CXC chemokines in angiogenesis

Strieter, Robert M.; Burdick, Marie D.; Gomperts, Brigitte N.; Belperio, John A.; Keane, Michael P.

doi:10.1016/j.cytogfr.2005.04.007

Cited by 358 publications

(219 citation statements)

References 157 publications

(133 reference statements)

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“…www.endocrinology-journals.org responsible for the ability of chemokines to attract neutrophils as well as a necessary motif involved in angiogenic properties of these chemokines (Strieter et al 2005). The co-regulation of CXCL1, CXCL3, CXCL5, CXCL6, and CXCL8 in tumors was puzzling.…”

Section: Discussionmentioning

confidence: 99%

CXC chemokines located in the 4q21 region are up-regulated in breast cancer

Bièche¹,

Chavey²,

Andrieu³

et al. 2007

Endocrine Related Cancer

158

162

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Recent data suggest that chemokines could be essential players in breast carcinogenesis. We previously showed that the CXC chemokine CXCL8 (interleukin-8) was overexpressed in estrogen receptor a (ERa)-negative breast cell lines. Analysis of CXCL8 chromosomal location showed that several CXC chemokines (CXCL1, CXCL2, CXCL3, CXCL4, CXCL4V1, CXCL5, CXCL6, CXCL7, and CXCL8) were localized in the same narrow region (360 kb in size) of chromosome 4. We thus hypothesized that they could belong to the same cluster. Quantification of these chemokines in breast tumors showed that samples expressing high CXCL8 also produced elevated levels of CXCL1, CXCL3, and CXCL5, and displayed low content of ERa. CXCL1, CXCL2, CXCL3, CXCL5, and CXCL8 were co-regulated both in tumors and in breast cancer cell lines. CXCL5 and CXCL8 were mainly produced by epithelial cells, whereas CXCL1, CXCL2, and CXCL3 had a high expression in blood cells. The overexpression of these chemokines in tumor cells was not the result of gene amplification, but rather of an enhanced gene transcription. Our data suggest that high CXCL8 expression in tumors is mainly correlated to activating protein-1 (AP-1) pathway and to a minor extent to NF-kB pathway. Interestingly, CXCL1, CXCL2, CXCL3, CXCL5, CXCL6, and CXCL8 chemokines were present at higher levels in metastases when compared with grade I and III biopsies. High levels of CXCL8, CXCL1, and CXCL3 accounted for a shorter relapse-free survival of ERa-positive patients treated with tamoxifen. In summary, we present evidences that multiple CXC chemokines are co-expressed in CXCL8-positive breast tumors. In addition, these chemokines could account for the higher aggressiveness of these types of tumors.

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Section: Discussionmentioning

confidence: 99%

CXC chemokines located in the 4q21 region are up-regulated in breast cancer

Bièche¹,

Chavey²,

Andrieu³

et al. 2007

Endocrine Related Cancer

158

162

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“…Neovascularization in fibroproliferative disorders is regulated by an opposing balance between angiogenic and angiostatic factors. Molecules that originally promote angiogenesis include ELR+ CXC chemokines, such as IL-8, whereas ELR– CXC chemokines, such as MIG and IP-10, behave as potent inhibitors of angiogenesis and benefit angiostasis [25]. An imbalance between the expression of pro-angiogenic and angiostatic CXC chemokines, such as an increase in IL-8 and a decrease in IP-10, favoring net angiogenic activity, has been demonstrated in lung fibrosis specimens in IPF [26].…”

Section: Discussionmentioning

confidence: 99%

Angiogenic and Angiostatic Chemokines in Idiopathic Pulmonary Fibrosis and Granulomatous Lung Disease

Anhenn

Theegarten³

et al. 2009

Respiration

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Background: Angiogenesis-angiostasis balance and leukocyte recruitment are influenced by different concentrations of distinct chemokines. Objective: To investigate the relative contribution of angiogenic and angiostatic CXC chemokines to the pathogenesis of idiopathic pulmonary fibrosis (IPF) and granulomatous lung diseases, we examined the in vitro production of an angiogenic chemokine (IL-8), and 2 angiostatic chemokines (IP-10 and MIG) by alveolar macrophages. Methods: Alveolar macrophages from 16 patients with granulomatous lung diseases [8 with sarcoidosis, 8 with extrinsic allergic alveolitis (EAA)], 16 patients with IPF, and 8 control subjects were cultured for 24 h. IL-8, IL-18, IP-10 and MIG in the culture supernatants were measured by a fluorescent bead-based multiplex technique. Results: In IPF patients, IL-8 was increased and correlated with bronchoalveolar lavage (BAL) neutrophils, whereas the levels of IP-10 and MIG were normal. In sarcoidosis and EAA patients, IL-8, IP-10, and MIG were all increased and IP-10 and MIG correlated with IL-18, a Th1 cytokine, and the percentage and number of BAL lymphocytes. Conclusions: The difference in the expression of CXC chemokines and a Th1 cytokine may contribute to the different immunopathogenesis, clinical course and responsiveness to treatment of these diseases.

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“…In addition to Th1 immune responses, it was recently reported that CXCL10 plays a role in maintaining glomerular podocyte function [9, 10]. Moreover, CXCL10 has been demonstrated to be involved in the regulation of mesangial cell proliferation [11, 12], endothelial cell proliferation and angiogenesis and intestinal epithelial cell proliferation [13, 14]. Furthermore, recent work demonstrated that CXCL10 was detected in the urine of transplant recipients [15].…”

Section: Introductionmentioning

confidence: 99%

IFN-Inducible Protein 10 (CXCL10) Regulates Tubular Cell Proliferation in Renal Ischemia-Reperfusion Injury

Furuichi

Wada

Kitajikma

et al. 2008

Nephron Exp Nephrol

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Although renal tubular cell proliferation after acute tubular necrosis is an important and essential response in the recovery of renal dysfunction in acute renal failure, the precise factors and mechanisms of tubular cell regeneration remain unclear. Here, we describe our studies using a neutralizing antibody (Ab) against interferon-inducible protein of 10 kDa (IP-10; CXCL10) that indicate a role for CXCL10 in tubular cell proliferation after renal ischemia-reperfusion injury. Tissue necrosis and interstitial infiltrating numbers were comparable between anti-CXCL10 Ab-treated and control mice treated with IgG at the 24 and 48 h time points after reperfusion. In contrast, the numbers of Ki67-positive proliferating tubular cells were significantly increased in anti-CXCL10 Ab-treated mice 48 h after reperfusion. In accordance with the in vivo findings,in vitro studies using murine tubular epithelial cells indicated an antiproliferative effect of CXCL10 upon the intensity of cell proliferation and the number of Ki67-positive cells. These data suggest that CXCL10 plays a role in the regulation of tubular cell proliferation following renal ischemia-reperfusion injury.

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CXC chemokines in angiogenesis

Cited by 358 publications

References 157 publications

CXC chemokines located in the 4q21 region are up-regulated in breast cancer

CXC chemokines located in the 4q21 region are up-regulated in breast cancer

Angiogenic and Angiostatic Chemokines in Idiopathic Pulmonary Fibrosis and Granulomatous Lung Disease

IFN-Inducible Protein 10 (CXCL10) Regulates Tubular Cell Proliferation in Renal Ischemia-Reperfusion Injury

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