Cd9 antigen mrna is induced by hypertonicity in two renal epithelial cell lines. Sheikh-Hamad, David, Joan D. Ferraris, Julia Dragolovich, Harry G. Preuss, Maurice B. Burg, and Arlyn Garc[acute]ia-P[acute]erez. Laboratory of Kidney and Electrolyte Metabolism, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892-1598
APStracts 2:0275C, 1995.
In diverse organisms, cells adapt to hyperosmotic stress by accumulating organic osmolytes. Mammalian renal medullary cells are routinely under osmotic stress. Two renal cell lines, MDCK and PAP -HT25, have been widely used to study mammalian osmotic regulation. In these epithelial cells, extracellular hypertonicity induces gene transcription of proteins directly involved in the metabolism and transport of organic osmolytes. This induction is relatively specific and not part of a generalized stress response. Little is known about the signal transduction pathway between cellular detection of extracellular osmolality and increased specific gene transcription. Here, we identify a cDNA product corresponding to CD9 antigen mRNA using differential mRNA display PCR on MDCK cells in isotonic versus hypertonic medium. CD9 antigen is a cell-surface glycoprotein originally found in cells of the immune system. Although CD9 antigen has been structurally characterized, its function is unclear. We further demonstrate that CD9 antigen mRNA is present in MDCK and PAP -HT25 cells and that its mRNA abundance is induced by extracellular hypertonicity, but not by heat stress. Also, we show that accumulation of organic osmolytes markedly attenuates the CD9 mRNA induction, as only recently demonstrated with genes involved in the hyperosmotic stress response. This suggests a role for CD9 antigen in this response. 

Received 14 February 1995; accepted in final form 28 June 1995.
APS Manuscript Number C83-5.
Article publication pending Am. J. Physiol. (Cell Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 30 July 1995.