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Phenotypic plasticity in the intercalated cell: the hensin pathway
Q Al-Awqati1, S Vijayakumar, C Hikita
1Department of Medicine, College of Physicians and Surgeons of Columbia University, New York, New York 10032, USA.
The American Journal of Physiology
|August 5, 1998
Summary
Metabolic acidosis can convert beta-intercalated cells to alpha-intercalated cells. A novel protein, hensin, acts as a molecular switch, driving this cell phenotype conversion and differentiation in vitro.
Area of Science:
- Nephrology
- Cell Biology
- Biochemistry
Background:
- Intercalated cells in the renal collecting duct regulate urine pH.
- Two main types, alpha and beta intercalated cells, have distinct proton and chloride/bicarbonate transporter localizations.
- Metabolic acidosis is hypothesized to induce a conversion from beta- to alpha-intercalated cells.
Purpose of the Study:
- To investigate the biochemical mechanisms underlying the plasticity of intercalated cell phenotypes.
- To identify molecular factors involved in the conversion of beta-intercalated cells to alpha-intercalated cells.
Main Methods:
- Utilized an immortalized cell line of beta-intercalated cells.
- Induction of phenotype conversion by plating cells at superconfluent density.
- Analysis of protein localization and cellular morphology.
Main Results:
- Beta-intercalated cells converted to the alpha-phenotype at high cell densities.
- A novel extracellular matrix protein, termed "hensin," was identified.
- Hensin mediated changes in cytoskeletal proteins, cell shape, and transporter (kAE1 and H+-ATPase) localization.
Conclusions:
- Hensin functions as a molecular switch regulating intercalated cell phenotype plasticity in vitro.
- The conversion process exhibits characteristics of terminal differentiation.
- These findings provide insights into the adaptive mechanisms of renal acid-base balance.