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Role for granulocyte colony stimulating factor in angiotensin II-induced neutrophil recruitment and cardiac fibrosis in mice.

Abstract：

BACKGROUND:Granulocyte colony stimulating factor (G-CSF) is a key mediator of neutrophil infiltration and is profibrotic in the liver, lung, and infarcted heart, but its roles in angiotensin II (Ang II)-induced hypertension and cardiac remodeling have not been fully determined. Thus, we sought to investigate the causal relation of G-CSF to neutrophil recruitment and cardiac fibrosis in C57BL/6J mice. METHODS:Hypertension and cardiac fibrosis were induced in wild-type (WT) mice receiving continuous infusion of Ang II (1,500ng/kg/min). After 7 days, heart sections were stained with hematoxylin and eosin, Masson's trichrome, and immunohistochemistry. The mRNA expression of cytokines was detected by real-time polymerase chain reaction analysis. The protein levels were measured by Western blot analysis. RESULTS:After Ang II infusion, myocardial G-CSF expression was significantly elevated in the hearts. Moreover, WT mice exhibited increased blood pressure, marked neutrophil accumulation, proinflammatory cytokine expression, reactive oxygen species production, and cardiac fibrosis after 7 days of Ang II infusion. However, administration of anti-G-CSF neutralizing antibody, but not with control immunoglobulin G, significantly attenuated these effects. In addition, neutralizing G-CSF antibody reversed Ang II-induced activation of ERK1/2, STAT3, and AKT signaling pathways in the hearts. CONCLUSIONS:This study demonstrates that G-CSF plays a critical role in hypertension and cardiac fibrosis and targeting this cytokine may be a novel therapeutic strategy to ameliorate hypertensive heart disease.

journal_name

Am J Hypertens

journal_title

American journal of hypertension

authors

Jiang HM,Wang HX,Yang H,Zeng XJ,Tang CS,Du J,Li HH

doi

10.1093/ajh/hpt095

subject

Has Abstract

pub_date

2013-10-01 00:00:00

pages

1224-33

issue

10

eissn

0895-7061

issn

1941-7225

pii

hpt095

journal_volume

26

pub_type

杂志文章

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