BACKGROUND: G-CSF is a critical regulator of hematopoietic cell proliferation, differentiation and survival. It has been reported that G-CSF attenuates renal injury during acute ischemia-reperfusion. In this study we evaluated the effects of G-CSF on the renal and cardiovascular systems of 2K1C hypertensive mice. METHODS: Male C57BL/6 mice were subjected to left renal artery clipping (2K1C) or sham operation and were then administered G-CSF (100 μg/kg/day) or vehicle for 14 days. RESULTS: Arterial pressure was higher in 2K1C + vehicle animals than in 2K1C + G-CSF (150±5 vs. 129±2 mmHg, p<0.01, n=8). Plasma angiotensin I, II and 1-7 concentrations were significantly increased in 2K1C + Vehicle when compared to the normotensive Sham group. G-CSF prevented the increase of these vasoactive peptides. The clipped kidney/contralateral kidney weight ratio showed a less atrophy of the ischemic kidney in the treated group (0.50±0.02 vs. 0.66±0.01, p<0.05). The infarction area in the clipped kidney was completely prevented in 7 out of 8 2K1C + G-CSF mice. Administration of G-CSF protected the clipped kidney from apoptosis. CONCLUSION: Our data indicate that G-CSF prevents kidney infarction and markedly attenuates the increases in plasma angiotensin levels and hypertension in 2K1C mice, reinforcing the protective effect of G-CSF on kidney ischemia.
BACKGROUND:G-CSF is a critical regulator of hematopoietic cell proliferation, differentiation and survival. It has been reported that G-CSF attenuates renal injury during acute ischemia-reperfusion. In this study we evaluated the effects of G-CSF on the renal and cardiovascular systems of 2K1C hypertensivemice. METHODS: Male C57BL/6 mice were subjected to left renal artery clipping (2K1C) or sham operation and were then administered G-CSF (100 μg/kg/day) or vehicle for 14 days. RESULTS: Arterial pressure was higher in 2K1C + vehicle animals than in 2K1C + G-CSF (150±5 vs. 129±2 mmHg, p<0.01, n=8). Plasma angiotensin I, II and 1-7 concentrations were significantly increased in 2K1C + Vehicle when compared to the normotensive Sham group. G-CSF prevented the increase of these vasoactive peptides. The clipped kidney/contralateral kidney weight ratio showed a less atrophy of the ischemic kidney in the treated group (0.50±0.02 vs. 0.66±0.01, p<0.05). The infarction area in the clipped kidney was completely prevented in 7 out of 8 2K1C + G-CSFmice. Administration of G-CSF protected the clipped kidney from apoptosis. CONCLUSION: Our data indicate that G-CSF prevents kidney infarction and markedly attenuates the increases in plasma angiotensin levels and hypertension in 2K1C mice, reinforcing the protective effect of G-CSF on kidney ischemia.
Authors: Bianca P Campagnaro; Clarissa L Tonini; Luciano M Doche; Breno V Nogueira; Elisardo C Vasquez; Silvana S Meyrelles Journal: DNA Cell Biol Date: 2013-06-20 Impact factor: 3.311
Authors: Ananda T Dias; Bianca P Rodrigues; Marcella L Porto; Agata L Gava; Camille M Balarini; Flavia P S Freitas; Zaira Palomino; Dulce E Casarini; Bianca P Campagnaro; Thiago M C Pereira; Silvana S Meyrelles; Elisardo C Vasquez Journal: J Transl Med Date: 2014-02-06 Impact factor: 5.531
Authors: Bianca P Campagnaro; Clarissa L Tonini; Breno V Nogueira; Dulce E Casarini; Elisardo C Vasquez; Silvana S Meyrelles Journal: Int J Hypertens Date: 2013-02-14 Impact factor: 2.420
Authors: Ananda T Dias; Amanda S Cintra; Jéssica C Frossard; Zaira Palomino; Dulce E Casarini; Isabele B S Gomes; Camille M Balarini; Agata L Gava; Bianca P Campagnaro; Thiago M C Pereira; Silvana S Meyrelles; Elisardo C Vasquez Journal: J Transl Med Date: 2014-09-16 Impact factor: 5.531