B-type natriuretic peptide overexpression ameliorates hepatorenal fibrocystic disease in a rat model of polycystic kidney disease
作者： Sara J. Holditch , Claire A. Schreiber , Peter C. Harris , Nicholas F. LaRusso , Marina Ramirez-Alvarado
DOI: 10.1016/J.KINT.2017.02.017
关键词:
摘要: Polycystic kidney disease (PKD) involves progressive hepatorenal cyst expansion and fibrosis, frequently leading to end-stage renal disease. Increased vasopressin cAMP signaling, dysregulated calcium homeostasis, and hypertension play major roles in PKD progression. The guanylyl cyclase A agonist, B-type natriuretic peptide (BNP), stimulates cGMP shows anti-fibrotic, anti-hypertensive, vasopressin-suppressive effects, potentially counteracting pathogenesis. Here, we assessed the impacts of guanylyl activation on PKD progression a rat model PKD. Sustained BNP production significantly reduced weight, cystic indexes concert with suppressed hepatic cystogenesis in vivo . In vitro , decreased epithelial cell proliferation, fibrotic gene expression, and increased intracellular calcium. Together, our data demonstrate multifaceted effects sustained of guanylyl polycystic liver Thus, targeting A-cGMP axis may provide novel therapeutic strategy for fibrocystic diseases.
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