmingham, July 2013.
Waheed A, Salvage SC, Orlowski A, Fry CH, Michael A, Aiello A, Jabr RI. Low-Na increases ventricular gap junction resistivity and phosphorylation levels of connexion 43 at Serine 368: Possible synergistic interaction between calcineurin and protein kinase C. Presented in 1) International Society for Heart Research , The world Congress, San Diego, USA, July 2013; and 2) International Unions of Physiological Society (IUPS) Congress, Birmingham, July 2013.
Clayton J, Kitney D, Hague T, Talstaya A, Fry CH, Jabr RI. Modulation of urinary bladder smooth muscle contractility and mucosal ATP release by inhibition of intracellular protein phosphatases. International Unions of Physiological Society (IUPS) Congress, Birmingham, July 2013.
Kitney D, Hague T, Jabr RI, Fry CH. The influence of heating (37-50C) on spontaneous contractile activity of isolated bladder preparations. Presented in 1) International Unions of Physiological Society (IUPS) Congress, Birmingham, July 2013 and 2) ICS, Spain, August 2013.
2012Salvage SC, Roberts M, Fry CH, Jabr RI. Low Na+ solution increases gap junction resistivity and connexin 43 phosphorylation at serine 368 in guinea pig atrial myocardium: a role for calcineurin. Physiological Society meeting, Edinburgh, UK, July 2012.
2011Manazza A, Salvage S, Fry CH, Jabr RI. Measurement of myocardial sarcoplasmic resistivity by dielectrophoresis and impedance analysis. Physiological Society meeting, Oxford, 2011 as well as the European working group on cardiac cellular electrophysiology group , Oslo, Norway, 2011.
Salvage S, Dillon PS, Fry CH, Jabr RI. Interrelationship between conduction velocity, intracellular Ca2+ and gap junctions. Physiological Society meeting, Oxford, 2011 as well as the European working group on cardiac cellular electrophysiology group , Oslo, Norway, 2011.
2009Lin Y-C, Fry CH, Jabr RI. Modulation of staircase response in mouse myocardium by isoprenaline Physiological Society meeting (Dublin, 2009)
Jabr RI, Fry CH. Calcineurin slows myocardial action potential conduction during rapid pacing by increasing intercellular resistivity. American Heart Association (North American section; Baltimore, 2009)
Fry CH, Gray R, Dillon P, Jabr RI. Electrophysiological properties of human myocardium from hypertrophic cardiomyopathy. American Heart Association (North American section; Baltimore, 2009)
Dhillon PS, Gray R, Kojodjojo P, Jabr RI, Chowdhury RA, Fry CH, Peters NS. The Relationship Between Gap Junction Conductance and Conduction Velocity in Intact Myocardium Authors: Circulation 2009.
2007Jabr RI, Gray R, Patel PM, Peters NS, Fry C H. Calcinuerin slows the conduction velocity in isolated guinea-pig papillary muscle. Abstract submitted to the European Cardiac Arrhythmias Society Congress to be held in Marseille, France, April 2007.
Chowdhury R, Inuabasi L, Jabr R, Nicholson Thomas DM, Hall MC, Kirubakaran S, Dhillon P, Garratt CJ, Peters NS. Multiple anatomical changes in a goat model of atrial fibrillation are associated with conduction velocity abnormalities at 3 months. Abstract submitted to the Heart Rhythm Society, the 28th Annual Scientific Sessions to be held in Denver, Colorado May 2007.
2006Jabr RI, Gorog DA, Bellahcene M, Dighe K, Marber MS. MAPKAPK-2 does not mediate the injury associated with P38-MAPK activation during myocardial ischaemia: Possible role of nuclear translocation of phosphorylated P38-MAPK. Heart, 2006:92(1), no.017.
2005Mesquita RS, Jabr RI, Marber MS, Heads.RJ. Calcineurin and Protein Kinase C Regulate cyclooxygenase-2 expression in the heart. Presented in the 2nd Annual Symposium of the American Heart Association Council on Basic Cardiovascular Sciences-Targeting Heart Failure: New Science, NewTools, New Strategies Keystone, CO, USA, 2005.
Jabr RI, Gorog DA, Bellahcene M, Dighe K, Marber MS. MAPKAPK-2 does not mediate the injury associated with P38-MAPK activation during myocardial ischaemia. J Mol Cell Cardiol, 2005:38(6), no.90.
2004Jabr RI, Perrino B, Clapp LH: Nuclear translocation of calcineurin A ß isoform in response to platelet-derived growth factor in cultured rat aortic smooth muscle cells. Biophysical J, Feb 2004
2001Jabr RI, Wilson AW, Perrino BA, Clapp LH: Characterisation of calcineurin in rat aortic smooth muscle. Journal of Physiology, Bristol, 5-7 September, 2001: 536P.
