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

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.

SUBMITTER: Guo J

PROVIDER: S-EPMC4072340 | biostudies-literature | 2014 Jul

REPOSITORIES: biostudies-literature

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

Guo Junli J Jie Wei W Shen Zhihua Z Li Mengsen M Lan Youling Y Kong Yueqiong Y Guo Shaoli S Li Tianfa T Zheng Shaojiang S

International journal of molecular medicine 20140507 1

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 wi ...[more]

PMID: 24804928

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Project description:BackgroundPreeclampsia (PE) is a complex pregnancy-related disease that endangers the safety of maternal and fetal. The purpose of this study is to reveal the pathogenesis of preeclampsia and discover new predictors from the perspective of peptidomics. The umbilical cord blood of PE and control group was analyzed by peptidomics. A peptide named Regulation of Proliferation Process in Preeclampsia (ROPPIP) was screened out to explore its role in the proliferation, migration and apoptosis of trophoblast cells in preeclampsia.MethodsWe compared and analyzed the umbilical cord blood of patients with PE and normal pregnant women using liquid chromatography-tandem mass spectrometry (LC-MS). hTR-8/Svneo cells cultured in vitro were divided into ROPPIP group and a disordered peptide group as control. Cell Counting Kit-8 (CCK-8) assay, flow cytometry, Transwell chamber assays and western blot analysis were performed to detect cell proliferation, invasion, migration and apoptosis, in addition to the expression of Matrix metalloproteinase-2 (MMP2), nuclear associated antigen Ki67, B-cell lymphoma-2 (Bcl2), Caspase 3, and β-actin protein.ResultsWe identified 133 differential peptides. Of these, 51 were up-regulated while 82 were down-regulated. the polypeptide SFGVRMATASPTDGNV with low differential expression in the serum of PE patients was selected for the study, we named the polypeptide as Regulation of Proliferation Process in PE (ROPPIP). The experiment shows that ROPPIP can up-regulate the expression levels of MMP2, Ki67, and Bcl2 in HTR-8/Svneo cells, down-regulate the expression of caspase-3, promote the proliferation and migration of HTR-8/Svneo cells and inhibit the apoptosis induced by cisplatin, the activation of the phosphatidylinositol-3-kinase/protein kinase B/mammalian target of rapamycin (PI3K/Akt/mTOR) signaling pathway may be associated with the function of ROPPIP.ConclusionsROPPIP promotes HTR-8/Svneo cells migration and proliferation, and inhibits apoptosis, by regulating the activation of the PI3K/AKT/mTOR signaling pathway.

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

Publications

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

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