Phenotypic plasticity in the intercalated cell: the hensin
pathway.
Al-Awqati, Qais, S. Vijayakumar, C. Hikita, J. Chen, and J. Takito.
Departments of Medicine and Physiology, College of Physicians and
Surgeons of Columbia University, 630 W 168th St, New York, NY,
10032
APStracts 5:0094F, 1998.
The collecting duct of the renal tubule contains two cell types, one
of which, the intercalated cell is responsible for acidification and
alkalinization of urine. These cells exist in a multiplicity of
morphologic forms, with two extreme types, and . The former,
acidifies the urine by an apical proton translocating ATPase and a
basolateral Cl:HCO3 exchanger which is an alternately spliced form of
band 3. This kidney form of band 3, kAE1, is present in the apical
membrane of the cell, which has the H+ ATPase on the basolateral
membrane. We had suggested previously that metabolic acidosis leads
to conversion of to types. To study the biochemical basis of this
plasticity we used an immortalized cell line of the cell and showed
that these cells convert to the phenotype when plated at
superconfluent density. At high density these cells localize a new
protein, which we term hensin to the extracellular matrix, and hensin
acts as a molecular switch capable of changing the phenotype of these
cells in vitro. Hensin induces new cytoskeletal proteins, makes the
cells assume a more columnar shape and re-targets kAE1 and the H+
ATPase. These recent studies suggest that the conversion of to cells,
at least in vitro bears many of the hallmarks of terminal
differentiation.
Received 24 December 1997; accepted in final form 1 May 1998.
APS Manuscript Number F409-7.
Article publication pending Am. J. Physiol. (Renal Physiology).
ISSN 1080-4757 Copyright 1998 The American Physiological Society.
Published in APStracts on 16 June 1998