Research ExplorerPublicationsCCR5 deficiency does not reduce hypertensive end-organ damag...

CCR5 deficiency does not reduce hypertensive end-organ damage in mice

Standard

CCR5 deficiency does not reduce hypertensive end-organ damage in mice. / Krebs, Christian; Fraune, Christoph; Schmidt-Haupt, Robin; Turner, Jan Eric; Panzer, Ulf; Quang, Michael N; Tannapfel, Andrea; Velden, Joachim; Stahl, Rolf A.K.; Wenzel, Ulrich.

In: AM J HYPERTENS, Vol. 25, No. 4, 4, 04.2012, p. 479-486.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Krebs, C, Fraune, C, Schmidt-Haupt, R, Turner, JE, Panzer, U, Quang, MN, Tannapfel, A, Velden, J, Stahl, RAK & Wenzel, U 2012, 'CCR5 deficiency does not reduce hypertensive end-organ damage in mice', AM J HYPERTENS, vol. 25, no. 4, 4, pp. 479-486. https://doi.org/10.1038/ajh.2011.243

APA

Krebs, C., Fraune, C., Schmidt-Haupt, R., Turner, J. E., Panzer, U., Quang, M. N., Tannapfel, A., Velden, J., Stahl, R. A. K., & Wenzel, U. (2012). CCR5 deficiency does not reduce hypertensive end-organ damage in mice. AM J HYPERTENS, 25(4), 479-486. [4]. https://doi.org/10.1038/ajh.2011.243

Vancouver

Krebs C, Fraune C, Schmidt-Haupt R, Turner JE, Panzer U, Quang MN et al. CCR5 deficiency does not reduce hypertensive end-organ damage in mice. AM J HYPERTENS. 2012 Apr;25(4):479-486. 4. https://doi.org/10.1038/ajh.2011.243

Bibtex

@article{f8560f84538a4e96aae4313bdbcf10a6,
title = "CCR5 deficiency does not reduce hypertensive end-organ damage in mice",
abstract = "BACKGROUND: CCR5 is expressed on infiltrating T cells in hypertensive mice and CCR5 antagonists reduce hypertension making CCR5 an interesting target in treatment of hypertension.METHODS: To evaluate the role of CCR5 in hypertensive renal and cardiac end-organ damage, we induced hypertension with desoxycorticosterone acetate (DOCA) and angiotensin II (Ang II) in wild-type (WT) and CCR5-deficient mice.RESULTS: CCR5 expression was increased in renal cortex and cardiac tissue as measured by quantitative PCR. Systolic blood pressure and renal function did not differ between hypertensive CCR5(-/-) and WT mice. DOCA + Ang II induced massive albuminuria and glomerular injury but no difference was found between CCR5(-/-) and WT mice. In addition, no difference was found for renal inflammation as measured by infiltrating T cells, macrophages, and CCL2 expression. The renal expression of the CCR5 ligands, CCL3, and CCL5 was increased in the kidney of hypertensive mice. For CCL3 the increase was significantly higher in CCR5(-/-) than in WT mice. DOCA + Ang II induced cardiac damage as assessed by heart weight, cardiac fibrosis as well as expression of fetal and matrix components but no significant difference was found between CCR5(-/-) and WT mice.CONCLUSIONS: CCR5 deficiency does not influence hypertensive renal and cardiac end-organ damage. Cells that infiltrate by expression of CCR5 are either not pathogenic or CCR5-positive leukocytes can migrate via alternative chemokine receptors. Beneficial effects of CCR5 antagonists in hypertension are most likely due to unspecific effects of the antagonists. Possibly, other chemokine receptors in concert with CCR5 are important for hypertensive injury.",
keywords = "Angiotensin II, Animals, Chemokine CCL2/biosynthesis, Chemokine CCL3/biosynthesis, Desoxycorticosterone, Heart, Hypertension/chemically induced, Kidney/pathology, Kidney Cortex/metabolism, Male, Mice, Myocardium/metabolism, Receptors, CCR5/deficiency",
author = "Christian Krebs and Christoph Fraune and Robin Schmidt-Haupt and Turner, {Jan Eric} and Ulf Panzer and Quang, {Michael N} and Andrea Tannapfel and Joachim Velden and Stahl, {Rolf A.K.} and Ulrich Wenzel",
year = "2012",
month = apr,
doi = "10.1038/ajh.2011.243",
language = "English",
volume = "25",
pages = "479--486",
journal = "AM J HYPERTENS",
issn = "0895-7061",
publisher = "Oxford University Press",
number = "4",

}

RIS

TY - JOUR

T1 - CCR5 deficiency does not reduce hypertensive end-organ damage in mice

AU - Krebs, Christian

AU - Fraune, Christoph

AU - Schmidt-Haupt, Robin

AU - Turner, Jan Eric

AU - Panzer, Ulf

AU - Quang, Michael N

AU - Tannapfel, Andrea

AU - Velden, Joachim

AU - Stahl, Rolf A.K.

