Neurodegenerative disease is a cause of progressive neuronal cell loss. As the lack of validated animal models makes it difficult to study neurodegeneration, the foremost objective of my study is to establish an effective in vitro neurodegenerative model system. Several studies have revealed the role of mesenchymal stromal cells (MSCs) and their secretome in rescuing neurodegeneration. Moreover, priming of MSCs to enhance their immunomodulatory function is a growing area of research. Hence the focus of my study is to evaluate the salutary effect of primed MSC secretome on the established neurodegenerative model system.

Despite extensive research into the design of biomaterials for cartilage reconstruction, there is still a need for the development of materials that have sufficient mechanical conformity to work synergistically with healthy cartilage and subchondral bone while remaining soft enough to allow tissue incorporation. My research focuses on the development of effective and cost-effective biomaterials-based strategies for the treatment of damaged and diseased organs and tissues, with a particular emphasis on cartilage tissue regeneration. My work involves designing and synthesizing bioinspired biomaterials that mimic the native microenvironment and then assess the efficacy of these novel scaffolds for improved chondrogenesis.

Polycomb group proteins and other proteins catalyze various histone modifications to regulate gene expression, while other proteins remove these modifications. Our group and others have shown that H2AK119ub1 catalyzed by Polycomb Repressive Complex I (PRC1) plays a crucial role in gene regulation during neuronal lineage specification in human pluripotent stem cells. The H2AK119ub1 mark is erased by histone H2A deubiquitinases that counteract the gene repression by PRC1. There are only about nine are histone H2A deubiquitinases namely USP3, USP12, USP16, USP21, USP22, USP44, BAP1, MYSM1 and BRCC36 and there are only few reports of these in hematopoietic stem cells. However, there are no reports of histone H2A deubiquitinases in neuronal lineage specification from human pluripotent stem cells. I aim to study the expression of histone H2A deubiquitinases in during neuronal differentiation, as well as study the effects of shRNA-mediated knockdown of H2A- DUBs on neuronal differentiation.