Relaxin—a pleiotropic hormone and its emerging role for experimental and clinical therapeutics

Dschietzig, Thomas; Bartsch, Cornelia; Baumann, Gert; Stangl, Karl

doi:10.1016/j.pharmthera.2006.03.004

Cited by 97 publications

(84 citation statements)

References 232 publications

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“…Locally produced relaxin may affect in an autocrine or paracrine way processes such as proliferation, fluid secretion, and NO synthesis. Relaxin is a 6 kDa peptide that is produced in a way similar to insulin from a preprohormone (for review, see Dschietzig et al (2006)). There is evidence that the relaxin precursors are as active as the mature peptide (Soloff et al 1992, Zarreh-Hoshyari-Khah et al 2001.…”

Section: Discussionmentioning

confidence: 99%

“…6A), but no significant changes were observed in Mmp2 (NZ4) and Mmp9 (NZ5), even with shorter (30 min) or longer (240 min) incubation periods, and higher relaxin concentration (500 ng/ml; not shown). As relaxin is known to increase nitric oxide (NO) production in several tissues (Dschietzig et al 2006), we tested its effect on the inducible nitric oxide synthase 2 (Nos2) of the vas deferens. Relaxin caused a significant increase in the mRNA levels for Nos2 (P!0.05, NZ5, Fig.…”

Section: Localization Of Relaxin In the Testis And Effect Of Relaxin mentioning

confidence: 99%

“…Relaxin has a wide spectrum of actions (Sherwood 2004, Dschietzig et al 2006. Its role in female reproduction is well known: relaxin is important during pregnancy and in preparation for parturition (Sherwood 2004), and it stimulates growth of the uterus in prepubertal animals (Bagnell et al 1993, Yan et al 2006.…”

Section: Introductionmentioning

confidence: 99%

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Locally produced relaxin may affect testis and vas deferens function in rats

Cardoso¹,

Nascimento²,

Royer³

et al. 2010

Reproduction

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We have previously shown that the rat testis and vas deferens contain high levels of the relaxin receptor, RXFP1. The present study was undertaken to determine the expression of relaxin in these tissues, and the effect of exogenous relaxin on Sertoli cell proliferation and on the mRNA levels of some proteins that may contribute to epithelial secretion and tissue reorganization in the vas deferens. Relaxin mRNA levels in testis and vas deferens were much lower than in the prostate. Sertoli cells seem to be an important source of relaxin mRNA in testis. Relaxin immunoreactivity was detected in the seminiferous epithelium but not in the interstitial compartment. The relaxin precursor was expressed in the vas deferens, and relaxin immunoreactivity was detected in apical cells of the vas deferens. Castration, but not treatment with the anti-estrogen ICI 182,780, dramatically reduced relaxin mRNA levels in the prostate and vas deferens, and this effect was prevented by testosterone. Rxfp1 mRNA levels in the vas deferens and prostate were not affected by castration or treatment with ICI 182,780. Exogenous relaxin increased the incorporation of 3 H-thymidine in cultured Sertoli cells, and treatment of the vas deferens with 100 ng/ml relaxin increased the mRNA levels for the cystic fibrosis chloride channel (cystic fibrosis transmembrane regulator) about three times, and doubled mRNA levels for the inducible form of nitric oxide synthase and metalloproteinase 7. These results suggest that locally produced relaxin acts as an autocrine or paracrine agent in the testis and vas deferens to affect spermatogenesis and seminal fluid composition.

