Regulation of autophagic flux by dynein-mediated autophagosomes trafficking in mouse coronary arterial myocytes.

ABSTRACT: Autophagic flux is an important process during autophagy maturation in coronary arterial myocytes (CAMs). Here, we defined the role and molecular mechanism of the motor protein dynein in the regulation of autophagic flux in CAMs. In mouse CAMs, dynein protein is abundantly expressed. Pharmacological or genetic inhibition of dynein activity dramatically enhanced 7-ketocholesterol (7-Ket)-induced expression of the autophagic marker LC3B and increased the cellular levels of p62, a selective substrate for autophagy. Inhibition of dynein activity increased 7-Ket-induced formation of autophagosomes (APs), but reduced the number of autophagolysosomes (APLs) in CAMs. Furthermore, 7-Ket increased the fusion of APs with lysosomes and the velocity of APs movement in mouse CAMs, which was abolished wh

SUBMITTER: Xu M 

PROVIDER: S-EPMC3855232 | biostudies-literature | 2013 Dec

REPOSITORIES: biostudies-literature