ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2011
Relaxin causes selective outward remodeling of brain parenchymal arterioles via activation of peroxisome proliferator-activated receptor-γ.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 51 citations in OpenAlex.
- Altered Cerebral Blood Flow and Potential Neuroprotective Effect of Human Relaxin-2 (Serelaxin) During Hypoxia or Severe Hypovolemia in a Sheep Model.International journal of molecular sciences · 2020Article
- Plasticity of the Maternal Vasculature During Pregnancy.Annual review of physiology · 2019Review
- The importance of comorbidities in ischemic stroke: Impact of hypertension on the cerebral circulation.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2018Review
- Impaired function of cerebral parenchymal arterioles in experimental preeclampsia.Microvascular research · 2018Article
- Targeting the Relaxin Pathway for Liver Disease Treatment.European medical journal. Hepatology · 2018Article
- The relaxin peptide family - potential future hope for neuroprotective therapy? A short review.Neural regeneration research · 2018Review
- Relaxin as a Therapeutic Target for the Cardiovascular Complications of Diabetes.Frontiers in pharmacology · 2018Review
- Vascular actions of relaxin: nitric oxide and beyond.British journal of pharmacology · 2017Review
- Serelaxin treatment reverses vascular dysfunction and left ventricular hypertrophy in a mouse model of Type 1 diabetes.Scientific reports · 2017Article
- Novel Anti-fibrotic Therapies.Frontiers in pharmacology · 2017Review
- Enhanced serelaxin signalling in co-cultures of human primary endothelial and smooth muscle cells.British journal of pharmacology · 2016Article
- Differential effects of relaxin deficiency on vascular aging in arteries of male mice.Age (Dordrecht, Netherlands) · 2015Article
- The cerebral circulation during pregnancy: adapting to preserve normalcy.Physiology (Bethesda, Md.) · 2015Review
- Relaxin activates peroxisome proliferator-activated receptor γ (PPARγ) through a pathway involving PPARγ coactivator 1α (PGC1α).The Journal of biological chemistry · 2015Article
- International Union of Basic and Clinical Pharmacology. XCV. Recent advances in the understanding of the pharmacology and biological roles of relaxin family peptide receptors 1-4, the receptors for relaxin family peptides.Pharmacological reviews · 2015Review
- Acute intravenous injection of serelaxin (recombinant human relaxin-2) causes rapid and sustained bradykinin-mediated vasorelaxation.Journal of the American Heart Association · 2014Article
- Localization of relaxin receptors in arteries and veins, and region-specific increases in compliance and bradykinin-mediated relaxation after in vivo serelaxin treatment.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2014Article
- Article
- Treatment for cerebral small vessel disease: effect of relaxin on the function and structure of cerebral parenchymal arterioles during hypertension.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2013Article
- Vasotrophic regulation of age-dependent hypoxic cerebrovascular remodeling.Current vascular pharmacology · 2013Review
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Brain parenchymal arterioles (PAs), but not pial arteries, undergo hypotrophic outward remodeling during pregnancy that involves peroxisome proliferator-activated receptor-γ (PPARγ) activation. Relaxin, a peptide hormone produced during pregnancy, is involved in systemic and renal artery remodeling and activates PPARγ in vitro. Thus, we hypothesized that relaxin is involved in the selective outward remodeling of PAs through a PPARγ-dependent mechanism. Nonpregnant rats were treated with relaxin (4 μg/h, osmotic minipump), relaxin plus PPARγ inhibitor GW9662 (10 mg/kg/d), or vehicle for 10 d. Vascular function and structure were compared in isolated and pressurized middle cerebral arteries (MCAs) and PAs taken from the same animals. Relaxin treatment increased serum relaxin to the level of pregnancy (54 ng/ml) and increased passive wall thickness (hypertrophy; 70 ± 5 vs. 54 ± 4 μm in vehicle; P<0.05) and inner diameter (outward remodeling; 10.6 ± 0.5 vs. 8.0 ± 0.6 μm in vehicle; P<0.05) in PAs, but not in MCAs. This hypertrophic outward remodeling was prevented by GW9662 that had diameters (57 ± 3 μm) and wall thickness (8.6 ± 1.0 μm) similar to vehicle. GW9662 also prevented relaxin-induced changes in PPARγ target gene expression. These results suggest that relaxin produced during pregnancy may be partly responsible for selective remodeling of PAs during pregnancy through a mechanism involving PPARγ
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