Sestrin2 regulates monocyte activation through AMPK ‐mTOR nexus under high‐glucose and dyslipidemic conditions

Sestrin2 expression levels were decreased upon high ‐glucose and oxidized LDL (OxLDL) treatments in monocytes with the alterations in adenosine monophosphate kinase (AMPK) and mechanistic target of rapamycin (mTOR) phosphorylation and activation. Further, we have observed that sestrin2 regulates monocyte activation, adhesion, and foam cell formatio n upon high‐glucose or OxLDL treatments through the AMPK–mTOR‐signaling pathway. Thus we conclude that sestrin2 could play a major role in the development of atherogenesis. AbstractThe vicious cycle between hyperinsulinemia and insulin resistance results in the progression of atherosclerosis in the vessel wall. The complex interaction between hyperglycemia and lipoprotein abnormalities promotes the development of atherogenesis. In the early phase of atherosclerosis, macrophage ‐derived foam cells play an important role in vascular remodeling. Mechanistic target of rapamycin (mTOR) signaling pathway has been identified to play an essential role in the initiation, progression, and complication of atherosclerosis. Recently sestrin2, an antioxidant, was shown to modulate TO R activity and thereby regulating glucose and lipid metabolism. But the role of sestrin2 in monocyte activation is still not clearly understood. Hence, this study is focussed on investigating the role of sestrin2 in monocyte activation under hyperglycemic and dyslipidemic conditions. High‐glucose and oxidized low‐density lipoprotein (LDL) treatments me...
Source: Journal of Cellular Biochemistry - Category: Biochemistry Authors: Tags: RESEARCH ARTICLE Source Type: research