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Polycystin-1 transforms the cAMP growth-responsive phenotype of M-1 cells
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Polycystin-1 transforms the cAMP growth-responsive phenotype of M-1 cells
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Journal Article
Polycystin-1 transforms the cAMP growth-responsive phenotype of M-1 cells
2001
Overview
Polycystin-1 transforms the cAMP growth-responsive phenotype of M-1 cells.
Polycystic kidney disease (PKD) is characterized by the abnormal proliferation of tubular epithelial cells. It was recently shown that the growth of PKD cyst-lining cells is stimulated by cyclic adenosine monophosphate (cAMP), whereas the growth of normal human kidney cortex cells is inhibited.
We have examined the effects of overexpressing the C-terminal cytosolic tail of mouse polycystin-1, as a membrane-targeted fusion protein, on cAMP-responsive cell proliferation in stably transfected M-1 cortical collecting duct cells. Two cell lines that express high levels of the polycystin-1 fusion protein and two control cell lines that do not express the fusion protein were tested.
Growth of parental M-1 cells and the control cell lines was inhibited by 8-Br-cAMP and by a variety of cAMP agonists. In contrast, growth of the polycystin-1–expressing clones was stimulated by cAMP. Consistent with this, the protein kinase A (PKA) inhibitor H-89 caused either a positive or a negative growth effect depending on the primary response to cAMP. PD98059 blocked the cAMP stimulation of cell proliferation, indicating that the pathway is MEK1 dependent.
Expression of the polycystin-1 C-terminal tail disrupts normal cellular signaling and transforms the stably transfected M-1 cells to an abnormal PKD cell proliferation phenotype.
Publisher
Elsevier Inc,Nature Publishing,Elsevier Limited
Subject
8-Bromo Cyclic Adenosine Monophosphate - pharmacology
/ Animals
/ Biological and medical sciences
/ Cell Division - drug effects
/ Cyclic AMP-Dependent Protein Kinases - antagonists & inhibitors
/ Cyclic AMP-Dependent Protein Kinases - metabolism
/ Enzyme Inhibitors - pharmacology
/ Gene Expression - physiology
/ Isoquinolines - pharmacology
/ Kidney Tubules, Collecting - cytology
/ Kidneys
/ Mice
/ Nephrology. Urinary tract diseases
/ Polycystic Kidney Diseases - genetics
/ Polycystic Kidney Diseases - metabolism
/ Recombinant Fusion Proteins - genetics
/ Recombinant Fusion Proteins - metabolism
