Biomolecular Science Center, Burnett School of Biomedical Sciences, College of Medicine, University of Central Florida, Orlando, 32816, USA.
Am J Physiol Heart Circ Physiol. 2011 Apr;300(4):H1442-50. doi: 10.1152/ajpheart.00917.2010. Epub 2011 Feb 4.
We investigated whether factors released from mouse embryonic stem (ES) cells primed with and without transforming growth factor (TGF)-β2 inhibit iodoacetic acid (IAA)- and H(2)O(2)-induced apoptosis in the cell culture system as well as after transplantation in the infarcted heart. We generated conditioned media (CMs) from ES cells primed with and without TGF-β2 and determined their effects on IAA- and H(2)O(2)-induced apoptosis in H9c2 cells. We also transplanted both ES-CMs in the infarcted heart to determine the effects on apoptosis and cardiac function after myocardial infarction (MI) at day (D)1 and D14. Terminal deoxynucleotidyltransferase-mediated dUTP nick end labeling (TUNEL) staining, apoptotic ELISA, and cell viability data demonstrated significantly (P < 0.05) reduced apoptosis with ES-CM compared with controls in both cell culture models. Moreover, TGF-β2-primed ES-CM (T-ES-CM) demonstrated enhanced beneficial effects, with further reduced (P < 0.05) apoptosis compared with ES-CM, suggesting the a presence of additional cytoprotective released factors after TGF-β2 treatment. Next, our in vivo apoptosis data suggested significant decrease in apoptosis with both ES-CMs compared with MI alone at D1 and D14. Notably, T-ES-CM demonstrated significant (P < 0.05) inhibition of apoptosis and fibrosis with improved cardiac function compared with ES-CM at D14, whereas no such effects were observed at D1. Next, we confirmed that apoptosis is mediated through a prosurvival Akt pathway. Moreover, we determined that after TGF-β2 treatment there was a two- to fivefold increase in cytoprotective released factors (interleukin-10, stem cell factor, tissue inhibitor of matrix metalloproteinase-1, and VEGF) with T-ES-CM compared with ES-CM. In conclusion, we suggest that factors released from ES cells with and without TGF-β2 treatment contain antiapoptotic factors that inhibit apoptosis in vitro and in vivo. We also suggest that T-ES-CM demonstrates additional beneficial effects that provide useful information for future therapeutic applications in regenerative medicine.
我们研究了从经转化生长因子(TGF)-β2 预培养和未经 TGF-β2 预培养的小鼠胚胎干细胞(ES)释放的因子是否能抑制细胞培养系统中碘乙酸(IAA)和 H2O2 诱导的细胞凋亡,以及在梗塞心脏中移植后的细胞凋亡。我们从经 TGF-β2 预培养和未经 TGF-β2 预培养的 ES 细胞中生成条件培养基(CM),并确定它们对 H9c2 细胞中 IAA 和 H2O2 诱导的细胞凋亡的影响。我们还将两种 ES-CM 都移植到梗塞的心脏中,以确定它们在心肌梗塞(MI)后第 1 天和第 14 天对细胞凋亡和心脏功能的影响。末端脱氧核苷酸转移酶介导的 dUTP 缺口末端标记(TUNEL)染色、凋亡 ELISA 和细胞活力数据表明,与对照组相比,ES-CM 在两种细胞培养模型中均显著(P < 0.05)减少了细胞凋亡。此外,TGF-β2 预培养的 ES-CM(T-ES-CM)显示出增强的有益作用,与 ES-CM 相比,细胞凋亡进一步减少(P < 0.05),这表明 TGF-β2 处理后存在其他细胞保护释放因子。接下来,我们的体内凋亡数据表明,与单独的 MI 相比,两种 ES-CM 在第 1 天和第 14 天都显著减少了凋亡。值得注意的是,与 ES-CM 相比,T-ES-CM 在第 14 天显著抑制了凋亡和纤维化,改善了心脏功能,而在第 1 天则没有观察到这种作用。接下来,我们证实凋亡是通过一种促生存 Akt 途径介导的。此外,我们确定,与 ES-CM 相比,T-ES-CM 中细胞保护释放因子(白细胞介素-10、干细胞因子、基质金属蛋白酶组织抑制剂-1 和血管内皮生长因子)的含量增加了两到五倍。综上所述,我们认为,经 TGF-β2 处理和未经 TGF-β2 处理的 ES 细胞释放的因子含有抗凋亡因子,能抑制体外和体内的细胞凋亡。我们还认为,T-ES-CM 具有额外的有益作用,为再生医学中的未来治疗应用提供了有用的信息。