Corin in Natriuretic Peptide Processing and Hypertension

Zhou, Yiqing; Wu, Qingyu

doi:10.1007/s11906-013-0415-7

Cited by 56 publications

(65 citation statements)

References 100 publications

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“…6 Pro-ANP and pro-BNP cardiac transcript levels were not significantly altered at Stage A (4 weeks) or Stage B (7 weeks) in DCM mice vs. controls (Figs. 3A & B).…”

Section: Resultsmentioning

confidence: 91%

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Depressed Corin Levels Indicate Early Systolic Dysfunction Before Increases of Atrial Natriuretic Peptide/B-Type Natriuretic Peptide and Heart Failure Development

et al. 2016

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Dilated cardiomyopathy is a major cause of heart failure that affects millions. Corin cleaves and biologically activates pro-atrial natriuretic peptide (pro-ANP) and pro-B-type natriuretic peptide (pro-BNP). High corin levels reduce the development of systolic dysfunction and heart failure in experimental dilated cardiomyopathy. Yet, patients with significant heart failure unexpectedly show low corin levels with high plasma ANP/BNP levels. Therefore, we examined the relationship between cardiac corin expression, ANP/BNP levels and the stages of heart failure. We used a well-established, dilated cardiomyopathy model to evaluate gene and protein expression as mice longitudinally developed Stages A-D heart failure. Cardiac systolic function (ejection fraction) continuously declined over time (P<0.001). Cardiac corin transcripts were decreased at early Stage B heart failure and remained low through Stages C-D (P<0.001). Cardiac corin levels were positively correlated with systolic function (r=0.96, P=0.003) and inversely with lung water (r=-0.92, P=0.001). In contrast, cardiac pro-ANP/BNP transcripts increased later (Stage C-D) and plasma levels rose only with terminal heart failure (Stage D, P<0.001). Immunoreactive plasma ANP and BNP levels were positively associated with plasma cyclic guanosine monophosphate (cGMP) levels (r=0.82, P=0.01 & r=0.8, P=0.02 respectively). In experimental dilated cardiomyopathy, corin levels declined early with progressive systolic dysfunction before the development of heart failure, while significant increases in plasma ANP, BNP and cGMP levels were found only in later Stage (C, D) heart failure. This dyssynchrony in expression of corin vs. ANP/BNP may impair cleavage-activation of pro-natriuretic peptides and thereby promote the transition from earlier to later stage heart failure.

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“…6 Pro-ANP and pro-BNP cardiac transcript levels were not significantly altered at Stage A (4 weeks) or Stage B (7 weeks) in DCM mice vs. controls (Figs. 3A & B).…”

Section: Resultsmentioning

confidence: 91%

“…6 ANP and BNP activate the guanylyl cyclase/natriuretic peptide receptor A (NPRA) signaling cascade to generate cyclic guanosine monophosphate (cGMP). 7, 8 In experimental DCM, increased corin expression has protective effects, positively modulating plasma cGMP levels, systolic function, myocardial fibrosis, HF and survival.…”

Section: Introductionmentioning

confidence: 99%

Depressed Corin Levels Indicate Early Systolic Dysfunction Before Increases of Atrial Natriuretic Peptide/B-Type Natriuretic Peptide and Heart Failure Development

et al. 2016

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“…Corin is expressed primarily in the heart (3)(4)(5), where it activates atrial natriuretic peptide (ANP), 3 which promotes sodium excretion and vessel relaxation, thereby reducing blood volume and pressure (6 -10). Variants and mutations in the genes encoding corin and ANP have been found in patients with hypertension and heart disease (11)(12)(13)(14)(15)(16)(17)(18)(19), supporting the importance of the corin and ANP pathway in maintaining normal blood pressure and cardiac function. Corin and ANP may also act locally in the pregnant uterus to promote trophoblast invasion and spiral artery remodeling (20 -23), which are critical for regulating maternal blood pressure.…”

mentioning

confidence: 90%

Distinct Roles of N-Glycosylation at Different Sites of Corin in Cell Membrane Targeting and Ectodomain Shedding

Wang

Zhou

Peng

et al. 2015

Journal of Biological Chemistry

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Background: Corin is a transmembrane protease containing 19 predicted N-glycosylation sites. Results: Corin mutants lacking individual N-glycosylation sites were studied for their biosynthesis and processing. Conclusion: N-Glycosylation at different sites plays distinct roles in preventing ectodomain shedding and promoting cell surface targeting and zymogen activation. Significance: The results are important for understanding how corin expression and activity are regulated.

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“…Corin deficiency prevents natriuretic peptide processing and causes hypertension in knockout mice [12, 13]. Corin variants have been found in people with hypertension [14–19]. …”

Section: Introductionmentioning

confidence: 99%

A novel cytoplasmic tail motif regulates mouse corin expression on the cell surface

Zhang

Wang

Dong

et al. 2015

Biochemical and Biophysical Research Communications

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Type II transmembrane serine proteases (TTSPs) are important in many biological processes. Cell surface expression is critical for TTSP activation and function. To date, the mechanism underlying TTSP cell surface expression is poorly understood. Corin is a TTSP and acts as the pro-atrial natriuretic peptide convertase that is essential for sodium homeostasis and normal blood pressure. In this study, we investigated how cytoplasmic tail sequences may regulate corin expression and activation on the cell surface. By site-directed mutagenesis, we made mouse corin proteins with truncations or point-mutations in the cytoplasmic tail. We expressed the mutants in transfected HEK293 cells and analyzed corin cell surface expression and activation by Western blotting and flow cytometry. We found that corin truncation mutants lacking a Lys-Phe-Gln sequence at residues 71–73 had higher levels of cell surface expression and activation compared with that in wild-type corin. When Lys-71, Phe-72 and Gln-73 residues were mutated together, but not individually, in corin with the full-length cytoplasmic tail, increased levels of cell surface expression and zymogen activation were also observed. These results indicate that residues Lys-71, Phe-72 and Gln-73 serve as a novel retention motif in the intracellular pathway to regulate corin cell surface expression and activation.

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Corin in Natriuretic Peptide Processing and Hypertension

Cited by 56 publications

References 100 publications

Depressed Corin Levels Indicate Early Systolic Dysfunction Before Increases of Atrial Natriuretic Peptide/B-Type Natriuretic Peptide and Heart Failure Development

Depressed Corin Levels Indicate Early Systolic Dysfunction Before Increases of Atrial Natriuretic Peptide/B-Type Natriuretic Peptide and Heart Failure Development

Distinct Roles of N-Glycosylation at Different Sites of Corin in Cell Membrane Targeting and Ectodomain Shedding

A novel cytoplasmic tail motif regulates mouse corin expression on the cell surface

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