ArticleCell proliferation2016
Progesterone modulates endothelial progenitor cell (EPC) viability through the CXCL12/CXCR4/PI3K/Akt signalling pathway.
Article in Cell proliferation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
21 citing papers in PubMed, 39 citations in OpenAlex.
- CXCL12/CXCR4 signaling governs ischemic neurovascular pathophysiology and repair: a multidimensional contextual analysis.Angiogenesis · 2026Review
- hucMSCs alleviate LPS-induced endothelial glycocalyx damage by secreting Cxcl12 to activate CXCR4.Stem cell research & therapy · 2026Article
- The role of CXCL12 axis in pancreatic cancer: New biomarkers and potential targets.Frontiers in oncology · 2023Review
- MicroRNAs in septic acute kidney injury.Burns & trauma · 2023Article
- Concanavalin A promotes angiogenesis and proliferation in endothelial cells through the Akt/ERK/Cyclin D1 axis.Pharmaceutical biology · 2022Article
- Construction and a preliminary study of paracrine effect of bone marrow-derived endothelial progenitor cell sheet.Cell and tissue banking · 2022Article
- Gambogic amide inhibits angiogenesis by suppressing VEGF/VEGFR2 in endothelial cells in a TrkA-independent manner.Pharmaceutical biology · 2021Article
- Solving the Puzzle: What Is the Role of Progestogens in Neovascularization?Biomolecules · 2021Review
- MFGE8 mitigates brain injury in a rat model of SAH by maintaining vascular endothelial integrity via TIGβ5/PI3K/CXCL12 signaling.Experimental brain research · 2021Article
- Bimodal Imaging-Visible Nanomedicine Integrating CXCR4 and VEGFa Genes Directs Synergistic Reendothelialization of Endothelial Progenitor Cells.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2020Article
- The Role of the CXCL12/CXCR4/CXCR7 Chemokine Axis in Cancer.Frontiers in pharmacology · 2020Review
- Silencing MicroRNA-137-3p, which Targets RUNX2 and CXCL12 Prevents Steroid-induced Osteonecrosis of the Femoral Head by Facilitating Osteogenesis and Angiogenesis.International journal of biological sciences · 2020Article
- Enzyme-Aided Extraction of Fucoidan by AMG Augments the Functionality of EPCs through Regulation of the AKT/Rheb Signaling Pathway.Marine drugs · 2019Article
- Advance of Stem Cell Treatment for Traumatic Brain Injury.Frontiers in cellular neuroscience · 2019Review
- Curcumin Attenuates gp120-Induced Microglial Inflammation by Inhibiting Autophagy via the PI3K Pathway.Cellular and molecular neurobiology · 2018Article
- Progesterone-mediated angiogenic activity of endothelial progenitor cell and angiogenesis in traumatic brain injury rats were antagonized by progesterone receptor antagonist.Cell proliferation · 2017Article
- Evaluation of velvet antler total protein effect on bone marrow‑derived endothelial progenitor cells.Molecular medicine reports · 2017Article
- Endothelial Progenitor Cells Correlated with Oxidative Stress after Mild Traumatic Brain Injury.Yonsei medical journal · 2017Article
- Mifepristone inhibits ovarian cancer metastasis by intervening in SDF-1/CXCR4 chemokine axis.Oncotarget · 2017Article
- CXCL12 enhances angiogenesis through CXCR7 activation in human umbilical vein endothelial cells.Scientific reports · 2017Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesProgesterone treatment can effectively increase levels of circulating endothelial progenitor cells (EPCs) and improve neurological functional outcome in a traumatic brain injury (TBI) rat model. However, the mechanisms of progesterone's effects on EPC viability remain elusive. The CXCL12/CXCR4 (CXC chemokine ligand 12/CXC chemokine receptor 4) signalling pathway regulates cell proliferation; we hypothesize that it mediates progesterone-induced EPC viability. MATERIALS AND
methodsEPCs were isolated from bone marrow-derived mononuclear cells (BM-MNCs) and treated with progesterone (5, 10 and 100 nm). MTS assay was used to investigate EPC viability. Protein expression was examined by Western blotting, ELISA assay and flow cytometry. Cell membrane and cytoplasm proteins were extracted with membrane and cytoplasm protein extraction kits. CXCR4 antagonist (AMD3100) and phosphatidylinositol 3-kinases (PI3K) antagonist (LY294002) were used to characterize underlying mechanisms.
resultsProgesterone-induced EPC viability was time- and dose-dependent. Administration of progesterone facilitated EPC viability and increased expression of CXCL12 and phosphorylated Akt (also known as protein kinase B, pAkt) activity (P < 0.05). Progesterone did not regulate CXCR4 protein expression in cultured EPC membranes or cytoplasm. However, progesterone-induced EPC viability was significantly attenuated by AMD3100 or LY294002. Inhibition of the signalling pathway with AMD3100 and LY294002 subsequently reduced progesterone-induced CXCL12/CXCR4/PI3K/pAkt signalling activity.
conclusionsThe CXCL12/CXCR4/PI3K/pAkt signalling pathway increased progesterone-induced EPC viability.
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