Paola Campagnola

Dr Paola Campagnolo

Lecturer in Molecular Cardiovascular Sciences
+44 (0)1483 684346
32 AY 04

Academic and research departments

School of Biosciences and Medicine.



Dr Paola Campagnolo is currently Lecturer of Molecular Cardiovascular Biology in the School of Biosciences and Medicine, Faculty of Health and Medical Sciences. Paola graduated in Biotechnology at the University of Padua, Italy. She then moved to Bristol to work under the supervision of Prof Paolo Madeddu at Bristol Heart Institute. In 2009, Paola completed her PhD in Cardiovascular Biology working on the isolation of a patient derived pro-angiogenic progenitor cell population. Next, Paola joined Prof Qingbo Xu's the BHF Centre of Excellence at King's College London as a BHF Research Associate to explore the use of stem cells for the repopulation of vascular grafts. In 2013, Paola joined Prof Molly Stevens' group at the Department of Materials at Imperial College London to undertake the study of novel bio- and nano- materials for cardiovascular tissue engineering.Paola has published extensively in top journals in the field of cardiovascular biology and material science with a total of over 646 citations.Paola is part of the editorial board of Editorial Board of Cardiovascular Biologics and Regenerative Medicine (specialty section of Frontiers in Cardiovascular Medicine), act as a reviewer for several journals, including PLoSONE and ATVB and is part of the reviewing board for the French National Agency of Research and the Italian Ministry of Health.

Research interests

My main research interests are (1) developing improved tissue engineered vascular grafts (2) study cell-cell and cell-material interaction in vascular cell within multicellular co-culture systems (3) long term bioreactor systems for multicellular cardiovascular constructs (4) epigenetic changes in cell-material interactions.

Research collaborations

Within the University of Surrey:Dr Kevin Maringer (Department of Microbial Sciences, FHMS)Dr Eirini Velliou (Department of Chemical Engineering, FEPS)Dr Patrizia Camelliti (Department of Biochemical Sciences, FHMS)Dr Costantina Lekakou (Department of Mechanical Engineering, FEPS)

External collaborations:Prof Paolo Madeddu (University of Bristol)Prof Molly Stevens (Imperial College London)Prof Qingbo Xu (Kings College London)Dr Nicola Smart (University of Oxford)Dr Ciro Chiappini (King's College London)

