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TGF-β2 处理增强了胚胎干细胞释放的细胞保护因子,并抑制了梗死心肌中的细胞凋亡。

TGF-β2 treatment enhances cytoprotective factors released from embryonic stem cells and inhibits apoptosis in infarcted myocardium.

机构信息

Biomolecular Science Center, Burnett School of Biomedical Sciences, College of Medicine, University of Central Florida, Orlando, 32816, USA.

出版信息

Am J Physiol Heart Circ Physiol. 2011 Apr;300(4):H1442-50. doi: 10.1152/ajpheart.00917.2010. Epub 2011 Feb 4.

Abstract

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.

摘要

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。

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