Role of guanylate binding protein-1 in vascular defects associated with chronic inflammatory diseases

被引：28

作者：

Hammon, Matthias ^{[2
]}

Herrmann, Martin ^{[3
]}

Bleiziffer, Oliver ^{[2
]}

Pryymachuk, Galyna ^{[2
]}

Andreoli, Laura ^{[4
]}

Munoz, Luis E. ^{[3
]}

Amann, Kerstin U. ^{[5
]}

Mondini, Michele ^{[6
]}

Gariglio, Marisa ^{[6
]}

Airo, Paolo ^{[4
]}

Schellerer, Vera S.

Hatzopoulos, Antonis K. ^{[7
]}

Horch, Raymund E. ^{[2
]}

Kneser, Ulrich ^{[2
]}

Stuerzl, Michael ^{[1
]}

Naschberger, Elisabeth ^{[1
]}

机构：

[1] Univ Med Ctr Erlangen, Dept Surg, Div Mol & Expt Surg, D-91054 Erlangen, Germany

[2] Univ Med Ctr Erlangen, Dept Plast & Hand Surg, D-91054 Erlangen, Germany

[3] Univ Med Ctr Erlangen, Dept Internal Med 3, Inst Clin Immunol & Rheumatol, D-91054 Erlangen, Germany

[4] Univ Clin Brescia, Brescia, Italy

[5] Univ Med Ctr Erlangen, Inst Pathol, Div Nephropathol, D-91054 Erlangen, Germany

[6] Univ Piemonte Orientale, Dept Clin & Expt Med, Novara, Italy

[7] Vanderbilt Univ, Sch Med, Dept Med, Div Cardiovasc Med, Nashville, TN 37212 USA

来源：

JOURNAL OF CELLULAR AND MOLECULAR MEDICINE | 2011年 / 15卷 / 07期

关键词：

rheumatic autoimmune disorders; guanylate binding protein-1; endothelial progenitor cells; inflammation; systemic lupus erythematosus; rheumatoid arthritis; systemic sclerosis; ENDOTHELIAL PROGENITOR CELLS; SYSTEMIC-LUPUS-ERYTHEMATOSUS; RHEUMATOID-ARTHRITIS; AUTOIMMUNE-DISEASES; PERIPHERAL-BLOOD; REVISED CRITERIA; ANGIOGENESIS; INTERFERON; GTPASE; CLASSIFICATION;

D O I：

10.1111/j.1582-4934.2010.01146.x

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Rheumatic autoimmune disorders are characterized by a sustained pro-inflammatory microenvironment associated with impaired function of endothelial progenitor cells (EPC) and concomitant vascular defects. Guanylate binding protein-1 (GBP-1) is a marker and intracellular regulator of the inhibition of proliferation, migration and invasion of endothelial cells induced by several pro-inflammatory cytokines. In addition, GBP-1 is actively secreted by endothelial cells. In this study, significantly increased levels of GBP-1 were detected in the sera of patients with chronic inflammatory disorders. Accordingly we investigated the function of GBP-1 in EPC. Interestingly, stable expression of GBP-1 in T17b EPC induced premature differentiation of these cells, as indicated by a robust up-regulation of both Flk-1 and von Willebrand factor expression. In addition, GBP-1 inhibited the proliferation and migration of EPC in vitro. We confirmed that GBP-1 inhibited vessel-directed migration of EPC at the tissue level using the rat arterio-venous loop model as a novel quantitative in vivo migration assay. Overall, our findings indicate that GBP-1 contributes to vascular dysfunction in chronic inflammatory diseases by inhibiting EPC angiogenic activity via the induction of premature EPC differentiation.

引用

页码：1582 / 1592

页数：11

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