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Putative endothelial progenitor cells do not promote vascular repair but attenuate pericyte-myofibroblast transition in UUO-induced renal fibrosis

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单位: [1]Huazhong Univ Sci & Technol, Tongji Med Coll, Tongji Hosp, Dept Nephrol, 1095 Jiefang Ave, Wuhan 430030, Hubei, Peoples R China [2]Huazhong Univ Sci & Technol, Tongji Med Coll, Tongji Hosp, Dept Nutr, 1095 Jiefang Ave, Wuhan 430030, Hubei, Peoples R China [3]Fifth Hosp Wuhan, Dept Nephrol, 122 Xianzheng Ave, Wuhan 430050, Hubei, Peoples R China
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关键词: Putative endothelial progenitor cells Microvesicles Renal fibrosis Pericyte-myofibroblast transition

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Background: Putative endothelial progenitor cells (pEPCs) have been confirmed to participate in alleviation of renal fibrosis in several ischaemic diseases. However, their mechanistic effect on renal fibrosis, which is characterized by vascular regression and further rarefaction-related pathology, remains unknown. Methods: To explore the effect and molecular mechanisms by which pEPCs act on unilateral ureteral obstruction (UUO)-induced renal fibrosis, we isolated pEPCs from murine bone marrow. In vivo, pEPCs (2x10(5) cells/day) and pEPC-MVs (microvesicles) were injected into UUO mice via the tail vein. In vitro, pEPCs were co-cultured with renal-derived pericytes. Pericyte-myofibroblast transition was evaluated using the myofibroblast marker alpha-smooth muscle actin (alpha-SMA) and pericyte marker platelet-derived growth factor receptor beta (PDGFR-beta). Results: Exogenous supply of bone marrow-derived pEPCs attenuated renal fibrosis by decreasing pericyte-myofibroblast transition without significant vascular repair in the UUO model. Our results indicated that pEPCs regulated pericytes and their transition into myofibroblasts via pEPC-MVs. Co-culture of pericytes with pEPCs in vitro suggested that pEPCs inhibit transforming growth factor-beta (TGF-beta)-induced pericyte-myofibroblast transition via a paracrine pathway. Conclusionp: EPCs effectively attenuated UUO-induced renal fibrosis by inhibiting pericyte-myofibroblast transition via a paracrine pathway, without promoting vascular repair.

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出版当年[2018]版:
大类 | 2 区 医学
小类 | 2 区 医学:研究与实验 3 区 细胞生物学
最新[2025]版:
大类 | 2 区 医学
小类 | 2 区 细胞与组织工程 2 区 细胞生物学 2 区 医学:研究与实验
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出版当年[2017]版:
Q1 MEDICINE, RESEARCH & EXPERIMENTAL Q2 CELL BIOLOGY
最新[2024]版:
Q1 CELL & TISSUE ENGINEERING Q1 CELL BIOLOGY Q1 MEDICINE, RESEARCH & EXPERIMENTAL

影响因子: 最新[2024版] 最新五年平均 出版当年[2017版] 出版当年五年平均 出版前一年[2016版] 出版后一年[2018版]

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第一作者单位: [1]Huazhong Univ Sci & Technol, Tongji Med Coll, Tongji Hosp, Dept Nephrol, 1095 Jiefang Ave, Wuhan 430030, Hubei, Peoples R China
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通讯机构: [1]Huazhong Univ Sci & Technol, Tongji Med Coll, Tongji Hosp, Dept Nephrol, 1095 Jiefang Ave, Wuhan 430030, Hubei, Peoples R China [2]Huazhong Univ Sci & Technol, Tongji Med Coll, Tongji Hosp, Dept Nutr, 1095 Jiefang Ave, Wuhan 430030, Hubei, Peoples R China
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