Regulation of CFTR Expression and Arginine Vasopressin Activity Are Dependent on Polycystin-1 in Kidney-Derived Cells | Zendy

Carolina Monteiro de Lemos Barbosa | Zendy; Jackson SouzaMenezes | Zendy; Andressa G. Amaral | Zendy; Luiz F. Onuchic | Zendy; Liudmila Cebotaru | Zendy; William B. Guggino | Zendy; Marcelo M. Morales | Zendy

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Regulation of CFTR Expression and Arginine Vasopressin Activity Are Dependent on Polycystin-1 in Kidney-Derived Cells

Author(s) -

Carolina Monteiro de Lemos Barbosa,

Jackson SouzaMenezes,

Andressa G. Amaral,

Luiz F. Onuchic,

Liudmila Cebotaru,

William B. Guggino,

Marcelo M. Morales

Publication year - 2016

Publication title -

cellular physiology and biochemistry

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 1.486

H-Index - 87

eISSN - 1421-9778

pISSN - 1015-8987

DOI - 10.1159/000438606

Subject(s) - endocrinology , medicine , vasopressin , pkd1 , aquaporin 2 , chloride channel , arginine , ussing chamber , transfection , polycystic kidney disease , autosomal dominant polycystic kidney disease , kidney , cystic fibrosis transmembrane conductance regulator , secretion , biology , microbiology and biotechnology , chemistry , cystic fibrosis , gene , biochemistry , mechanical engineering , amino acid , water channel , engineering , inlet

Autosomal dominant polycystic kidney disease (ADPKD) is characterized by the development of multiple, progressive, fluid-filled renal cysts that distort the renal parenchyma, leading to end-stage renal failure, mainly after the fifth decade of life. ADPKD is caused by a mutation in the PKD1 or PKD2 genes that encode polycystin-1 (PC-1) and polycystin-2 (PC-2), respectively. PC-1 is an important regulator of several signaling pathways and PC-2 is a nonselective calcium channel. The CFTR chloride channel is responsible for driving net fluid secretion into the cysts, promoting cyst growth. Arginine vasopressin hormone (AVP), in turn, is capable of increasing cystic intracellular cAMP, contributing to cell proliferation, transepithelial fluid secretion, and therefore to disease progression. The aim of this study was to assess if AVP can modulate CFTR and whether PC-1 plays a role in this potential modulation.

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