Ischemia-induced loss of epithelial polarity: Potential role of the actin cytoskeleton

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Abstract

Proximal tubule cells play a major role in the reabsorption of ions, water, and solutes from the glomerular filtrate. This is accomplished, in large part, by a surface membrane polarized into structurally, biochemically, and physiologically distinct apical and basolateral membrane domains separated by cellular junctional complexes. Establishment and maintenance of these unique membrane domains is essential for the normal functioning of proximal tubular cells and is dependent on cortical actin cytoskeletal-surface membrane interactions. Ischemia results in the duration-dependent loss of apical and basolateral surface membrane lipid and protein polarity. This loss of surface membrane polarity is associated with disruption of the cortical actin microfilament network and the opening of cellular tight junctions. Surface membrane lipids and proteins are then free to diffuse laterally within the membrane bilayer into the alternate membrane domain. Functionally, ischemia-induced loss of epithelial polarity is, in part, responsible for reduced sodium and glucose reabsorption. With recovery, proximal tubule cells undergo remodeling of the surface membrane such that the unique apical and basolateral membrane domains are reestablished allowing normal cellular function to return.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Renal Fluid and Electrolyte Physiology
Volume260
Issue number6 29-6
StatePublished - 1991
Externally publishedYes

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Actin Cytoskeleton
Ischemia
Membranes
Membrane Proteins
Membrane Lipids
Tight Junctions
Actins
Sodium
Maintenance
Ions
Glucose
Water

Keywords

  • Ischemic injury
  • Lipid
  • Proximal tubule
  • Sodium-potassium-activated adenosinetriphosphatase
  • Surface membranes

ASJC Scopus subject areas

  • Physiology

Cite this

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