Bironaite D, Baltriukiene D, Uralova N, Stulpinas A, Bukelskiene V, Imbrasaite A, Kalvelyte A
Department of Developmental Biology, Institute of Biochemistry, Vilnius, Lithuania.
Cell Biol Int. 2009 Jul;33(7):711-9. doi: 10.1016/j.cellbi.2009.03.007. Epub 2009 Apr 17.
Apoptosis in heart failure has been intensively investigated in vitro and in vivo. Stem cells have therapeutic value in the direct treatment of diseases, including cardiovascular disease. The main drawback of stem cell therapy is their poor survival in the diseased tissues. Since intracellular mitogen-activated protein kinases (MAPKs) actively participate in the regulation of cell survival and of proapoptotic signals, the ability to manipulate the mechanisms of MAPKs activation in myogenic stem cells might increase the survival of transplanted stem cells. Our results clearly demonstrate sustained activation of all three MAPKs, ERK, JNK and p38 in myogenic stem cells after exposure to the NO inducer, NOC-18. Inhibition of MAPKs phosphorylation by specific inhibitors revealed the anti-apoptotic role of MAPKs in myogenic stem cells.
心力衰竭中的细胞凋亡已在体外和体内进行了深入研究。干细胞在包括心血管疾病在内的疾病直接治疗中具有治疗价值。干细胞治疗的主要缺点是它们在患病组织中的存活率低。由于细胞内丝裂原活化蛋白激酶（MAPK）积极参与细胞存活和促凋亡信号的调节，操纵成肌干细胞中MAPK激活机制的能力可能会提高移植干细胞的存活率。我们的结果清楚地表明，在暴露于NO诱导剂NOC-18后，成肌干细胞中所有三种MAPK，即ERK、JNK和p38均持续激活。用特异性抑制剂抑制MAPK磷酸化揭示了MAPK在成肌干细胞中的抗凋亡作用。
Zotero 插件