Beclin-1/LC3-II dependent macroautophagy was uninfluenced in ischemia-challenged vascular endothelial cells

摘要: Abstract Autophagy has been extensively studied and occurs in many biological settings. However, a question remains as to whether ischemia enhances Beclin-1/LC3-II-dependent macroautophagy vascular endothelial cells, previously thought. Furthermore, the effect of level autophagy on cell or skin flap survival still requires elucidation. We created lethal model human umbilical cells (HUVECs), performed quantitative proteomics bioinformatics analyses, verified autophagic status both in vitro in vivo. The significantly upregulated proteins encoded by autophagy-related genes (ATGs) included ATG2A, ATG3, ATG4B, ATG5, ATG7, ATG9A, ATG12, ATG16, ATG101. enhanced lysosomal were cathepsin B, D, lysosome-associated membrane protein 1 (LAMP1), LAMP2. differentially expressed excluded Beclin-1, microtubule-associated light chain 3 (LC3)-I, LC3-II. Western blot analyses that expression levels LC3-I, LC3-II neither nor downregulated ischemia-challenged HUVECs. was not rapamycin ischemic HUVECs but appeared be inhibited chloroquine. Our in vivo study rats showed downregulation jeopardized survival. In conclusion, Ischemia canonical in vivo, contradiction previous studies. An appropriate homeostasis can minimize damage.