Renal Corin Is Essential for Normal Blood Pressure and Sodium Homeostasis

Zhou, Tiantian; Zhang, Shengnan; Du, Chunyu; Wang, Kun; Gu, Xiabing; Sun, Shujun; Zhang, Xianrui; Niu, Yayan; Wang, Can; Li, Meng; Dong, Ningzheng; Wu, Qingyu

doi:10.3390/ijms231911251

Cited by 8 publications

(18 citation statements)

References 87 publications

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“…45 Renal corin function increases natriuresis during excessive salt ingestion in mice. 46 Black CORIN gene variants did not affect NP expression, circulating NP levels, BP, or hypertension in candidate gene analysis. Underrepresented populations require more research on CV genetics.…”

Section: Recent Studiesmentioning

confidence: 80%

Role of Corin in Cardiovascular Disease

Askin,

Poyraz

2023

Cor Vasa

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Transmembránová serinová proteáza II. typu corin, která se vyskytuje ve významném množství v srdci, aktivuje natriuretické peptidy. Do oběhu je corin uvolňován z myocytů. Cirkulující solubilní corin je spojen s hypertenzí, srdečním selháním, infarktem myokardu, preeklampsií i s cévními mozkovými příhodami. Naše výsledky naznačují, že solubilní corin může fungovat jako senzitivní a specifi cký biomarker predikující riziko rozvoje kardiovaskulárních onemocnění (KVO). Cirkulující solubilní corin lze bohužel obtížně použít v klinické praxi. Tento přehled shrnuje výsledky nejnovějších studií zkoumajících souvislost mezi corinem a KVO a naznačuje směry dalšího výzkumu s cílem zpřesnit predikci rizika, prognózu a farmakoterapii KVO a podpořit jeho rutinní stanovování v rámci laboratorního vyšetření.

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Section: Recent Studiesmentioning

confidence: 80%

Role of Corin in Cardiovascular Disease

Askin,

Poyraz

2023

Cor Vasa

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“…The strain of the Corin KO mice was published ( 17 , 47 ). Briefly, two loxP loci were inserted in the Corin gene, flanking exon 4, to generate Cor flox mice, which were crossed with CMV-Cre mice expressing Cre in all tissues.…”

Section: Methodsmentioning

confidence: 99%

“…Briefly, two loxP loci were inserted in the Corin gene, flanking exon 4, to generate Cor flox mice, which were crossed with CMV-Cre mice expressing Cre in all tissues. The resultant mice with the null Corin allele were verified by DNA genotyping and analysis of Corin mRNA and protein expression by RT-PCR and western blotting, respectively ( 17 , 47 ). The Corin KO mice were hypertensive [systolic blood pressure: ∼118 vs. ∼107 mm Hg in wild-type (WT) mice] and bred into the C57BL/6J background, as reported previously ( 17 , 47 ).…”

Section: Methodsmentioning

confidence: 99%

“…The resultant mice with the null Corin allele were verified by DNA genotyping and analysis of Corin mRNA and protein expression by RT-PCR and western blotting, respectively ( 17 , 47 ). The Corin KO mice were hypertensive [systolic blood pressure: ∼118 vs. ∼107 mm Hg in wild-type (WT) mice] and bred into the C57BL/6J background, as reported previously ( 17 , 47 ). High levels of blood pressure in the Corin KO mice remained similar at different ages ( Supplementary Figure S1 ).…”

Section: Methodsmentioning

confidence: 99%

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Corin deficiency impairs cardiac function in mouse models of heart failure

Niu

Zhou

Zhang

et al. 2023

Front. Cardiovasc. Med.

