Abstract
Autophagy is an intracellular degradation system that disassembles cytoplasmic components through autophagosomes with lysosomes. Autophagic dysregulation may be related vascular diseases including hypertension, pulmonary hypertension and atherosclerosis. Recently, there are increasing interests about involvement of autophagy in survival and function of vascular smooth muscle cells. In hypertensive rat, impaired relaxation and augmented contraction elevate peripheral resistance. We observed expression levels of autophagic markers beclin1, LC3I/II and p62 in mesenteric arteries and aorta from control rats and hypertensive rats. Significantly increased beclin1 and LC3II were observed in hypertensive rats compared with control rats. We checked the expression level of p62, autophagosome cargo protein, which is degraded by autolysosomes. The level of p62 was significantly decreased in hypertensive rats. In this study, we assumed that alterations in autophagic flux change function of mesenteric arteries from hypertensive rats.Support or Funding InformationThis work was supported by the Basic Science Research Program of the National Research Foundation of Korea (NRF) funded by the Ministry of Education, Science and Technology (NRF‐2018R1D1A1B07041820) and Brain Korea 21 PLUS Project for Medical Science, Yonsei University.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
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