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Articles in PresS, published online ahead of print December 3, 2002
Am J Physiol Renal Physiol, 10.1152/ajprenal.00210.2002
Submitted on June 5, 2002
Accepted on November 22, 2002
1 Department of Medicine, Indiana University, Indianapolis, IN, USA; Department of Medicine, Roudebush VAMC, Indianapolis, IN, USA
2 Department of Biology, University of North Dakota, Grand Forks, ND, USA
3 Departmentof Biochemistry and Molecular Biology, Colorado State University, Fort Collins, CO, USA
* To whom correspondence should be addressed. E-mail: bmolitor{at}iupui.edu.
Ischemic injury induces actin cytoskeleton disruption and aggregation, but mechanisms affecting these changes remain unclear. To determine the role of ADF/cofilin participation in ischemic-induced actin cytoskeletal breakdown, we utilized porcine kidney cultured cells, LLC-PKA4.8, and adenovirus containing wild type, constitutively active and inactive Xenopus ADF/cofilin cDNAs linked to GFP (XAC-GFP) in an ATP depletion model. High adenoviral infectivity (70%) in LLC-PKA4.8 cells resulted in linearly increasing XAC(wt)-GFP and pXAC(wt)-GFP (inactive) expression. ATP depletion rapidly induced dephosphorylation, and therefore activation, of endogenous pcofilin as well as pXAC(wt)-GFP, in conjunction, with the formation of fluorescent XAC(wt)-GFP/actin aggregates and rods. No significant actin cytoskeletal alterations occurred with short term ATP depletion of LLC-PKA4.8 cells expressing GFP or the constitutively inactive mutant, XAC(S3E)-GFP, but cells expressing the constitutively active mutant demonstrated nearly instantaneous actin disruption with aggregate and rod formation. Confocal image 3-D volume reconstructions of normal and ATP depleted LLC-PKA4.8 cells demonstrated 25 minutes of ATP depletion induced a rapid increase in XAC(wt)-GFP apical and basal signal in addition to XAC-GFP/actin aggregate formation. These data demonstrate XAC(wt)-GFP participates in ischemia-induced actin cytoskeletal alterations and determines the rate and extent of these ATP depletion-induced cellular alterations.
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