Progesterone modulates endothelial progenitor cell (<scp>EPC</scp>) viability through the<scp>CXCL</scp>12/<scp>CXCR</scp>4/<scp>PI</scp>3K/Akt signalling pathway

Yu, Peng; Zhang, Zhifei; Li, Shengjie; Wen, Xiaolong; Quan, Wei; Tian, Qilong; Chen, Jieli; Zhang, Jianning; Jiang, Rongcai

doi:10.1111/cpr.12231

Cited by 36 publications

(25 citation statements)

References 64 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This decrease in the quantity of EPCs may be attributed to the steroid-induced decrease in nitric oxide activity leading to EPC senescence and apoptosis [43,44]. In the process of vascular repair, recent studies have shown that SDF-1α-mediated signaling pathways play important roles in enhancing EPC mobilization and functions in ischemic disease models [23,24,45]. In our study, systematic and local changes in the expression of SDF-1α and the quantitative variations of EPCs in rat peripheral blood potentially revealed the mechanism of miR-137-3p silencing in promoting micro-vessel repair in SONFH.…”

Section: Discussionmentioning

confidence: 99%

“…It is well known that stromal cell-derived factor-1α (SDF-1α) is the product of CXCL12. Activation of the SDF-1α/C-X-C chemokine receptor 4 (CXCR4) axis has been implicated in the process of angiogenesis, including recruitment of endothelial progenitor cells (EPCs) [23,24] and endothelial cell migration [25]. EPCs are a type of bone marrow-derived premature progenitor cells [26], which are characterized as CD45 low /CD34 + /VEGFR2 + [27].…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Silencing MicroRNA-137-3p, which Targets RUNX2 and CXCL12 Prevents Steroid-induced Osteonecrosis of the Femoral Head by Facilitating Osteogenesis and Angiogenesis

Kong¹,

Zuo²,

Wang³

et al. 2020

Int. J. Biol. Sci.

View full text Add to dashboard Cite

The main pathogenesis of steroid-induced osteonecrosis of the femoral head (SONFH) includes decreased osteogenic capacity of bone marrow-derived mesenchymal stem cells (BMSCs) and damaged blood supply to the femoral head. MicroRNAs (miRNAs) have been shown to play prominent roles in SONFH development. However, there is no report that a specific miRNA targeting two genes in two different pathogenic pathways has been applied to this disease. The present study investigated the effects of transplantation of miR-137-3p-silenced BMSCs on the prevention and early treatment of SONFH. First, western blotting and dual luciferase assays were employed to verify that miR-137-3p directly targets Runx2 and CXCL12. Then, silencing of miR-137-3p was found to facilitate osteogenic differentiation of BMSCs, which was confirmed by alkaline phosphatase (ALP) staining, alizarin red staining and qRT-PCR. Silencing of miR-137-3p also promoted angiogenesis by human umbilical vein endothelial cells (HUVECs) in the presence or absence of glucocorticoids. Thereafter, overexpression of Runx2 and CXCL12 without the 3′ untranslated region (3′UTR) partially rescued the effects of miR-137-3p on osteogenesis and angiogenesis, respectively. This finding further supported the hypothesis that miR-137-3p exerts its functions partly by regulating the genes, Runx2 and CXCL12. We also demonstrated that SONFH was partially prevented by transplantation of miR-137-3p-silenced BMSCs into a rat model. Micro-CT and histology showed that the transplantation of miR-137-3p-silenced BMSCs significantly improved bone regeneration. Additionally, the results of enzyme-linked immunosorbent assays (ELISA) and flow cytometry suggested that stromal cell-derived factor-1α (SDF-1α) and endothelial progenitor cells (EPCs) participated in the process of vascular repair. Taken together, these findings show that silencing of miR-137-3p directly targets the genes, Runx2 and CXCL12, which can play critical roles in SONFH repair by facilitating osteogenic differentiation and mobilizing EPCs.Key words: steroid-induced osteonecrosis of the femoral head, miR-137-3p, bone marrow-derived mesenchymal stem cells, CXCL12 (SDF-1α), Runx2, endothelial progenitor cells

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Silencing MicroRNA-137-3p, which Targets RUNX2 and CXCL12 Prevents Steroid-induced Osteonecrosis of the Femoral Head by Facilitating Osteogenesis and Angiogenesis

Kong¹,

Zuo²,

Wang³

et al. 2020

Int. J. Biol. Sci.

