Dr Andrea Markou

Learning cell biology presents challenges for undergraduates due to its intricate nature, demanding comprehension of complex cell structures and functions within the human body. To address this, the integration of game design principles into non-game contexts, known as gamification, offers an innovative solution. While traditional learning methods encompass lectures and tutorials, the introduction of gamified elements can foster active learning and provide alternative didactic strategies. This presentation centres on evaluating the impact of gamification in improving students' learning experiences and comprehension of cell biology. This case study employs gamification through collaborative creation of edible 3D cell membrane models, evaluated by instructional staff. This process is accompanied by quiz-style activities targeting cell functions, along with a Pictionary-style component featuring various cell organelles. The session will offer insights garnered from this initiative, encompassing student and lecturer preferences, encountered challenges, identified opportunities, and the rationale behind its current structure, as well as future plans. The outcomes of this initiative revealed an improvement in collaborative teamwork, leading to enhanced communication skills and the reinforcement of fundamental subject knowledge. Challenges within the classroom context encompass student participation in activities and their preconceptions of an ideal undergraduate biosciences educational environment. By engaging students through active, game-inspired learning methodologies, educators can elevate understanding and engagement in intricate subjects like cell biology.

Abstract The aquaporin‐4 (AQP4) water channel is abundantly expressed in the glial cells of the central nervous system and facilitates brain swelling following diverse insults, such as traumatic injury or stroke. Lack of specific and therapeutic AQP4 inhibitors highlights the need to explore alternative routes to control the water permeability of glial cell membranes. The cell surface abundance of AQP4 in mammalian cells fluctuates rapidly in response to changes in oxygen levels and tonicity, suggesting a role for vesicular trafficking in its translocation to and from the cell surface. However, the molecular mechanisms of AQP4 trafficking are not fully elucidated. In this work, early and recycling endosomes were investigated as likely candidates of rapid AQP4 translocation together with changes in cytoskeletal dynamics. In transiently transfected HEK293 cells a significant amount of AQP‐eGFP colocalised with mCherry‐Rab5‐positive early endosomes and mCherry‐Rab11‐positive recycling endosomes. When exposed to hypotonic conditions, AQP4‐eGFP rapidly translocated from intracellular vesicles to the cell surface. Co‐expression of dominant negative forms of the mCherry‐Rab5 and ‐Rab11 with AQP4‐eGFP prevented hypotonicity‐induced AQP4‐eGFP trafficking and led to concentration at the cell surface or intracellular vesicles respectively. Use of endocytosis inhibiting drugs indicated that AQP4 internalisation was dynamin‐dependent. Cytoskeleton dynamics‐modifying drugs also affected AQP4 translocation to and from the cell surface. AQP4 trafficking mechanisms were validated in primary human astrocytes, which express high levels of endogenous AQP4. The results highlight the role of early and recycling endosomes and cytoskeletal dynamics in AQP4 translocation in response to hypotonic and hypoxic stress and suggest continuous cycling of AQP4 between intracellular vesicles and the cell surface under physiological conditions.

The aquaporins (AQPs) form a family of integral membrane proteins that facilitate the movement of water across biological membrane by osmosis, as well as facilitating the diffusion of small polar solutes. AQPs have been recognised as drug targets for a variety of disorders associated with disrupted water or solute transport, including brain oedema following stroke or trauma, epilepsy, cancer cell migration and tumour angiogenesis, metabolic disorders, and inflammation. Despite this, drug discovery for AQPs has made little progress due to a lack of reproducible high-throughput assays and difficulties with the druggability of AQP proteins. However, recent studies have suggested that targetting the trafficking of AQP proteins to the plasma membrane is a viable alternative drug target to direct inhibition of the water-conducting pore. Here we review the literature on the trafficking of mammalian AQPs with a view to highlighting potential new drug targets for a variety of conditions associated with disrupted water and solute homeostasis.