The DNA-dependent protein kinase catalytic subunit exacerbates endotoxemia-induced myocardial microvascular injury by disrupting the MOTS-c/JNK pathway and inducing profilin-mediated lamellipodia degradation
Rongjun Zou, Wanting Shi, Xing Chang, Miao Zhang, Songtao Tan, Ruibin Li, Hao Zhou, Yukun Li, Ge Wang, Weihui Lv, Xiaoping Fan
Abstract
DNA-PKcs inactivation during endotoxemia could be a worthwhile therapeutic strategy to restore MOTS-c expression, prevent JNK-induced profilin phosphorylation, improve F-actin polymerization, and enhance lamellipodial integrity, ultimately ameliorating endothelial barrier function and reducing myocardial microvascular injury.
Topics & Concepts
Cell biologyROCK1Protein kinase ABiologyPhosphorylationMolecular biologyChemistryCancer researchGDF15 and Related BiomarkersMechanisms of cancer metastasisMacrophage Migration Inhibitory Factor