Role of the chemokines CCL3/MIP-1α and CCL5/RANTES in sponge-induced inflammatory angiogenesis in mice

Barcelos, Lucíola da Silva; Coelho, Amanda M.; Russo, Remo C.; Guabiraba, Rodrigo; Souza, Adriano Lopes de; Bruno-Lima, Guilherme; Proudfoot, Amanda E. I.; Andrade, Sílvia Passos; Teixeira, Mauro Martins

doi:10.1016/j.mvr.2009.04.009

Cited by 41 publications

(36 citation statements)

References 48 publications

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“…28 Barcelos et al found that antagonism of RANTES receptors with Met-RANTES reduced atherosclerotic plaque formation in mice. 29 Braunersreuther et al reported that RANTES plays a central role in promoting late-stage atherosclerosis in the context of accelerated atherosclerosis in ApoE -/-mice promoted by high-fat diet. 30 Fractalkine (CX3CL1) is a unique member of the CX3C chemokine subfamily.…”

Section: Discussionmentioning

confidence: 99%

Independent Roles of Monocyte Chemoattractant Protein-1, Regulated on Activation, Normal T-Cell Expressed and Secreted and Fractalkine in the Vulnerability of Coronary Atherosclerotic Plaques

Li¹,

Guo²,

Luan³

et al. 2012

Circ J

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Section: Discussionmentioning

confidence: 99%

Independent Roles of Monocyte Chemoattractant Protein-1, Regulated on Activation, Normal T-Cell Expressed and Secreted and Fractalkine in the Vulnerability of Coronary Atherosclerotic Plaques

Li¹,

Guo²,

Luan³

et al. 2012

Circ J

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“…CCL5 is a potent chemoattractant for many cell types, such as monocytes, NK cells (74,75), memory T cells (75), eosinophils (76), and dendritic cells (77), many of which are present in KS lesions. CCL5 levels correlated with neovascularization in a mouse model of angiogenesis (78), and CCL5 is thought to play a pivotal role in the recruitment of endothelial progenitors that are essential for neovascularization through interaction with CCR5 (79). KS is characterized by chronic inflammation and neoangiogenesis, and the observed kaposin B-induced increase in CCL5 has the potential to mediate these effects and contribute significantly to KS tumorigenesis.…”

Section: Figmentioning

confidence: 98%

Kaposi's Sarcoma-Associated Herpesvirus Kaposin B Induces Unique Monophosphorylation of STAT3 at Serine 727 and MK2-Mediated Inactivation of the STAT3 Transcriptional Repressor TRIM28

King

2013

J Virol

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Kaposi's sarcoma-associated herpesvirus (KSHV) is the etiologic agent of primary effusion lymphoma (PEL), multicentric Castleman's disease (MCD), and the inflammation-driven neoplasm Kaposi's sarcoma (KS). A triad of processes, including abnormal proliferation of endothelial cells, aberrant angiogenesis, and chronic inflammation, characterize KS lesions. STAT3 is a key transcription factor governing these processes, and deregulation of STAT3 activity is linked to a wide range of cancers, including PEL and KS. Using primary human endothelial cells (ECs), I demonstrate that KSHV infection modulated STAT3 activation in two ways: (i) KSHV induced uncoupling of canonical tyrosine (Y) and serine (S) phosphorylation events while (ii) concomitantly inducing the phosphorylation and inactivation of TRIM28 (also known as KAP-1 or TIF-1␤), a newly identified negative regulator of STAT3 activity. KSHV infection of primary ECs induced chronic STAT3 activation characterized by a shift from the canonical dual P-STAT3 Y705 S727 form to a mono P-STAT3 S727 form. Expression of the latent protein kaposin B promoted the unique phosphorylation of STAT3 at S727, in the absence of Y705, activated the host kinase mitogen-activated protein kinase-activated protein (MAPKAP) kinase 2 (MK2), and stimulated increased expression of STAT3-dependent genes, including CCL5, in ECs. TRIM28-mediated repression of STAT3 is relieved by phosphorylation of S473, and in vitro kinase assays identified TRIM28 S473 as a bona fide target of MK2. Together, these data suggest that kaposin B significantly contributes to the chronic inflammatory environment that is a hallmark of KS by unique activation of the proto-oncogene STAT3, coupled with MK2-mediated inactivation of the STAT3 transcriptional repressor TRIM28.

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“…34 CCL5 activation of CCR5-mediated angiogenesis is controversial, as studies have shown its ability to both promote and inhibit endothelial cell function. 35,36 Activation of the CCL5/CCR5 chemokine/receptor has been found to promote the recruitment of EPC to promote neovascularization during wound healing and shown to be important for sustaining the granulation phase. 37 …”

Section: Chemokines Regulating Angiogenesismentioning

confidence: 99%

Chemokine Regulation of Angiogenesis During Wound Healing

Bodnar

2015

Advances in Wound Care

131

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Role of the chemokines CCL3/MIP-1α and CCL5/RANTES in sponge-induced inflammatory angiogenesis in mice

Abstract: Thus, endogenous CCL3 appears not to play a role in driving sponge-induced inflammatory angiogenesis in mice. The effects of CCL5 were anti-angiogenic and appeared to be mediated via activation of CCR5.

Cited by 41 publications

References 48 publications

Independent Roles of Monocyte Chemoattractant Protein-1, Regulated on Activation, Normal T-Cell Expressed and Secreted and Fractalkine in the Vulnerability of Coronary Atherosclerotic Plaques

Independent Roles of Monocyte Chemoattractant Protein-1, Regulated on Activation, Normal T-Cell Expressed and Secreted and Fractalkine in the Vulnerability of Coronary Atherosclerotic Plaques

Kaposi's Sarcoma-Associated Herpesvirus Kaposin B Induces Unique Monophosphorylation of STAT3 at Serine 727 and MK2-Mediated Inactivation of the STAT3 Transcriptional Repressor TRIM28

Chemokine Regulation of Angiogenesis During Wound Healing

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