My publications


Barcelos LS, Duplaa C, Kraenkel N, Graiani G, Invernici G, Katare R, Siragusa M, Meloni M, Campesi I, Monica M, Simm A, Campagnolo P, Mangialardi G, Stevanato L, Alessandri G, Emanueli C, Madeddu P (2009) Human CD133(+) Progenitor Cells Promote the Healing of Diabetic Ischemic Ulcers by Paracrine Stimulation of Angiogenesis and Activation of Wnt Signaling, CIRCULATION RESEARCH 104 (9) pp. 1095-U199 LIPPINCOTT WILLIAMS & WILKINS
Di Bernardini E, Campagnolo P, Margariti A, Zampetaki A, Karamariti E, Hu Y, Xu Q (2014) Endothelial lineage differentiation from induced pluripotent stem cells is regulated by microRNA-21 and transforming growth factor ²2 (TGF-²2) pathways.,The Journal of Biological Chemistry 289 (6) pp. 3383-3393 The American Society for Biochemistry and Molecular Biology, Inc.
Finding a suitable cell source for endothelial cells (ECs) for
cardiovascular regeneration is a challenging issue for regenerative
medicine. In this paper, we describe a novel mechanism
regulating induced pluripotent stem cells (iPSC) differentiation
into ECs, with a particular focus on miRNAs and their targets.
We first established a protocol using collagen IV and VEGF to
drive the functional differentiation of iPSCs into ECs and compared
the miRNA signature of differentiated and undifferentiated
cells. Among the miRNAs overrepresented in differentiated
cells, we focused on microRNA-21 (miR-21) and studied its
role in iPSC differentiation. Overexpression of miR-21 in predifferentiated
iPSCs induced EC marker up-regulation and in
vitro and in vivo capillary formation; accordingly, inhibition of
miR-21 produced the opposite effects. Importantly, miR-21
overexpression increased TGF- 2 mRNA and secreted protein
level, consistent with the strong up-regulation of TGF- 2
during iPSC differentiation. Indeed, treatment of iPSCs with
TGF -2 induced EC marker expression and in vitro tube formation.
Inhibition of SMAD3, a downstream effector of TGF -2,
strongly decreased VE-cadherin expression. Furthermore,TGF -2
neutralization and knockdown inhibited miR-21-induced EC
marker expression. Finally, we confirmed the PTEN/Akt pathway
as a direct target of miR-21, and we showed that PTEN
knockdown is required for miR-21-mediated endothelial differentiation.
In conclusion, we elucidated a novel signaling pathway
that promotes the differentiation of iPSC into functional
ECs suitable for regenerative medicine applications.
Gubernator M, Slater SC, Spencer HL, Spiteri I, Sottoriva A, Riu F, Rowlinson J, Avolio E, Katare R, Mangialardi G, Oikawa A, Reni C, Campagnolo P, Spinetti G, Touloumis A, Tavare S, Prandi F, Pesce M, Hofner M, Klemens V, Emanueli C, Angelini G, Madeddu P (2015) Epigenetic Profile of Human Adventitial Progenitor Cells Correlates With Therapeutic Outcomes in a Mouse Model of Limb Ischemia, ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY 35 (3) pp. 675-688 LIPPINCOTT WILLIAMS & WILKINS
Avolio E, Alvino V, Ghorbel M, Campagnolo P (2016) Perivascular cells and tissue engineering: current applications and untapped potential,Pharmacology and Therapeutics 171 pp. 83-92 Elsevier
The recent development of tissue engineering provides exciting new perspectives for the replacement of failing organs and the repair of damaged tissues. Perivascular cells, including vascular smooth muscle cells, pericytes and other tissue specific populations residing around blood vessels, have been isolated from many organs and are known to participate to the in situ repair process and angiogenesis. Their potential has been harnessed for cell therapy of numerous pathologies; however, in this Review we will discuss the potential of perivascular cells in the development of tissue engineering solutions for healthcare. We will examine their application in the engineering of vascular grafts, cardiac patches and bone substitutes as well as other tissue engineering applications and we will focus on their extensive use in the vascularization of engineered constructs. Additionally, we will discuss the emerging potential of human pericytes for the development of efficient, vascularized and non-immunogenic engineered constructs.
Luongo G, Campagnolo Paola, Perez JE, Kosel J, Georgiou TK, Regoutz A, Payne DJ, Stevens MM, Ryan MP, Porter AE, Dunlop IE (2017) Scalable high-affinity stabilization of magnetic iron
oxide nanostructures by a biocompatible antifouling
ACS Applied Materials & Interfaces 9 (46) pp. 40059-40069 American Chemical Society
Iron oxide nanostructures have been widely developed for biomedical applications,
due to their magnetic properties and biocompatibility. In clinical application, the stabilization of
these nanostructures against aggregation and non-specific interactions is typically achieved using
weakly anchored polysaccharides, with better-defined and more strongly anchored synthetic
polymers not commercially adopted due to complexity of synthesis and use. Here, we show for
the first time stabilization and biocompatibilization of iron oxide nanoparticles by a synthetic
homopolymer with strong surface anchoring and a history of clinical use in other applications,
poly(2-methacryloyloxyethy phosphorylcholine) (poly(MPC)). For the commercially important
case of spherical particles, binding of poly(MPC) to iron oxide surfaces and highly effective