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IntroductionCorin is a protease in the natriuretic peptide system. Deleterious CORIN variants are associated with hypertension and heart disease. It remains unclear if and to what extent corin deficiency may contribute to heart failure (HF).MethodsCorin knockout (KO) mice were used as a model. Cardiac function was assessed by echocardiography and tissue analysis in Corin KO mice at different ages or subjected to transverse aortic constriction (TAC), which increased pressure overload. Heart and lung tissues were analyzed for cardiac hypertrophy and lung edema using wheat germ agglutinin, Sirius red, Masson's trichrome, and Prussian blue staining. Recombinant corin was tested for its effect on cardiac function in the TAC-operated Corin KO mice. Selected gene expression in the heart was examined by RT-PCR. ELISA was used to analyze factors in plasma.ResultsCorin KO mice had progressive cardiac dysfunction with cardiac hypertrophy and fibrosis after 9 months of age, likely due to chronic hypertension. When Corin KO mice were subjected to TAC at 10–12 weeks of age, cardiac function decreased more rapidly than in similarly treated wild-type mice. When the TAC-operated Corin KO mice were treated with recombinant corin protein, cardiac dysfunction, hypertrophy, and fibrosis were ameliorated. The corin treatment also decreased the gene expression associated with cardiac hypertrophy and fibrosis, increased plasma cGMP levels, lowered plasma levels of N-terminal pro-atrial natriuretic peptide, angiotensin II, and aldosterone, and lessened lung edema in the Corin KO mice subjected to TAC.ConclusionCorin deficiency impairs cardiac function and exacerbates HF development in mice. Corin protein may be used to reduce cardiac hypertrophy and fibrosis, suppress the renin-angiotensin-aldosterone system, and improve cardiac function in HF.

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“…In th cellular region, there are two frizzled domains, eight LDLR class-A repeats, an SR main, and a C-terminal protease domain (Figure 1). Corin-mediated pro-ANP c occurs not only in the heart, but also in non-cardiac tissues, including the kidne and uterus [114,116,117]. Disruption of the Corin gene prevents pro-ANP proce mice, causing salt-sensitive hypertension that is also observed in ANP KO mice mans, dysfunctional CORIN variants are associated with impaired pro-ANP pro and hypertensive diseases [40,[118][119][120][121].…”

Section: Corin In Pro-anp Processingmentioning

confidence: 99%

Type II Transmembrane Serine Proteases as Modulators in Adipose Tissue Phenotype and Function

Zhang

et al. 2023

Biomedicines

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Adipose tissue is a crucial organ in energy metabolism and thermoregulation. Adipose tissue phenotype is controlled by various signaling mechanisms under pathophysiological conditions. Type II transmembrane serine proteases (TTSPs) are a group of trypsin-like enzymes anchoring on the cell surface. These proteases act in diverse tissues to regulate physiological processes, such as food digestion, salt-water balance, iron metabolism, epithelial integrity, and auditory nerve development. More recently, several members of the TTSP family, namely, hepsin, matriptase-2, and corin, have been shown to play a role in regulating lipid metabolism, adipose tissue phenotype, and thermogenesis, via direct growth factor activation or indirect hormonal mechanisms. In mice, hepsin deficiency increases adipose browning and protects from high-fat diet-induced hyperglycemia, hyperlipidemia, and obesity. Similarly, matriptase-2 deficiency increases fat lipolysis and reduces obesity and hepatic steatosis in high-fat diet-fed mice. In contrast, corin deficiency increases white adipose weights and cell sizes, suppresses adipocyte browning and thermogenic responses, and causes cold intolerance in mice. These findings highlight an important role of TTSPs in modifying cellular phenotype and function in adipose tissue. In this review, we provide a brief description about TTSPs and discuss recent findings regarding the role of hepsin, matriptase-2, and corin in regulating adipose tissue phenotype, energy metabolism, and thermogenic responses.

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Renal Corin Is Essential for Normal Blood Pressure and Sodium Homeostasis

Cited by 8 publications

References 87 publications

Role of Corin in Cardiovascular Disease

Role of Corin in Cardiovascular Disease

Corin deficiency impairs cardiac function in mouse models of heart failure

Type II Transmembrane Serine Proteases as Modulators in Adipose Tissue Phenotype and Function

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