Jabr RI, Wilson AW, Clapp LH: Ca2+ modulates vascular smooth muscle KATP channels via protein phosphatase-2B. Biophysical Journal 2001:80:627a.
2000Wilson AW, Jabr RI Clapp LH: Modulation of Glibenclamide-sensitive background K+ current by extracellular Ca2+ in isolated rat aortic smooth muscle cells. Journal of Physiology (London) 2000: 525P, 77P.
1999Al-Saeedi F, Juggi JS, Jabr RI, Al-Zaid NS: Intracellular kinetics of activator Ca2+ after ischemic preconditioning as determined by force-frequency relationship. J Mol Cell Cardiol, May 1999.
Ghadanfer E.A., Juggi JS, Jabr RI, Al-Zaid NS: Effect of preconditioning temperature on cardioprotection during global ischemia-reperfusion. J Mol Cell Cardiol, May 1999.
Jabr RI, Juggi JS, Joseph S, Barac-Nieto M: An increase in myocardial shortening velocity precedes arterial hypertension in spontaneously hypertensive rats. J Mol Cell Cardiol, May 1999.
1997Jabr RI, Hume JR: Effects of lysophosphatidylcholine on membrane currents in renal artery smooth muscle cells. Circulation 1997:94(8), pp1I-353, 2060.
Jabr RI, Hume JR: Prominent role of sarcoplasmic reticulum Ca2+ stores in canine hypoxic pulmonary vasoconstriction. Biophysical Journal 1997:72(2), pp. A184.
1996Jabr RI, Ahn DS, Hume JR: Characterization of three types of delayed rectifier potassium channels in canine pulmonary artery smooth muscle cells. Biophysical Journal Feb 1996:70(2), pp. A188.
1995Cole WC, Jabr RI, Aiello AE, Morales E: Cardiac non-selective cation current activated by oxy-radical stress and lysophosphatidylcholine: Voltage-dependence and block by Ni2+. Biophysical Journal 1995:68:A210.
1994Aiello EA, Jabr RI, Cole WC: Cardiac action potential shortening and arrhythmias during reperfusion after ischemia: Role of coronary vasoconstriction due to oxy-radical stress. Biophysical Journal 1994:66:A83.
Jabr RI, Cole WC: Oxygen-derived free -radical stress activates non-selective cation current in guinea-pig ventricular myocytes: Role of sulfhydryl groups. Biophysical Journal1994:66:A434.
Jabr RI, Leblanc N, Cole WC: Abnormal Ca2+ release activates Ca2+ -activated K+ channels in rabbit coronary myocytes during oxygen radicals stress. International Symposium on Resistance Arteries, Vermont, USA,1994.
1993Jabr RI, Cole WC: Oxygen radicals stimulates Na+/Ca2+ exchange and non-selective cation currents in guinea-pig ventricular myocytes. Biophysical Journal 1993:64:A397: 227.
1992Sigurdsson S, Jabr RI, Miller AL, Stephens NL, Cole WC: Whole-cell and single channel K+ currents in isolated canine bronchial smooth muscle cells. Biophysical Journal 1992:61:A251: 1446.
Jabr RI, Leblanc N, Cole WC: Abnormal sarcoplasmic reticulum (SR) Ca2+ release may mediate activation of Ca2+-dependent K+ current in coronary myocytes during oxygen-radical stress. Biophysical Journal 1992:61: A433: 2490.
1991Jabr RI, Cole WC: Effects of oxygen radicals on electrical activity and membrane currents in heart are mediated by abnormal Ca2+ release from sarcoplasmic reticulum. Circulation 1991:2:II-283; 1127.
1990Cole WC, McPherson CD, Jabr RI, Miller AL: Alterations in action potentials and contraction associated with perfusion of guinea-pig right ventricle: Protection by oxy-radical scavengers. Journal of Molecular and Cellular Cardiology 1990:22(suppl 1):S40.
Jabr RI, Cole WC: Alterations in electrical activity and membrane ionic currents after exposure of guinea-pig ventricular myocytes to oxy-radical. Journal of Molecular and Cellular Cardiology 1990:22(suppl 1):S35.
1987Jabr RI, Braveny P, Juggi JS: Preservation of the conduction system during ischemic heart arrest and cardioplegia. PACE 1987:10(3):598.
1986Braveny P, Juggi JS, Jabr RI: Post-arrest electrical instability of perfused rat heart. Journal of Molecular and Cellular Cardiology 1986:18(suppl 21): 274.