17&amp;beta;-estradiol promotes recovery after myocardial infarction by enhancing homing and angiogenic capacity of bone marrow-derived endothelial progenitor cells through ER&amp;alpha;-SDF-1/CXCR4 crosstalking

Yuan, Zhize; Lee, Kang; Wang, Zhe; Chen, Anqing; Zhao, Qiang; Li, Haiqing

doi:10.1093/abbs/gmy127

Cited by 22 publications

(20 citation statements)

References 35 publications

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“…Hence, it is necessary to study the mechanism of H/R-EPC-exosomes to EPCs, a type of hematopoietic stem cell, promote vascular repair, including vascular proliferation and remodeling, when organs suffer from ischemic injury or endothelial damage [22,23]. EPCs have been identified to participate in the alleviation of cardiac fibrosis in several cardiovascular diseases [24,25]. Several studies have described effective EPC-mediated attenuation of renal/fibrosis via exosomes [5,26].…”

Section: Discussionmentioning

confidence: 99%

YBX-1 mediated sorting of miR-133 into hypoxia/reoxygenation-induced EPC-derived exosomes to increase fibroblast angiogenesis and MEndoT

et al. 2019

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Background: Myocardial fibrosis is a common pathophysiological change in cardiovascular disease, which can cause cardiac dysfunction and even sudden death. Excessively activated fibroblasts proliferate and secret excessive extracellular matrix (ECM) components, resulting in normal cardiac structural damage and cardiac fibrosis. We previously found that human endothelial progenitor cell (EPC)-derived exosomes, after hypoxia/reoxygenation (H/R) induction, could significantly increase the mesenchymal-endothelial transition (MEndoT) compared to normal culture EPC-derived exosomes. Exosomes have been shown to carry different nucleic acids, including microRNAs. However, the effects of microRNAs in EPC-derived exosomes on MEndoT and myocardial fibrosis remain unknown. Methods: EPCs were isolated from human peripheral blood, and fibroblasts were isolated from rat hearts, then transfected with miR-133 inhibitor, si-YBX-1, and ov-YBX-1 into EPCs. After H/R induction for 48 h, isolation and characterization of exosomes derived from human EPCs were performed. Finally, fibroblasts were treated by exosome at 48 h. The expression of miR-133 was measured by qRT-PCR; YBX-1 expression was measured by qRT-PCR and western blot. Angiopoiesis was measured by tube formation assay. Endothelial markers and fibrosis markers were measured by western blot. Results: H/R treatment promoted miR-133 expression in EPCs and EPC-derived exosomes. miR-133 could be incorporated into exosomes and transmitted to cardiac fibroblasts, increasing the angiogenesis and MEndoT of cardiac fibroblasts. miR-133 silencing in H/R-induced EPCs could inhibit miR-133 expression in EPCs and EPCsderived exosomes. miR-133 silencing in H/R-induced EPCs could inhibit the angiogenesis and MEndoT of cardiac fibroblasts and reverse the effect of H/R treatment. Additionally, miR-133 was specially sorted into H/R-induced EPCderived exosomes via YBX-1. YBX-1 silencing inhibited miR-133 transfer and reduced fibroblast angiogenesis and MEndoT. Conclusion: miR-133 was specially sorted into H/R-induced EPC-derived exosomes via YBX-1 to increase fibroblast angiogenesis and MEndoT.

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Section: Discussionmentioning

confidence: 99%

YBX-1 mediated sorting of miR-133 into hypoxia/reoxygenation-induced EPC-derived exosomes to increase fibroblast angiogenesis and MEndoT

et al. 2019

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“…A lot of homing-related genes have been identified, such as CXCR4 [38], IGF2/IGF2R, CXCL12 [39][40][41].…”

Section: Esc/ipsc-ecs Normal Epcs and Ipah-epcs Have Characteristicsmentioning

confidence: 99%

Using human pluripotent stem cell differentiated endothelial cells to study the differential regulation in PAH

Qin¹,

Yang²

2020

Preprint

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Aims Endothelial cells (ECs) have been applied in clinic to treat pulmonary arterial hypertension (PAH), a disease characterized by disordered pulmonary vasculature. However, lack of enough transplantable cells before the deterioration of patient condition is current limitation to apply cell therapy in cardiovascular diseases. So, we thought it necessary to continue to differentiate embryo stem cells (ESCs)/induced-pluripotent stem cells (iPSCs) into endothelial cells (ECs) and identify their characteristics. Methods and results Comparing previous reported methods of human pluripotent cell differentiation toward vascular cells/ Hemogenic Endothelial cells/ endothelial colony-forming cells, we established a highly efficient differentiation protocol to get cells that match phenotype of isolated ECs from health donors. This protocol, including two stages, early mesoderm endothelial progenitor stage and EC marker expression stage. In the first stage, Rock inhibitor Y27632 and DMSO plays an important role in inducing-APLNR + mesoderm and promotes EC differentiation potential; later on SB431542 and BMP4 drives cells toward EC lineage. Meanwhile, an improved protocol with chemically-defined medium (CDM) has similar differentiation efficiency,again demonstrating that a large number of clinically needed cells could be obtained with simple factors. ESC/iPSC-ECs, normal EPCs and IPAH-EPCs have the characteristics of early EPCs marked by CD133 and mesenchymal stem cells. Microarray analysis further revealed IPAH-derived EPCs features of rapid proliferation and weak immune regulation. At last, a model Zebrafish xenograft was utilized to assess the functionality of differentiated ESC/iPSC-ECs. ConclusionsWe established a highly efficient differentiation protocol to get ESC/iPSC-ECs with characteristics of phenotype and molecular matched with early-EPCs from health donors, and revealed the molecular pathogenesis in PAH.

