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Updated: May 24, 2026
A Modified Two Kidney One Clip Mouse Model of Renin Regulation in Renal Artery Stenosis
Published on: October 26, 2020
Granulocyte colony stimulating factor prevents kidney infarction and attenuates renovascular hypertension
Breno V Nogueira1, Zaira Palomino, Marcella L Porto
1Department of Morphology, Health Sciences Center, Federal University of Espirito Santo (UFES), Vitoria, ES, Brasil.
Insights
Granulocyte-colony stimulating factor (G-CSF) prevents kidney infarction and reduces hypertension in a mouse model of renal ischemia. G-CSF also attenuates increases in vasoactive peptides, reinforcing its protective effects on kidney ischemia.
Area of Science:
- Nephrology
- Cardiovascular Medicine
- Hematology
Background:
- Granulocyte-colony stimulating factor (G-CSF) regulates hematopoietic cells and is known to attenuate renal ischemia-reperfusion injury.
- The effects of G-CSF on the renal and cardiovascular systems in hypertension models require further investigation.
Purpose of the Study:
- To evaluate the protective effects of G-CSF on renal and cardiovascular systems in a two-kidney, one-clip (2K1C) hypertensive mouse model.
Main Methods:
- Male C57BL/6 mice underwent 2K1C surgery or sham operation.
- Mice received daily injections of G-CSF (100 μg/kg) or vehicle for 14 days.
Main Results:
- G-CSF treatment significantly lowered arterial pressure in 2K1C mice compared to vehicle controls (129±2 vs. 150±5 mmHg).
- G-CSF prevented the elevation of plasma angiotensin I, II, and 1-7 levels observed in 2K1C mice.
- G-CSF administration reduced ischemic kidney atrophy and prevented infarction and apoptosis in the clipped kidney.
Conclusions:
- G-CSF demonstrates significant protective effects against kidney infarction and hypertension in the 2K1C mouse model.
- G-CSF attenuates increases in plasma angiotensin levels, highlighting its role in managing renovascular hypertension and 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 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.
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