Kidney ischemia–reperfusion regulates expression and distribution of tubulin subunits, β-actin and rho GTPases in proximal tubules

Ischemic injury is characterized by a loss of cell polarity and a release of proximal tubule epithelial cells resulting from cytoskeletal reorganization. This study used a reversible unilateral renal ischemia–reperfusion model to investigate the expression and distribution of cytoskeletal components and Rho GTPases at protein and mRNA levels in proximal tubule fractions. Ischemia strongly increased β-actin and α-tubulin expressions that were predominantly found in nuclear fractions. Rho GTPases and caveolin-1 expression were upregulated by ischemia and were enriched mainly in Triton-soluble membranes. Rac1 expression was stimulated in the soluble fractions during reperfusion. Rho GTPases mRNA levels were similarly regulated by ischemia–reperfusion suggesting that changes in their expressions could occur at gene or mRNA levels. ERM protein expression and distribution were unaffected by ischemia–reperfusion. Together, these data show that renal ischemia–reperfusion induced expression and redistribution of actin and microtubule cytoskeleton components in addition to Rho GTPases in proximal tubules, suggesting that they participate in an adaptive response to cellular lesions.