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“…Recent studies have shown that stromal cell-derived factor 1 (SDF-1), also known as CXC motif chemokine 12 (CXCL12), and also CXCR4 signaling pathways may play important roles in hematopoiesis and immunity [18]. In women, estrogen exerts a cardiovascular protective effect on endothelial progenitor cells through estrogen receptor-a (ER-a) and the SDF-1/CXCR4 signaling pathway [19]. CXCL12 and CXCR4 gene polymorphisms are correlated with an increased genetic risk of CAD and the severity of coronary stenosis [19].…”

Section: Introductionmentioning

confidence: 99%

“…In women, estrogen exerts a cardiovascular protective effect on endothelial progenitor cells through estrogen receptor-a (ER-a) and the SDF-1/CXCR4 signaling pathway [19]. CXCL12 and CXCR4 gene polymorphisms are correlated with an increased genetic risk of CAD and the severity of coronary stenosis [19].…”

Section: Introductionmentioning

confidence: 99%

MicroRNA-668-3p Protects Against Oxygen-Glucose Deprivation in a Rat H9c2 Cardiomyocyte Model of Ischemia-Reperfusion Injury by Targeting the Stromal Cell-Derived Factor-1 (SDF-1)/CXCR4 Signaling Pathway

Gao

Liu

2020

Med Sci Monit

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Departmental sources Background: Ischemia-reperfusion injury (IRI) results from the restoration of blood supply to ischemic organs, including the heart. Expression of microRNA-668-3p (miR-668-3p) is known to protect the kidney from IRI. This study aimed to investigate the role of miR-668-3p in oxygen-glucose deprivation (OGD) in a rat H9c2 cardiomyocyte model of IRI. Material/Methods: Rat H9c2 cardiomyocytes were cultured in glucose-free Dulbecco's modified Eagle's medium (DMEM) under anaerobic conditions, followed by oxygenation, to create the OGD model of IRI. The luciferase reporter assay evaluated the interaction between stromal cell-derived factor-1 (SDF-1), or CXC motif chemokine 12 (CXCL12), and miR-668-3p. Protein and mRNA levels of SDF-1, CXCR4, Bcl2, Bax, cleaved caspase-3, endothelial nitric oxide synthase (eNOS), and phosphorylated endothelial nitric oxide synthase (p-eNOS) were analyzed by Western blot and quantitative reverse transcription-polymerase chain reaction (RT-qPCR), and apoptosis were assessed by flow cytometry. Enzyme-linked immunosorbent assay (ELISA) measured reactive oxygen species (ROS), including malondialdehyde (MDA), nitric oxide (NO), p-eNOS, and the inflammatory cytokines, tumor necrosis factor-a (TNF-a), interleukin-1b (IL-1b), IL-6, and monocyte chemoattractant protein-1 (MCP-1) in H9c2 cell supernatants. Results: In the OGD rat H9c2 cardiomyocyte model of IRI, miR-668-3p levels were reduced. Overexpression of miR-668-3p inhibited SDF-1, CXCR4, the expression of inflammatory cytokines, markers of oxidative stress, and p-eNOS. The overexpression of SDF-1 reversed these findings. Overexpression of SDF-1 promoted cell apoptosis, which was reduced by miR-668-3p. Conclusions: In the OGD rat H9c2 cardiomyocyte model of IRI, miR-668-3p suppressed mediators of inflammation and oxidative stress and enhanced cell viability through the SDF-1/CXCR4 signaling pathway.

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17β-estradiol promotes recovery after myocardial infarction by enhancing homing and angiogenic capacity of bone marrow-derived endothelial progenitor cells through ERα-SDF-1/CXCR4 crosstalking

Cited by 22 publications

References 35 publications

YBX-1 mediated sorting of miR-133 into hypoxia/reoxygenation-induced EPC-derived exosomes to increase fibroblast angiogenesis and MEndoT

YBX-1 mediated sorting of miR-133 into hypoxia/reoxygenation-induced EPC-derived exosomes to increase fibroblast angiogenesis and MEndoT

Using human pluripotent stem cell differentiated endothelial cells to study the differential regulation in PAH

MicroRNA-668-3p Protects Against Oxygen-Glucose Deprivation in a Rat H9c2 Cardiomyocyte Model of Ischemia-Reperfusion Injury by Targeting the Stromal Cell-Derived Factor-1 (SDF-1)/CXCR4 Signaling Pathway

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