Chronic photoperiodic manipulation induced chronodisruption upregulates HSP60 during early pro-atherogenic remodeling in thoracic aorta of C57BL/6J mice

Abstract Background Circadian disruption is often associated with aggravation of atherosclerosis; however, the pathophysiological mechanisms underlying atherogenic initiation in normolipidemic diet remains unclear. Most studies done for understanding circadian induced atherosclerosis have been carried out murine model hyperlipidemia atherosclerosis. The present study investigates pro-atherogenic events response to chronic photoperiodic manipulation chronodisruption (PMCD) C57BL/6J mice fed laboratory chow diet. Results results were compared by high fat fructose (HFHF) combined effects HFHF and PMCD on also investigated possible synergy both variants. HFHF+PMCD groups recorded increments body weight gains serum lipid parameters (TC, TG, LDL-cholesterol, VLDL) a decrement HDL-cholesterol as control group. However, group gain similar that group, but (TG significantly elevated HDL levels lowered. prominent hypertrophic remodeling, higher collagen deposition, elastin derangement, along endothelial dysfunction, its activation, macrophage infiltration, observed thoracic aorta all three experimental groups. But mRNA immunoblots heat shock protein 60 (HSP60) was found be maximum followed Conclusion Laboratory feeding coupled mediated overexpress HSP60 turn plays central role remodeling mice.