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Am J Physiol Cell Physiol (October 17, 2001). doi:10.1152/ajpcell.00122.2001
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Articles in PresS, published online ahead of print October 16, 2001
Am J Physiol Cell Physiol, 10.1152/ajpcell.00122.2001
Submitted on March 8, 2001
Accepted on October 16, 2001

Cyclic AMP-dependent protein kinase and proliferation differ in normal and polycystic kidney epithelia

Carmela Marfella-Scivittaro1, Andrea Quinones2, and Stephanie A Orellana3*

1 Pediatrics, Case Western Reserve University, Cleveland, Ohio, USA; Pediatrics, Rainbow Babies and Children's Hospital, Cleveland, Ohio, USA
2 Pediatrics, Case Western Reserve University, Cleveland, Ohio, USA
3 Pediatrics, Case Western Reserve University, Cleveland, Ohio, USA; Pediatrics, Rainbow Babies and Children's Hospital, Cleveland, Ohio, USA; Physiology and Biophysics, Case Western Reserve University, Cleveland, Ohio, USA

* To whom correspondence should be addressed. E-mail: sao3{at}po.cwru.edu.

Developmental control of cell proliferation is crucial, and abnormal principal cell proliferation may contribute to cystogenesis in polycystic kidney disease. This study investigates roles for cAMP and its primary effector, cAMP-dependent protein kinase (cAPK), in control of cell proliferation in filter-grown non-cystic (NC) and cystic (CY) -derived principal cell cultures. Both had similar cAMP pathway characteristics upstream of cAPK subunit distribution, but differed in predicted cAPK subtype distribution. Functionally, cultures were proliferative prior to polarization, with constitutively higher proliferation in CY. Non-cystic cultures achieved levels similar to CY upon pharmacological manipulation of cAMP production, cAPK activation, or inhibition of cAPK subtype I activity. Inhibition of overall cAPK activity, or of cAPK subtype II anchoring, diminished cAMP/cAPK-mediated proliferation in NC but had no effect on CY. Polarized CY monolayers remained proliferative, but NC lost responsiveness. No large proliferation changes resulted from treatments of polarized cultures, however polarized NC and CY differed in post-stimulation handling of cAPK catalytic and Type II{alpha} regulatory subunits. Results support cAPK subtype regulation of pre-polarization proliferation in normal principal cells, altered regulation of cAPK in cystic cells, and suggest differences at or downstream of cAPK can contribute to altered proliferation in a developmental renal disease.




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