individualization of magnetite nanoparticles (20 nm) are demonstrated. Next-generation highaspect
ratio nanowires (both magnetite/maghemite and core-shell iron/iron oxide) are
furthermore stabilized by poly(MPC)-coating, with nanowire cytotoxicity at large concentrations
significantly reduced. The synthesis approach is exploited to incorporate functionality into the
poly(MPC) chain is demonstrated by random copolymerization with an alkyne-containing
monomer for click-chemistry. Taking these results together, poly(MPC) homopolymers and
random copolymers offer a significant improvement over current iron oxide nanoformulations,
combining straightforward synthesis, strong surface-anchoring and well-defined molecular
Sweilam Mona N., Cordery Sarah F., Totti Stella, Velliou Eirini G., Campagnolo Paola, Varcoe John R., Delgado-Charro M. Begoña, Crean Carol (2020) Textile-based non-invasive lithium drug monitoring: a proof-of-concept study for wearable sensing,Biosensors and Bioelectronics 150 111897 Elsevier
Flexible wearable chemical sensors are emerging tools which target diagnosis and monitoring of medical conditions. One of the potential applications of wearable chemical sensors is therapeutic drug monitoring for drugs that have a narrow therapeutic range such as lithium. We have investigated the possibility of developing a fibre-based device for non-invasive lithium drug monitoring in interstitial fluid. A flexible cotton-based lithium sensor was coupled with a carbon fibre-based reference electrode to obtain a potentiometric device. In vitro reverse iontophoresis experiments were performed to extract Li+ from under porcine skin by applying a current density of 0.4 mA cm-2 via two electrodes. Carbon fibre-based reverse iontophoresis electrodes were fabricated and used instead of a conventional silver wire-based version and comparable results were obtained. The fibre-based Li+ sensor and reference electrodes were capable of determining the Li+ concentration in samples collected via reverse iontophoresis and the results compared well to those obtained by ion chromatography. Additionally, biocompatibility of the used materials have been tested. Promising results were obtained which confirm the possibility of monitoring lithium in interstitial fluid using a wearable sensor.
Mastrullo Valeria, Cathery William, Velliou Eirini, Madeddu Paolo, Campagnolo Paola (2020) Angiogenesis in Tissue Engineering: As Nature Intended?,Frontiers in Bioengineering and Biotechnology Frontiers Media
Despite the steady increase in the number of studies focusing on the development of
tissue engineered constructs, solutions delivered to the clinic are still limited. Specifically,
the lack of mature and functional vasculature greatly limits the size and complexity of
vascular scaffold models. If tissue engineering aims to replace large portions of tissue
with the intention of repairing significant defects, a more thorough understanding of the
mechanisms and players regulating the angiogenic process is required in the field. This
review will present the current material and technological advancements addressing the
imperfect formation of mature blood vessels within tissue engineered structures.
Cheung Yin P., Mastrullo Valeria, Maselli Davide, Butsabong Teemapron, Madeddu Paolo, Maringer Kevin, Campagnolo Paola (2020) A Critical Role for Perivascular Cells in Amplifying Vascular Leakage Induced by Dengue Virus Non-Structural Protein 1,mSphere American Society for Microbiology
Dengue is the most prevalent arthropod-borne viral disease affecting humans, with
severe dengue typified by potentially fatal microvascular leakage and hypovolaemic shock.
Blood vessels of the microvasculature are composed of a tubular structure of endothelial cells
ensheathed by perivascular cells (pericytes). Pericytes support endothelial cell barrier
formation and maintenance through paracrine and contact-mediated signalling, and are critical
to microvascular integrity. Pericyte dysfunction has been linked to vascular leakage in
noncommunicable pathologies such as diabetic retinopathy, but has never been linked to
infection-related vascular leakage. Dengue vascular leakage has been shown to result in part
from the direct action of the secreted dengue virus (DENV) non-structural protein NS1 on
endothelial cells. Using primary human vascular cells, we show here that NS1 also causes
pericyte dysfunction, and that NS1-induced endothelial hyperpermeability is more pronounced
in the presence of pericytes. Notably, NS1 specifically disrupted the ability of pericytes to
support endothelial cell function in a 3D microvascular assay, with no effect on pericyte viability
or physiology. These effects are mediated at least in part through contact-independent
paracrine signals involved in endothelial barrier maintenance by pericytes. We therefore
identify a role for pericytes in amplifying NS1-induced microvascular hyperpermeability in
severe dengue, and thus show that pericytes can play a critical role in the aetiology of an
infectious vascular leakage syndrome. These findings open new avenues of research for the
development of drugs and diagnostic assays for combating infection-induced vascular
leakage, such as severe dengue.