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Epithelial cell polarity and disease

¹Department of Medicine, Mount Sinai School of Medicine, New York, New York 10029, USA.

The American Journal of Physiology

|April 1, 1997

Summary

Autosomal dominant polycystic kidney disease (ADPKD) involves faulty epithelial cell polarity, leading to abnormal protein localization and cyst formation. This study explores the mechanisms behind these polarity defects in ADPKD kidneys.

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Area of Science:

Nephrology
Cell Biology
Molecular Medicine

Background:

Epithelial polarity is crucial for kidney function, enabling vectorial transport via precise protein localization.
Disruptions in protein polarization can cause diseases like autosomal dominant polycystic kidney disease (ADPKD).

Purpose of the Study:

To investigate the mechanisms underlying aberrant membrane protein polarization in ADPKD.
To understand how altered polarity contributes to cyst development and fluid secretion in ADPKD.

Main Methods:

Analysis of membrane protein localization in ADPKD cyst epithelia.
Investigation of fetal gene expression patterns in ADPKD kidneys.

Main Results:

ADPKD exhibits abnormal apical localization of Na-K-ATPase and epidermal growth factor (EGF) receptors.
Aberrant expression of fetal genes, including Na-K-ATPase beta2-subunit, is observed in ADPKD kidneys.
Polycystin overexpression and failure to downregulate fetal genes are implicated in ADPKD polarity defects.

Conclusions:

Aberrant protein polarization, particularly of Na-K-ATPase and EGF receptors, contributes to ADPKD pathogenesis.
Failure to downregulate fetal gene expression is a key mechanism driving polarity abnormalities in ADPKD.
Understanding these mechanisms offers insights into potential therapeutic targets for ADPKD.

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