Tissue inhibitor of metalloproteinase-1 promotes hematopoietic differentiation via caspase-3 upstream the MEKK1/MEK6/p38α pathway

Dassé, Emilie; Bridoux, Lucie; Baranek, Thomas; Lambert, Elise; Salesse, Stéphanie; Sowa, M; Martiny, Laurent; Trentesaux, Chantal; Petitfrere, E.

doi:10.1038/sj.leu.2404540

Cited by 29 publications

(22 citation statements)

References 29 publications

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“…In the hematopoietic system, TIMP-1 was initially found to enhance the proliferation of erythroid cells and promote hematopoietic differentiation [18,39,40]. More recently, we found that TIMP-1 À/À mice present a consistent decrease in BM cellularity, including LT-HSC numbers, but no alterations in the respective percentages of circulating myeloid cells, B lymphocytes, or T lymphocytes.…”

Section: Q9mentioning

confidence: 76%

The tissue inhibitor of metalloproteinases 1 increases the clonogenic efficiency of human hematopoietic progenitor cells through CD63/PI3K/Akt signaling

Rossi

Forte

Migliardi

et al. 2015

Experimental Hematology

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Section: Q9mentioning

confidence: 76%

The tissue inhibitor of metalloproteinases 1 increases the clonogenic efficiency of human hematopoietic progenitor cells through CD63/PI3K/Akt signaling

Rossi

Forte

Migliardi

et al. 2015

Experimental Hematology

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“…The inhibition of TIMP-1 expression in hMSCs significantly promoted cell growth and differentiation into adult cells of the osteogenic lineage, indicating that TIMP-1 is an endogenous attenuator of these processes. Previous reports have shown that TIMP-1 inhibits epithelial cell proliferation and osteoblastic differentiation (23,24) but stimulates differentiation in hematopoietic progenitor cells, B cells, and Burkitt lymphoma cells (25)(26)(27). However, none of these studies has provided information regarding the underlying molecular mechanisms.…”

Section: Discussionmentioning

confidence: 99%

Tissue inhibitor of metalloproteinase-1 (TIMP-1) regulates mesenchymal stem cells through let-7f microRNA and Wnt/β-catenin signaling

Egea

Zahler

Rieth

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

116

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Tissue inhibitor of metalloproteinases 1 (TIMP-1) is a matrix metalloproteinase (MMP)-independent regulator of growth and apoptosis in various cell types. The receptors and signaling pathways that are involved in the growth factor activities of TIMP-1, however, remain controversial. RNA interference of TIMP-1 has revealed that endogenous TIMP-1 suppresses the proliferation, metabolic activity, and osteogenic differentiation capacity of human mesenchymal stem cells (hMSCs). The knockdown of TIMP-1 in hMSCs activated the Wnt/β-catenin signaling pathway as indicated by the increased stability and nuclear localization of β-catenin in TIMP-1-deficient hMSCs. Moreover, TIMP-1 knockdown cells exhibited enhanced β-catenin transcriptional activity, determined by Wnt/β-catenin target gene expression analysis and a luciferase-based β-cateninactivated reporter assay. An analysis of a mutant form of TIMP-1 that cannot inhibit MMP indicated that the effect of TIMP-1 on β-catenin signaling is MMP independent. Furthermore, the binding of CD63 to TIMP-1 on the surface of hMSCs is essential for the TIMP-1-mediated effects on Wnt/β-catenin signaling. An array analysis of microRNAs (miRNAs) and transfection studies with specific miRNA inhibitors and mimics showed that let-7f miRNA is crucial for the regulation of β-catenin activity and osteogenic differentiation by TIMP-1. Let-7f was up-regulated in TIMP-1-depleted hMSCs and demonstrably reduced axin 2, an antagonist of β-catenin stability. Our results demonstrate that TIMP-1 is a direct regulator of hMSC functions and reveal a regulatory network in which let-7f modulates Wnt/β-catenin activity.plasticity | osteogenesis | canonical Wnt signaling

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“…Caspase-3, a key regulator y protease from which many signaling pathways merge for the execution of apoptosis, participates in apoptosis induced by bcl-2/ bax, p38 and JAK-STAT [19,20] . We detected the caspase-3 expression in HepG2 cells after treatment with PE.…”

Section: Involvement Of Caspase-3 In Hepg2 Cell Apoptosis Induced By Pementioning

confidence: 99%

Exogenous phosphatidylethanolamine induces apoptosis of human hepatoma HepG2 cells via the bcl-2/bax pathway

Yao¹,

Huang²,

Li³

et al. 2009

WJG

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AIM:To investigate the signaling pathways implicated in phosphatidylethanolamine (PE)-induced apoptosis of human hepatoma HepG2 cells. METHODS:Inhibitory effects of PE on human h e p a t o m a H e p G 2 c e l l s w e r e d e t e c t e d b y 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Cell cycle, apoptosis and mitochondrial transmembrane potential (ΔΨm) were analyzed by flow cytometry. Immunocytochemical assay and Western blotting were used to examine Bcl-2, Bax and caspase-3 protein levels in HepG2 cells treated with PE. RESULTS:PE inhibited the growth of HepG2 cells in a dose-and time-dependent manner. It did not affect the cell cycle, but induced apoptosis. PE significantly decreased ΔΨm at 0.25, 0.5 and 1 mmol/L, respectively, suggesting that PE induces cell apoptosis by decreasing the mitochondrial transmembrane potential. The Bcl-2 expression level induced by different concentrations of PE was lower than that in control groups. However, the Bax expression level induced by PE was higher than that in the control group. Meanwhile, PE increased the caspase-3 expression in a dose-and time-dependent manner. CONCLUSION:Exogenous PE induces apoptosis of human hepatoma HepG2 cells via the bcl-2/bax pathway.

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Tissue inhibitor of metalloproteinase-1 promotes hematopoietic differentiation via caspase-3 upstream the MEKK1/MEK6/p38α pathway

Cited by 29 publications

References 29 publications

The tissue inhibitor of metalloproteinases 1 increases the clonogenic efficiency of human hematopoietic progenitor cells through CD63/PI3K/Akt signaling

The tissue inhibitor of metalloproteinases 1 increases the clonogenic efficiency of human hematopoietic progenitor cells through CD63/PI3K/Akt signaling

Tissue inhibitor of metalloproteinase-1 (TIMP-1) regulates mesenchymal stem cells through let-7f microRNA and Wnt/β-catenin signaling

Exogenous phosphatidylethanolamine induces apoptosis of human hepatoma HepG2 cells via the bcl-2/bax pathway

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