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Study of Epigenetic regulation of ERK5 by histone methylase, Enhancer of Zeste Homolog (EZH)-2, during ox-LDL-induced endothelial to mesenchymal transition (EndMT)

Implementing Organization

Principal Investigator
Prof. Umesh CS Yadav
Jawaharlal Nehru University, New Delhi
CO-Principal Investigator
Prof. Rakesh K. Tyagi
Jawaharlal Nehru University, New Delhi-110067

Project Overview

Endothelial to mesenchymal transition (EndMT) is a cellular pathological process that occurs during embryonic development and is linked to diseases like endothelial dysfunction (ED) and atherosclerosis. The increase in oxidized-low density lipoprotein (oxLDL) levels during metabolic disorders creates an oxidative microenvironment in the vasculature, affecting endothelial cells (ECs) function and homeostasis. Exposure to oxLDL leads to decreased Erk5 expression, downregulation of endothelial cell marker genes, and increased expression of inflammatory markers. These alterations can compromise EC homeostasis and promote ED. However, the mechanism of epigenetic modifications enabled during EndMT and its impact on key EC and mesenchymal marker genes is unknown. The study proposes investigating how oxLDL-rich environments enable EZH2 mediated epigenetic modifications in Erk5 gene expression and promote EndMT during metabolic stress conditions. The aim is to identify and validate EZH2 histone methylase as a novel therapeutic target for preventing and treating atherosclerosis in metabolically predisposed individuals. The study aims to unravel the crosstalk between Erk5 and EZH2, identifying a novel target for the prevention and therapy of metabolic stress-induced atherosclerosis.

Source

Source
Anusandhan National Research Foundation/Science and Engineering Research Board (SERB), DST 2023-24
Funding Organization
Quick Information
Area of Research
Life Sciences & Biotechnology
Start Date
2023
End Date
2026
Status
Ongoing
Contact
umeshcsyadav@gmail.com
Output
No. of Research Paper
00
Technologies (If Any)
00
No. of PhD Produced
00
Publications
00
No. of Patents
Filed : 00
Grant : 00
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