AU - Wenzel, Ulrich

PY - 2012/4

Y1 - 2012/4

N2 - BACKGROUND: CCR5 is expressed on infiltrating T cells in hypertensive mice and CCR5 antagonists reduce hypertension making CCR5 an interesting target in treatment of hypertension.METHODS: To evaluate the role of CCR5 in hypertensive renal and cardiac end-organ damage, we induced hypertension with desoxycorticosterone acetate (DOCA) and angiotensin II (Ang II) in wild-type (WT) and CCR5-deficient mice.RESULTS: CCR5 expression was increased in renal cortex and cardiac tissue as measured by quantitative PCR. Systolic blood pressure and renal function did not differ between hypertensive CCR5(-/-) and WT mice. DOCA + Ang II induced massive albuminuria and glomerular injury but no difference was found between CCR5(-/-) and WT mice. In addition, no difference was found for renal inflammation as measured by infiltrating T cells, macrophages, and CCL2 expression. The renal expression of the CCR5 ligands, CCL3, and CCL5 was increased in the kidney of hypertensive mice. For CCL3 the increase was significantly higher in CCR5(-/-) than in WT mice. DOCA + Ang II induced cardiac damage as assessed by heart weight, cardiac fibrosis as well as expression of fetal and matrix components but no significant difference was found between CCR5(-/-) and WT mice.CONCLUSIONS: CCR5 deficiency does not influence hypertensive renal and cardiac end-organ damage. Cells that infiltrate by expression of CCR5 are either not pathogenic or CCR5-positive leukocytes can migrate via alternative chemokine receptors. Beneficial effects of CCR5 antagonists in hypertension are most likely due to unspecific effects of the antagonists. Possibly, other chemokine receptors in concert with CCR5 are important for hypertensive injury.

AB - BACKGROUND: CCR5 is expressed on infiltrating T cells in hypertensive mice and CCR5 antagonists reduce hypertension making CCR5 an interesting target in treatment of hypertension.METHODS: To evaluate the role of CCR5 in hypertensive renal and cardiac end-organ damage, we induced hypertension with desoxycorticosterone acetate (DOCA) and angiotensin II (Ang II) in wild-type (WT) and CCR5-deficient mice.RESULTS: CCR5 expression was increased in renal cortex and cardiac tissue as measured by quantitative PCR. Systolic blood pressure and renal function did not differ between hypertensive CCR5(-/-) and WT mice. DOCA + Ang II induced massive albuminuria and glomerular injury but no difference was found between CCR5(-/-) and WT mice. In addition, no difference was found for renal inflammation as measured by infiltrating T cells, macrophages, and CCL2 expression. The renal expression of the CCR5 ligands, CCL3, and CCL5 was increased in the kidney of hypertensive mice. For CCL3 the increase was significantly higher in CCR5(-/-) than in WT mice. DOCA + Ang II induced cardiac damage as assessed by heart weight, cardiac fibrosis as well as expression of fetal and matrix components but no significant difference was found between CCR5(-/-) and WT mice.CONCLUSIONS: CCR5 deficiency does not influence hypertensive renal and cardiac end-organ damage. Cells that infiltrate by expression of CCR5 are either not pathogenic or CCR5-positive leukocytes can migrate via alternative chemokine receptors. Beneficial effects of CCR5 antagonists in hypertension are most likely due to unspecific effects of the antagonists. Possibly, other chemokine receptors in concert with CCR5 are important for hypertensive injury.

KW - Angiotensin II

KW - Animals

KW - Chemokine CCL2/biosynthesis

KW - Chemokine CCL3/biosynthesis

KW - Desoxycorticosterone

KW - Heart

KW - Hypertension/chemically induced

KW - Kidney/pathology

KW - Kidney Cortex/metabolism

KW - Male

KW - Mice

KW - Myocardium/metabolism

KW - Receptors, CCR5/deficiency

U2 - 10.1038/ajh.2011.243

DO - 10.1038/ajh.2011.243

M3 - SCORING: Journal article

C2 - 22258337

VL - 25

SP - 479

EP - 486

JO - AM J HYPERTENS

JF - AM J HYPERTENS

SN - 0895-7061

IS - 4

M1 - 4

ER -