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SCF 通过 PI3K/AKT 和 MMP-2/-9 信号通路增加心脏干细胞迁移。

SCF increases cardiac stem cell migration through PI3K/AKT and MMP‑2/‑9 signaling.

机构信息

Cardiovascular Institute of Affiliated Hospital, Hainan Medical College, Haikou 571199, P.R. China.

Department of Pathology, School of Basic Medicine Science, Guangdong Medical College, Zhanjiang 524023, P.R. China.

出版信息

Int J Mol Med. 2014 Jul;34(1):112-8. doi: 10.3892/ijmm.2014.1773. Epub 2014 May 7.

DOI:10.3892/ijmm.2014.1773
PMID:24804928
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4072340/
Abstract

The transplantation of cardiac stem cells (CSCs) is thought to be responsible for improving the performance of injured heart induced by myocardial infarction (MI). However, the mechanisms involved in the migration of activated CSCs post‑MI remain to be clarified. In this study, CSCs were isolated from rat hearts and a cellular migration assay was performed using a 24‑well Transwell system. Stem cell factor (SCF) induced CSC migration in a concentration‑dependent manner, which could be blocked with an SCF antibody as well as a PI3K/AKT inhibitor, LY294002. Moreover, SCF induced the expression and activity of matrix metalloproteinase (MMP)‑2 and MMP‑9 in a concentration‑ and time‑dependent manner, as measured by quantitative RT‑PCR, western blot analysis and gelatin zymography. Results of western blot analysis revealed phosphorylated AKT was markedly increased in SCF‑treated CSCs and that inhibition of SCF/c‑Kit signaling or phospho‑AKT activity significantly attenuated the SCF‑induced expression of MMP‑2 and MMP‑9. Thus, our results showed that SCF partially mediated CSC migration via the activation of PI3K/AKT/MMP‑2/‑9 signaling.

摘要

心脏干细胞 (CSC) 的移植被认为可改善心肌梗死 (MI) 所致受损心脏的功能。然而，涉及 MI 后激活的 CSC 迁移的机制仍有待阐明。在本研究中，从大鼠心脏中分离出 CSC，并使用 24 孔 Transwell 系统进行细胞迁移分析。干细胞因子 (SCF) 以浓度依赖性方式诱导 CSC 迁移，该迁移可被 SCF 抗体以及 PI3K/AKT 抑制剂 LY294002 阻断。此外，SCF 以浓度和时间依赖性方式诱导基质金属蛋白酶 (MMP)-2 和 MMP-9 的表达和活性，通过定量 RT-PCR、western blot 分析和明胶酶谱法进行测量。Western blot 分析结果显示，在 SCF 处理的 CSC 中，磷酸化 AKT 明显增加，而抑制 SCF/c-Kit 信号或磷酸化 AKT 活性可显著减弱 SCF 诱导的 MMP-2 和 MMP-9 的表达。因此，我们的结果表明，SCF 通过激活 PI3K/AKT/MMP-2/9 信号通路部分介导 CSC 迁移。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e964/4072340/2316f348b618/IJMM-34-01-0112-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e964/4072340/09f85b5ec22e/IJMM-34-01-0112-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e964/4072340/d8c5680e1ebe/IJMM-34-01-0112-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e964/4072340/fd98b41851be/IJMM-34-01-0112-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e964/4072340/2316f348b618/IJMM-34-01-0112-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e964/4072340/09f85b5ec22e/IJMM-34-01-0112-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e964/4072340/d8c5680e1ebe/IJMM-34-01-0112-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e964/4072340/fd98b41851be/IJMM-34-01-0112-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e964/4072340/2316f348b618/IJMM-34-01-0112-g03.jpg

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本文引用的文献

[1]
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Int J Mol Med. 2012-9-11

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