Chemokines as mediators of angiogenesis

Mehrad, Borna; Keane, Michael P.; Strieter, Robert M.

doi:10.1160/th07-01-0040

Cited by 180 publications

(152 citation statements)

References 120 publications

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“…Monoclonal antibodies targeting chemokines or chemokine receptors involved in angiogenesis have been used to modulate a dysbalance of angiogenesis and angiostasis under pathological conditions [173]. Idiopathic pulmonary fibrosis, an often fatal pulmonary fibroproliferative lung disease, is characterized by a dysregulation of tissue repair and neovascularisation as reflected by overexpression in the lung of the angiogenic ELR?…”

Section: Effects In Angiogenesis/fibroproliferationmentioning

confidence: 99%

Platelet-derived chemokines: pathophysiology and therapeutic aspects

Flad

Brandt

2010

Cell. Mol. Life Sci.

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The identification of chemokines in blood platelets has strengthened our view of these cells as participants in immune host defense. Platelet chemokines representing prestored and rapidly releasable proteins may play a major role as first-line inflammatory mediators. This is evident from their capability to recruit early inflammatory cells such as neutrophil granulocytes and monocytes and even to exhibit direct antimicrobial activity. However, insight is growing that platelet chemokines may be also long-term regulators, e.g., by activating T lymphocytes, by modulating the formation of endothelium and even thrombocytopoiesis itself. This review deals with the individual and cooperative functionality of platelet chemokines, as well as their potential as a basis for therapeutic intervention in the pathology of inflammation, infection, allergy and tumors. Within this context, therapeutic strategies based on the use of antibodies, modified chemokines, chemokine-binding proteins and chemokine receptor antagonists as well as first clinical studies will be addressed.

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Section: Effects In Angiogenesis/fibroproliferationmentioning

confidence: 99%

Platelet-derived chemokines: pathophysiology and therapeutic aspects

Flad

Brandt

2010

Cell. Mol. Life Sci.

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“…Thus, CXC chemokines are not only responsible for leukocyte recruitment to inflamed tissues, they also regulate the inflammatory reaction leading to angiogenesis, tissue repair and new tissue generation [64,65,66]. Recent evidence indicates that endothelial cells express specific CXC receptors (CXCR), such as CXCR1, CXCR2, CXCR3 and CXCR4, which induce endothelial cell chemotaxis and form blood vessels [67].…”

Section: Inflammation and Angiogenesismentioning

confidence: 99%

Mast Cells and Basophils: A Potential Link in Promoting Angiogenesis during Allergic Inflammation

Crivellato

Travan

Ribatti

2009

Int Arch Allergy Immunol

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Mast cells and basophils are granulated metachromatic cells which possess complex and partially overlapping roles in acquired and innate immunity, including both effector and regulatory activities. Mast cells and basophils cooperate in exacerbating and/or modulating inflammation as well as in mediating subsequent tissue repair. Mast cells release a series of potent proangiogenic molecules during inflammation that stimulate vessel sprouting and new vessel formation. Recent data suggest that basophils may also play a role in inflammation-related angiogenesis, principally but not exclusively through the expression of several forms of vascular endothelial growth factors and their receptors. This review focuses on the potential cooperative link between mast cells and basophils in promoting angiogenesis during allergic inflammation. We discuss the multifaceted roles of mast cells and basophils in inflammatory mechanisms of allergic diseases and whether these cells can be both source and target of proangiogenic mediators.

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“…CXCL6 [granulocyte chemotactic protein-2 (GCP2)] is a member of the CXC chemokine family, which is characterized by the presence of four conserved cysteine residues near the amino terminus forming the Cys-X-Cys or "CXC" motif [13]. The CXC chemokine family is divided into ELR+ and ELR- chemokines based on the presence or absence of the amino acid sequence Glu-Leu-Arg (ELR) [14].…”

Section: Introductionmentioning

confidence: 99%

HIF-1a Plays a Role in the Chemotactic Migration of Hepatocarcinoma Cells Through the Modulation of CXCL6 Expression

Tian

Huang

Zhao

et al. 2014

Cell Physiol Biochem

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Background/Aims: Hypoxia promotes the progression and metastasis of hepatocellular carcinoma (HCC). Hypoxia inducible factor-α (HIF-1α) regulates the expression of various chemokines involved in tumor growth, angiogenesis and metastasis. Methods: The role of HIF-1α in HCC tumor growth and invasion and the prognosis of patients with HCC was investigated in cell lines and patient samples. HIF-1α mRNA and protein levels were assessed by qRT-PCR and western blotting. Silencing of HIF-1α downregulated the expression of granulocyte chemotactic protein-2 (GCP-2)/CXCL6, a CXC ELR+ chemokine, in HCC cells, and a luciferase assay showed that HIF-1α binds to a hypoxia response element in the promoter of CXCL6 and regulates its transcription. Induction of HIF-1α by hypoxia promoted the migration and invasion of HCC cells in vitro, and this effect was suppressed by an anti-CXCL6 antibody. Results: HIF-1α is upregulated in HCC cell lines and tissues and its effect on promoting invasion and metastasis is mediated by its direct interaction with the pro-angiogenic chemokine CXCL6. CXCL6 expression was associated with poor prognosis of HCC patients. Conclusion: HIF-1α promotes HCC progression and metastasis by upregulating CXCL6 transcription in HCC cells, providing a potential novel therapeutic target for the treatment of HCC.

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Chemokines as mediators of angiogenesis

Cited by 180 publications

References 120 publications

Platelet-derived chemokines: pathophysiology and therapeutic aspects

Platelet-derived chemokines: pathophysiology and therapeutic aspects

Mast Cells and Basophils: A Potential Link in Promoting Angiogenesis during Allergic Inflammation

HIF-1a Plays a Role in the Chemotactic Migration of Hepatocarcinoma Cells Through the Modulation of CXCL6 Expression

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