Epoetin Alfa and Its Nonerythropoietic Derivative, Carbamylerythropoietin, Stimulate Chemotaxis of Circulating Endothelial Progenitor Cells via Intracellular Nitric Oxide Production.

Schuler, Anna; Beem, Elaine; Sautina, Laura; Zharikov, Sergey; Segal, Mark S.

doi:10.1097/00042871-200701010-00777

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“…To determine whether stimulation of NO underlies the chemotactic effect of relaxin on BMDECs, we inhibited NOS with 10M of the arginine analog L-NAME, a low concentration that does not lower basal levels of NO but effectively blocks agonistinduced increases in NO. 18 The ability of relaxin to stimulate chemotaxis was blocked by low-level L-NAME, but importantly the basal level of migration was unaffected by these low levels of L-NAME ( Figure 2G). …”

Section: Relaxin Stimulates No In Human Cd34 ؉ Bmdecs Via Pi3k/aktmentioning

confidence: 95%

Relaxin increases human endothelial progenitor cell NO and migration and vasculogenesis in mice

Segal¹,

Sautina²,

Li³

et al. 2012

Blood

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The ovarian peptide hormone, relaxin, circulates during pregnancy, contributing to profound maternal vasodilation through endothelial and nitric oxide (NO)-dependent mechanisms. Circulating numbers of bone marrow-derived endothelial cells (BMDECs), which facilitate angiogenesis and contribute to repair of vascular endothelium, increase during pregnancy. Thus, we hypothesized that relaxin enhances BMDEC NO production, circulating numbers, and function. Recombinant human relaxin-2 (rhRLX) stimulated PI3K/Akt B-dependent NO production in human BMDECs within minutes, and activated BMDEC migration that was inhibited by L-N G -nitroarginine methyl ester. In BMDECs isolated from relaxin/ insulin-like family peptide receptor 2 gene (Rxfp2) knockout and wild-type mice, but not Rxfp1 knockout mice, rhRLX rapidly increased NO production. Similarly, rhRLX increased circulating BMDEC number in Rxfp2 knockout and wild-type mice, but not Rxfp1 knockout mice as assessed by colony formation and flow cytometry. IntroductionDramatic changes in systemic and renal hemodynamics occur during pregnancy. There is a marked decrease in systemic vascular resistance and reciprocal increases in cardiac output and global arterial compliance, accompanied by a modest decline in mean arterial pressure. The renal circulation participates in this maternal vasodilatory response; consequently, renal plasma flow and glomerular filtration rate rise by 80% and 50%, respectively. Although understanding of the mechanisms underlying these maternal adaptations to pregnancy is incomplete, there is increasing evidence that the ovarian peptide hormone relaxin plays a key role. 1 Originally isolated from the ovary by Hisaw, 2 relaxin was named for its ability to relax the pubis symphysis in some species. In nonhuman primates, it was subsequently shown by the same investigators to cause morphologic changes in endothelial cells of endometrial blood vessels consistent with hypertrophy and hyperplasia, and enlargement of arterioles and capillaries. 3 Humans have 3 relaxin genes, designated relaxin-1, -2, and -3. 4 Rats and mice each have 2 relaxin genes designated relaxin-1 and -3. Human relaxin-2, as well as rat and mouse relaxin-1 gene products, are true orthologs, insofar as they are secreted by the corpus luteum during pregnancy and circulate. Humans, rats, and mice have 1 relaxin receptor, the LGR7 (leucine rich repeat-containing G protein coupled) receptor recently renamed relaxin/insulin-like family peptide 1 receptor, RXFP1. Although human relaxin may also bind to the LGR8 receptor (RXFP2), albeit with reduced affinity, 5 the preferred ligand for RXFP2 is insulin-like 3 (INSL3). Recently, 2 new receptors have been described for relaxin-3, GPCR135 and 142, 6 although GPCR142 is a pseudogene in rats.Infusion of recombinant human relaxin-2 (rhRLX) in nonpregnant conscious female and male rats significantly decreases renal and systemic vascular resistances, and increases cardiac output, renal blood flow, glomerular filtration, and global arterial compliance, ...

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Section: Relaxin Stimulates No In Human Cd34 ؉ Bmdecs Via Pi3k/aktmentioning

confidence: 95%

Relaxin increases human endothelial progenitor cell NO and migration and vasculogenesis in mice

Segal¹,

Sautina²,

Li³

et al. 2012

Blood

View full text Add to dashboard Cite

show abstract

Epoetin Alfa and Its Nonerythropoietic Derivative, Carbamylerythropoietin, Stimulate Chemotaxis of Circulating Endothelial Progenitor Cells via Intracellular Nitric Oxide Production.

Cited by 1 publication

References 0 publications

Relaxin increases human endothelial progenitor cell NO and migration and vasculogenesis in mice

Relaxin increases human endothelial progenitor cell NO and migration and vasculogenesis in mice

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