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Am J Physiol Regul Integr Comp Physiol 296: R1282-R1289, 2009. First published February 4, 2009; doi:10.1152/ajpregu.90992.2008
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WATER AND ELECTROLYTE HOMEOSTASIS

Rosiglitazone decreases blood pressure and renal injury in a female mouse model of systemic lupus erythematosus

Marcia Venegas-Pont,1 Julio C. Sartori-Valinotti,1 Christine Maric,1 Lorraine C. Racusen,2 Porter H. Glover,1 Gerald R. McLemore, Jr.,1 Allison V. Jones,1 Jane F. Reckelhoff,1 and Michael J. Ryan1

1Department of Physiology and Biophysics and the Center for Excellence in Cardiovascular Renal Research, University of Mississippi Medical Center, Jackson, Mississippi; and 2Department of Pathology, Johns Hopkins Hospital, Baltimore, Maryland

Submitted 9 December 2008 ; accepted in final form 27 January 2009

Women with systemic lupus erythematosus (SLE) exhibit a high prevalence of hypertension and renal injury. Rosiglitazone (Rosi), a peroxisome proliferator activator receptor gamma (PPAR{gamma}) agonist, has renal protective and antihypertensive effects. We tested whether Rosi ameliorates hypertension and renal injury in a female mouse model of SLE (NZBWF1). Thirty-week-old SLE and control (NZW/LacJ) mice (n ≥ 6/group) were fed Rosi (5 mg·kg–1·day–1 in standard chow) or standard chow for 4 wk. SLE mice had increased blood pressure (BP in mmHg) compared with controls (139 ± 4 vs. 111 ± 4, P < 0.05). Rosi treatment lowered BP in SLE mice (127 ± 4, P < 0.05) but not in controls (111 ± 4). Urinary albumin (µg/mg creatinine) was increased in SLE mice compared with controls (12,396 ± 6,525 vs. 50 ± 6) and reduced with Rosi treatment (148 ± 117). Glomerulosclerosis (% of glomeruli with sclerosis) was reduced in Rosi-treated SLE mice (4.2 ± 1.6 vs. 0.4 ± 0.3, P < 0.05). Renal monocyte/macrophage numbers (cell number/1,320 points counted) were reduced in SLE mice treated with Rosi (32.6 ± 11.0 vs. 10.6 ± 3.6, P < 0.05) but unchanged in controls (3.7 ± 1.6 vs. 3.7 ± 2.0). Renal osteopontin expression, a cytokine-regulating macrophage recruitment, was reduced in Rosi-treated SLE mice. Urinary endothelin (in pg/mg creatinine) was increased in SLE mice compared with controls (1.9 ± 0.59 vs. 0.6 ± 0.04, P < 0.05) and reduced in SLE mice treated with Rosi (0.8 ± 0.11, P < 0.05). PPAR{gamma} protein expression in the renal cortex was significantly lower in SLE mice compared with controls and was unaffected by Rosi. These data suggest that Rosi may be an important therapeutic option for the treatment of SLE hypertension and renal injury.

lupus; inflammation; endothelin; glomerulosclerosis; proliferator activated receptor gamma


Address for reprint requests and other correspondence: M. J. Ryan, Assistant Professor, Univ. of Mississippi Medical Center, Dept. of Physiology & Biophysics, 2500 North State St., Jackson, MS 39216-4505 (e-mail: mjryan{at}physiology.umsmed.edu)






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