Enhancement of dynein-mediated autophagosome trafficking and autophagy maturation by ROS in mouse coronary arterial myocytes
作者： Ming Xu , Xiao‐Xue Li , Yang Chen , Ashley L. Pitzer , Yang Zhang
DOI: 10.1111/JCMM.12326
关键词:
摘要: Dynein-mediated autophagosome (AP) trafficking was recently demonstrated to contribute the formation of autophagolysosomes (APLs) and autophagic flux process in coronary arterial myocytes (CAMs). However, it remains unknown how function dynein as a motor protein for AP is regulated under physiological pathological conditions. The present study tested whether dynein-mediated autophagy maturation by redox signalling associated with lysosomal Ca2+ release machinery. In primary cultures CAMs, reactive oxygen species (ROS) including H2O2 O2−. (generated xanthine/xanthine oxidase) significantly increased ATPase activity movement, which were accompanied fusion APL formation. Inhibition (erythro-9-(2-hydroxy-3-nonyl)adenine) (EHNA) or disruption complex dynamitin (DCTN2) overexpression blocked ROS-induced activation, movement formation, resulted an accumulation along failed breakdown AP. Antagonism nicotinic acid adenine dinucleotide phosphate (NAADP)-mediated NED-19 PPADS abolished ROS-enhanced activation CAMs. parallel, all these changes also enhanced NADPH oxidase-1 (Nox1) gene Incubation high glucose led marked production compared normoglycaemic while Nox1 inhibitor ML117 abrogated this effect. Moreover, suppressed caused glucose. Taken together, data suggest that ROS important players regulate dynein-dependent leading efficient
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