Department of Biological Sciences
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Item The multifaceted role of lncRNA MEG3 in kidney disease: a focus on mechanisms, therapeutic and diagnostic potential(Elsevier, 2025-09) Majumder, Syamantak; Gaikwad, Anil BhanudasKidney disease represents a global health challenge, affecting millions of people and contributing to significant morbidity and mortality. Long noncoding RNAs are potentially emerging as regulators in cellular processes and are involved in pathophysiological alterations in kidney disease. Among these, MEG3 has gained attention for its diverse regulatory roles in fibrosis, apoptosis and inflammation. MEG3 dysregulation has been implicated in conditions like chronic kidney disease, acute kidney injury, diabetic kidney disease and renal cell carcinoma. However, its involvement in endoplasmic reticulum (ER) stress and autophagy, crosstalk in kidney disease, is poorly understood. Hence, this review aims to highlight the role of MEG3 as a therapeutic and diagnostic viewpoint in kidney disease and its regulatory mechanism in ER stress and autophagy.Item Chloroquine attenuates hypoxia-mediated autophagy to curb thrombosis- an ex vivo and in vivo study(2024-04) Mukherjee, Sudeshna; Majumder, Syamantak; Chowdhury, Shibasish; Chowdhury, RajdeepHypoxia can trigger the activation of blood platelets, leading to thrombosis. If not addressed clinically, it can cause severe complications and fatal consequences as well. The current treatment regime for thrombosis is often palliative and includes long-term administration of anticoagulants, which has the risk of over-bleeding in injury and other secondary effects as well. This demands a deeper understanding of the process and exploration of an alternative therapeutic avenue. Interestingly, recent studies demonstrate that platelets though atypical and enucleated, possess components of autophagy machinery. This cellular homeostatic process though well-studied in non-platelet cells, is under-explored in platelets.Item Janus Kinase 2 Regulates Transcription Factor EB Expression and Autophagy Completion in Glomerular Podocytes(JASN, 2017-09) Majumder, SyamantakThe nonreceptor kinase Janus kinase 2 (JAK2) has garnered attention as a promising therapeutic target for the treatment of CKD. However, being ubiquitously expressed in the adult, JAK2 is also likely to be necessary for normal organ function. Here, we investigated the phenotypic effects of JAK2 deficiency. Mice in which JAK2 had been deleted from podocytes exhibited an elevation in urine albumin excretion that was accompanied by increased podocyte autophagosome fractional volume and p62 aggregation, which are indicative of impaired autophagy completion. In cultured podocytes, knockdown of JAK2 similarly impaired autophagy and led to downregulation in the expression of lysosomal genes and decreased activity of the lysosomal enzyme, cathepsin D. Because transcription factor EB (TFEB) has recently emerged as a master regulator of autophagosome-lysosome function, controlling the expression of several of the genes downregulated by JAK2 knockdown, we questioned whether TFEB is regulated by JAK2. In immortalized mouse podocytes, JAK2 knockdown decreased TFEB promoter activity, expression, and nuclear localization. In silico analysis and chromatin immunoprecipitation assays revealed that the downstream mediator of JAK2 signaling STAT1 binds to the TFEB promoter. Finally, overexpression of TFEB in JAK2-deficient podocytes reversed lysosomal dysfunction and restored albumin permselectivity. Collectively, these observations highlight the homeostatic actions of JAK2 in podocytes and the importance of TFEB to autophagosome-lysosome function in these cells. These results also raise the possibility that therapeutically modulating TFEB activity may improve podocyte health in glomerular disease.