RhoGTPases and end-binding protein 1 (EB1) expression associated with apelininduced proximal tubule function improvement in the post-ischemic kidney.

SARA M. MOLINAS; FLORENCIA HIDALGO; FLORENCIA BARSI; MARÍA EUGENIA TABORRA; TOMÁS RIVABELLA MAKNIS; JAVIER GIRARDINI ; M. CECILIA LAROCCA; LILIANA A. MONASTEROLO

Rosario

Congreso; REUNIÓN ANUAL SAFIS 2019; 2019

Sociedad Argentina de Fisiología (SAFIS)

Understanding the mechanisms of kidney repair after ischemic injury is critical in the researchof new therapeutic strategies. The repair process is accomplished by migration of new cells intothe region, reconstituting the functional tubular epithelium. Ischemia?reperfusion induceschanges in expression and distribution of Rho GTPases in proximal tubules. Similarly to RhoGTPases, EB1 is an important regulator of microtubule and actin dynamics, essential for kidneytubular cell-migration and epithelial remodelling. Furthermore, in certain scenarios, EB1regulatory function overlaps with Rho GTPases signalling. Increasing evidence indicates thatthe adipokine apelin and its receptor, APJ, may be potential target for the treatment of kidneydisease. The aim of this study was to evaluate the effects of apelin on functional parameters andthe expression of RhoGTPases and EB1 in the post-ischemic kidney. Male Wistar rats (n= 4 pergroup) underwent 40 min unilateral renal ischemia followed by 24 h reperfusion (IR) or shamsurgery (C). Apelin 50ug/Kg/d i.p. was administered during 3 days prior to IR (IR+Ap).Increased fractional glucose excretion in IR was prevented by Ap treatment (C: 0.0042 +/-0.001%; IR: 0.25 +/- 0.06*; IR+Ap: 0.0097 +/- 0.004#). Western blot analysis of corticalplasma membrane fractions showed diminished levels of the RhoGTPases Cdc42 (C: 1 +/-0.24; IR: 0.19 +/- 0.02*; IR+Ap: 0.64 +/- 0.10#) and RhoA (C: 1 +/- 0.19; IR: 0.11 +/- 0.05*;IR+Ap: 0.43 +/- 0.18#; *p