EARLY RECOVERY OF THE ACTIN CYTOSKELETON DURING RENAL ISCHEMIC-INJURYIN-VIVO

The actin cytoskeleton of proximal tubule cells is important for both the maintenance of membrane domains and attachment to neighboring cell s and underlying substrata, Adenosine triphosphate (ATP) depletion dur ing ischemic injury causes early alterations in the actin cytoskeleton , resulting in loss of membrane domains and cellular attachment, We ex amined the actin cytoskeleton during recovery from ischemic injury, As shown previously in cell culture studies, ATP depletion to 14% of con trol values from in vivo ischemia resulted in decreases in G-actin con sistent with net polymerization of the cytoskeleton, After 20 minutes of recovery restored ATP levels to 24% of control values, percent G-ac tin increased back to control values, yet cytoplasmic actin polymerize d with little evidence of apical recovery, After 120 minutes of recove ry, ATP levels had increased to 48% of control values with little qual itative or quantitative change in actin polymerization from 20 minutes of recovery, When ATP levels recovered to 65% of control values at 36 0 minutes after ischemia, movement of F-actin back toward the apical s urface was observed, These data, along with prior data using maleic ac id, suggest that thresholds of cellular ATP may cause differing effect s on distinct cellular actin pools, We conclude that actin cytoskeleta l recovery occurs very early and may be necessary for reestablishment of polarity essential for normal reabsorptive functions. (C) 1996 by t he National Kidney Foundation, Inc.