Urotensin II Induces Migration of Endothelial Progenitor Cells via Activation of the RhoA/Rho Kinase Pathway

Xu, Shixin; Jiang, Hong; Wu, Bing; Yang, Jian; Chen, Sisi

doi:10.1620/tjem.219.283

Cited by 21 publications

(24 citation statements)

References 25 publications

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“…Many signaling pathways, such as P38 MAPK (Tang et al 2011), Notch/Jagged1 (Ii et al 2010), and RhoA/Rock (Xu et al 2009), influence the differentiation and biological functions of EPCs. Whether PIN-induced regulation of EPCs involves other signaling pathways remains to be investigated.…”

Section: Discussionmentioning

confidence: 99%

Pinocembrin, a major flavonoid in propolis, improves the biological functions of EPCs derived from rat bone marrow through the PI3K-eNOS-NO signaling pathway

et al. 2012

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The number and quality of endothelial progenitor cells (EPCs) are damaged to varying degrees in patients at risk for developing atherosclerosis. The improvement of the quantity and functions of EPCs can enhance repair of injured endothelial monolayer resulting in inhibiting atherosclerosis. The purpose of this study was to investigate the effect of pinocembrin (PIN), a major flavonoid in propolis on the differentiation and biological functions of EPCs and the potential mechanisms of these effects. Flow cytometry analysis revealed that PIN treatment increased the number of CD34? , CD133 ?

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Section: Discussionmentioning

confidence: 99%

Pinocembrin, a major flavonoid in propolis, improves the biological functions of EPCs derived from rat bone marrow through the PI3K-eNOS-NO signaling pathway

et al. 2012

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“…EPCs were isolated from male Sprague-Dawley rats weighing 120-160 g provided by the Experimental Animal Center of Wuhan University, as previously described (4,6). The University of Wuhan's Animal Ethics Committee approved all animal procedures.…”

Section: Methodsmentioning

confidence: 99%

“…Isolation and characterization of EPCs and confirmation of endothelial cell lineage were performed as previously described (4). Fluorescent chemical detection of EPCs was performed on attached EPCs after 7 days in culture.…”

Section: Urotensin II Promotes the Proliferation Of Endothelial Progementioning

confidence: 99%

“…mRNA for GPR14 is widely expressed in cardiovascular tissues, including myocytes, vascular smooth muscle cells (VMSCs) and endothelial cells (ECs) (1,3), as well as in endothelial progenitor cells (EPCs) (1,4). UII has been observed to be highly expressed in cardiovascular tissues and atherosclerotic plaque (3).…”

Section: Introductionmentioning

confidence: 99%

“…A previous study showed that EPCs express the UII receptor and UII induces the migration of EPCs in a dose-response manner. Moreover, the chemotactic effect of UII is mediated via activation of the RhoA/Rho kinase pathway (4). In this study, we examined the potential proliferation function of UII in EPCs and the role of mitogenactivated protein kinase (MAPK) signaling in this process.…”

Section: Introductionmentioning

confidence: 99%

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Urotensin II promotes the proliferation of endothelial progenitor cells through p38 and p44/42 MAPK activation

Wen

Jiang

2012

Mol Med Report

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Abstract. Urotensin II (UII) is a vasoactive peptide with many potent effects in the cardiorenovascular system and is also possibly involved in the pathogenesis of atherosclerosis. Endothelial progenitor cells (EPCs) are involved in angiogenesis and vascular homeostasis and may be important in the maintenance of endothelial integrity. The aim of this study was to investigate whether UII has an effect on the proliferation of bone marrow-derived EPCs and the possible signaling mechanisms involved. Bone marrow-derived EPCs were isolated from male Sprague-Dawley rats and cultured in medium containing 5% fetal bovine serum. Cells were incubated with UII for 24 h. The proliferation of EPCs was analyzed by MTT assay. Western blotting was performed to determine the phosphorylation levels of mitogen-activated protein kinases (MAPKs). The results demonstrated that UII promoted the proliferation of EPCs in a concentrationdependent manner in a certain range, and the proliferation was largely suppressed by inhibitors of GPR14 and MAPKs (p38 and p44/42). UII significantly increased the phosphorylation levels of p38MAPK and p44/42MAPK, and these effects were significantly inhibited by respective inhibitors. These findings indicate that UII promotes the proliferation of rat bone marrow-derived EPCs through a process that involves MAPK activation, and provides novel insights regarding the role of UII in the EPC-mediated repair of atherosclerotic injury.

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Inhibition of U‐II/UT signaling ameliorates cystitis‐associated bladder hyperactivity by targeting the RhoA/Rho‐kinase pathway

Liu

Sun

et al. 2022

The Kaohsiung J of Med Scie

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Urotensin II (U‐II) and its receptor (UT) are involved in the pathogenesis of various diseases; however, their association with the development of cystitis has not been elucidated. The present study was designed to investigate the functional role of U‐II/UT signaling in cyclophosphamide (CYP)‐induced cystitis. A total of 60 female rats were randomly divided into the control and CYP‐treated groups. Intraperitoneal injection of CYP successfully induced cystitis in rats of the CYP‐treated group. The protein and mRNA expression levels of U‐II and UT were significantly enhanced in rat bladder tissues of the CYP‐treated group. Furthermore, the results of the immunofluorescence staining analysis demonstrated that CYP treatment apparently increased the expression levels of UT in the urothelium layer, detrusor smooth muscle, and bladder interstitial Cajal‐like cells. The selective antagonist of UT, SB657510 (10 μm), significantly suppressed the CYP‐induced increase in the spontaneous contractions of muscle strips and ameliorated the bladder hyperactivity of CYP‐treated rats. Moreover, CYP treatment significantly increased the protein expression levels of Ras homolog family member (Rho) A and Rho‐associated protein kinase 2 in rat bladder tissues. Following pretreatment with the Rho‐kinase inhibitor Y‐27632 (10 μm), the inhibitory effects of SB657510 (10 μm) on the spontaneous contractions of muscle strips were eliminated. In conclusion, the results of the present study suggested that activation of U‐II/UT signaling promoted the development of cystitis‐associated‐bladder hyperactivity by targeting the RhoA/Rho‐kinase pathway, indicating that the U‐II/UT signaling could serve as a novel target for the treatment of interstitial cystitis/bladder pain syndrome.

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Urotensin II Induces Migration of Endothelial Progenitor Cells via Activation of the RhoA/Rho Kinase Pathway

Cited by 21 publications

References 25 publications

Pinocembrin, a major flavonoid in propolis, improves the biological functions of EPCs derived from rat bone marrow through the PI3K-eNOS-NO signaling pathway

Pinocembrin, a major flavonoid in propolis, improves the biological functions of EPCs derived from rat bone marrow through the PI3K-eNOS-NO signaling pathway

Urotensin II promotes the proliferation of endothelial progenitor cells through p38 and p44/42 MAPK activation

Inhibition of U‐II/UT signaling ameliorates cystitis‐associated bladder hyperactivity by targeting the RhoA/Rho‐kinase pathway

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