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Section: Discussionmentioning

confidence: 99%

Section: Localization Of Relaxin In the Testis And Effect Of Relaxin mentioning

confidence: 99%

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Locally produced relaxin may affect testis and vas deferens function in rats

Cardoso¹,

Nascimento²,

Royer³

et al. 2010

Reproduction

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“…[6][7][8][9][10] Relaxin has been shown to inhibit the collagen-promoting actions of transforming growth factor-b1 (TGF-b1) and angiotensin II in rat cardiac fibroblasts, 11 and was more recently shown to inhibit TGF-b1 signaling through stimulation of the nitric oxide (NO) pathway to inhibit Smad2 phosphorylation. 12 Of further significance are the findings that relaxin also stimulates vasodilation and coronary flow via NO signaling, increases angiogenesis by upregulating vascular endothelial growth factor and basic fibroblast growth factor [6][7][8][13][14][15] and inhibits cardiomyocyte apoptosis by altering the Bcl2/Bax ratio; 16 promoting its therapeutic potential.…”

mentioning

confidence: 99%

Relaxin remodels fibrotic healing following myocardial infarction

Samuel

Cendrawan

Gao

et al. 2011

Laboratory Investigation

101

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In the setting of myocardial infarction (MI), implanted stem cell viability is low and scar formation limits stem cell homing, viability, and integration. Thus, interventions that favorably remodel fibrotic healing may benefit stem cell therapies. However, it remains unclear whether it is feasible and safe to remodel fibrotic healing post-MI without compromising ventricular remodeling and dysfunction. This study, therefore, determined the anti-fibrotic and other effects of the hormone, relaxin in a mouse model of MI. Adult male mice underwent left coronary artery ligation-induced MI and were immediately treated with recombinant human relaxin (MI þ RLX) or vehicle (MI þ VEH) over 7 or 30 days, representing time points of early and mature fibrotic healing. Cardiac function was assessed by echocardiography and catheterization, while comprehensive immunohistochemistry, morphometry, and western blotting were performed to explore the relaxin-induced mechanisms of action post-MI. RLX significantly inhibited the MI-induced progression of cardiac fibrosis over 7 and 30 days, which was associated with a reduction in TGF-b1 expression, myofibroblast differentiation, and cardiomyocyte apoptosis in addition to a promotion of matrix metalloproteinase-13 levels and de novo blood vessel growth (all Po0.05 vs respective measurements from MI þ VEH mice). Despite the evident fibrotic healing post-MI, relaxin did not adversely affect the incidence of ventricular free-wall rupture or the extent of LV remodeling and dysfunction. These combined findings demonstrate that RLX favorably remodels the process of fibrotic healing post-infarction by lowering the density of mature scar tissue in the infarcted myocardium, border zone, and non-infarcted myocardium, and may, therefore, facilitate cell-based therapies in the setting of ischemic heart disease.

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“…Do niedawna ten polipeptydowy hormon kojarzony był wyłącznie z funkcjonowaniem żeńskiego systemu rozrodczego. Tymczasem, od początku lat osiemdziesiątych, zaczęto dostrzegać jego plejotropowy charakter [2,3]. Oznacza to, że relaksyna 2 posiada wielokierunkowe działanie na tkanki reprodukcyjne jak i inne.…”

Section: Wprowadzenieunclassified

Relaxin 2 – a pregnancy hormone involved in the process of carcinogenesis

Domińska¹

2013

Ginekol Pol

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Streszczenie Relaksyna 2 jest polipeptydem o budowie podobnej do insuliny i insulino-podobnych czynników wzrostu (IGFs). Hormon ten nie wchodzi jednak w interakcje z receptorami insulinowymi Słowa kluczowe: relaksyna 2 / nowotworzenie / LGR7 / LGR8 / Abstract Relaxin 2 is a polypeptide hormone structurally related to insulin and insulin-like growth factors (IGFs). However, it does not interact with insulin receptors and has a decidedly different biological properties. Relaxin 2 activates LGR 7 and LGR 8 relaxin receptors, that belong to the leucine-rich repeat-containing (LRR),

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Relaxin—a pleiotropic hormone and its emerging role for experimental and clinical therapeutics

Cited by 97 publications

References 232 publications

Locally produced relaxin may affect testis and vas deferens function in rats

Locally produced relaxin may affect testis and vas deferens function in rats

Relaxin remodels fibrotic healing following myocardial infarction

Relaxin 2 – a pregnancy hormone involved in the process of carcinogenesis

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