View full text Add to dashboard Cite

show abstract

“…Steroid hormones (eg, estrogen and progesterone) are able to up‐regulate the mRNA and protein expression of CXCR4 in human ESCs for implantation and pregnancy . In addition, the CXCL12/CXCR4 signaling pathway enhances progesterone‐induced endothelial progenitor cell viability . The above evidences suggest that CXCL12/CXCR4 axis plays an important role in embryonic development during the early pregnancy.…”

Section: Introductionmentioning

confidence: 92%

“…16 In addition, the CXCL12/CXCR4 signaling pathway enhances progesterone-induced endothelial progenitor cell viability. 18 The above evidences suggest that CXCL12/CXCR4 axis plays an important role in embryonic development during the early pregnancy.…”

mentioning

confidence: 98%

Abortifacient metapristone (RU486 derivative) interrupts CXCL12/CXCR4 axis for ovarian metastatic chemoprevention

Zheng

Chen

et al. 2017

Molecular Carcinogenesis

View full text Add to dashboard Cite

Recent global epidemiological studies revealed the lower ovarian cancer death from long-term use of oral contraceptives. However, the underlying mechanism of action is not clear. Here, we use the abortifacient metapristone (RU486 derivative) to test the hypothesis that the contraceptives might interrupt CXCL12/CXCR4 chemokine axis to inhibit ovarian cancer metastasis. Metapristone at concentrations (

show abstract

“…Akt signaling pathway has a close relationship with cell viability and migration. Some studies showed that it was involved in progesterone-induced EPC viability ( 3 ). Notch signaling pathway is highly conserved, and plays a key role in neovascularization and angiogenesis process.…”

Section: Introductionmentioning

confidence: 99%

Evaluation of velvet antler total protein effect on bone marrow-derived endothelial progenitor cells

Xiao

et al. 2017

Molecular Medicine Reports

View full text Add to dashboard Cite

Lu Rong, velvet antler (VA), is a traditional Chinese medicine, which is used as a food supplement and therapeutic drug in China, Japan, Russia, New Zealand and Southeast Asia. The regenerative characteristics of VA have resulted in great research interest, particularly regarding the fields of organ grafting and stem cell differentiation. Various VA proteomic studies verified that proteins act as the primary bioactive components of VA. The present study aimed to investigate if VA proteins (VA-pro) influence endothelial progenitor cell (EPC) viability. Various methods have previously been used to investigate VA-pro, including freeze-drying technology, ultrasonic wave methods, high performance liquid chromatography-mass spectrometry, EPCs extraction and culture. Results demonstrated that VA-pro promoted EPCs proliferation and migration, particularly at a concentration of 1 mg/ml. Furthermore, VA-pro increased the activation level of Notch1 intracellular domain and Hes1, and the level of phosphorylated-Akt and phosphorylated-mechanistic target of rapamycin. VA-pro may therefore affect EPC viability via regulation of the Notch and Akt signaling pathways. The present study revealed the effects and potential molecular mechanism of VA-pro on EPCs, and suggested an association between VA regeneration characteristics and the optimization of EPC viability. These findings may contribute to EPC transplantation research and aid in providing a novel treatment method for vascular diseases in the future.

show abstract

Progesterone modulates endothelial progenitor cell (EPC) viability through theCXCL12/CXCR4/PI3K/Akt signalling pathway

Abstract: The CXCL12/CXCR4/PI3K/pAkt signalling pathway increased progesterone-induced EPC viability.

Cited by 36 publications

References 64 publications

Silencing MicroRNA-137-3p, which Targets RUNX2 and CXCL12 Prevents Steroid-induced Osteonecrosis of the Femoral Head by Facilitating Osteogenesis and Angiogenesis

Silencing MicroRNA-137-3p, which Targets RUNX2 and CXCL12 Prevents Steroid-induced Osteonecrosis of the Femoral Head by Facilitating Osteogenesis and Angiogenesis

Abortifacient metapristone (RU486 derivative) interrupts CXCL12/CXCR4 axis for ovarian metastatic chemoprevention

Evaluation of velvet antler total protein effect on bone marrow-derived endothelial progenitor cells

Contact Info

Product

Resources

About