RANTES/CCL5-induced pro-angiogenic effects depend on CCR1, CCR5 and glycosaminoglycans

Suffee, Nadine; Hlawaty, Hanna; Meddahi‐Pellé, Anne; Maillard, Loïc; Louedec, Liliane; Haddad, Oualid; Martin, Loı̈c; Laguillier, Christelle; Richard, Benjamin; Oudar, Olivier; Letourneur, Didier; Charnaux, Nathalie; Sutton, Angéla

doi:10.1007/s10456-012-9285-x

Cited by 92 publications

(79 citation statements)

References 47 publications

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“…The anti-inflammatory and immunomodulatory activities of resveratrol were further confirmed by the inhibition of many chemokines in both subsets, particularly IL-8, MCP-1, CCL3, CCL4, and RANTES and of the growth factors G-CSF and GM-CSF (in M1 cells) and VEGF (in M2 cells). These inflammatory mediators, beside their active role in recruiting leukocytes into inflammatory sites, may stimulate endothelial cell migration, spreading, and neo-vessel formation, thus promoting the angiogenesis associated with the progression of atherosclerotic plaque [28]. The inhibitory effects of resveratrol on TNF- α , IL-6, IL-8, MCP-1, CCL-4, RANTES, and G-CSF in the M1 macrophage subset and on TNF- α , IL-12, IL-8, MCP-1, CCL3, CCL-4, RANTES, and VEGF in M2 macrophages together with metalloproteinases inhibition may be added to a variety of resveratrol antiatherogenic actions, since these molecules are known to be involved in inflammatory responses in arterial walls during progression of atherosclerosis [29].…”

Section: Discussionmentioning

confidence: 99%

Resveratrol Counteracts Inflammation in Human M1 and M2 Macrophages upon Challenge with 7-Oxo-Cholesterol: Potential Therapeutic Implications in Atherosclerosis

Buttari

Profumo

Segoni

et al. 2014

Oxidative Medicine and Cellular Longevity

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Macrophages consist of two main subsets: the proinflammatory M1 subset and the anti-inflammatory M2 one. 7-oxo-cholesterol, the most abundant cholesterol autoxidation product within atherosclerotic plaque, is able to skew the M1/M2 balance towards a proinflammatory profile. In the present study, we explored the ability of the polyphenolic compound resveratrol to counteract the 7-oxo-cholesterol-triggered proinflammatory signaling in macrophages. Resveratrol-pretreated human monocyte-derived M1 and M2 macrophages were challenged with 7-oxo-cholesterol and analyzed for phenotype and endocytic ability by flow cytometry, for metalloproteinase- (MMP-) 2 and MMP-9 by gelatin zymography, and for cytokine, chemokine, and growth factor secretome by a multiplex immunoassay. We also investigated the NF-κB signaling pathway. In the M1 subset, resveratrol prevented the downregulation of CD16 and the upregulation of MMP-2 in response to 7-oxo-cholesterol, whereas in M2 macrophages it prevented the upregulation of CD14, MMP-2, and MMP-9 and the downregulation of endocytosis. Resveratrol prevented the upregulation of several proinflammatory and proangiogenic molecules in both subsets. We identified modulation of NF-κB as a potential mechanism implicated in 7-oxo-cholesterol and resveratrol effects. Our results strengthen previous findings on the immunomodulatory ability of resveratrol and highlight its role as potential therapeutic or preventive compound, to counteract the proatherogenic oxysterol signaling within atherosclerotic plaque.

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Section: Discussionmentioning

confidence: 99%

Resveratrol Counteracts Inflammation in Human M1 and M2 Macrophages upon Challenge with 7-Oxo-Cholesterol: Potential Therapeutic Implications in Atherosclerosis

Buttari

Profumo

Segoni

et al. 2014

Oxidative Medicine and Cellular Longevity

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“…The chemokine (C-C motif) ligand 5 (also CCL5) is also known as RANTES (regulated on activation, normal T cell expressed and secreted) [33]. It is of interest that the RANTES/CCL5-activity seems to be related to the in vitro promotion of endothelial cell migration, spreading and neo-vessel formation [33].…”

Section: Resultsmentioning

confidence: 99%

“…It is of interest that the RANTES/CCL5-activity seems to be related to the in vitro promotion of endothelial cell migration, spreading and neo-vessel formation [33]. RANTES/CCL5-mediated angiogenesis depends at least partly on VEGF secretion by ECs [33].…”

Section: Resultsmentioning

confidence: 99%

Key Proteins Involved in Spheroid Formation and Angiogenesis in Endothelial Cells After Long-Term Exposure to Simulated Microgravity

Dittrich

Grimm

Sahana

et al. 2018

Cell Physiol Biochem

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Background/Aims: Cardiovascular complications are common in astronauts returning from a prolonged spaceflight. These health problems might be driven by complex modulations of gene expression and protein synthesis in endothelial cells (ECs). Studies on the influence of microgravity on phenotype, growth pattern and biological processes of ECs can help to understand these complications. Methods: We exposed ECs (EA.hy926) to a Random Positioning Machine (RPM). Proteins associated with cell structure, angiogenesis and endothelial dysfunction were investigated in distinct pools of multicellular spheroids (MCS), adherent cells (AD) and tubular structures (TS) formed after a 35-day RPM-exposure. Results: Combining morphological and molecular approaches, we found AD, MCS and TS with changes in the synthesis and release of proteins involved in three-dimensional growth. Fibronectin and monocyte chemoattractant protein-1 (MCP-1) mRNAs and protein contents were elevated along with an increased secretion of vascular endothelial growth factor (VEGF), interleukin (IL)-6, IL-8, MCP-1, intercellular adhesion molecule 1 (ICAM-1), vascular cell adhesion molecule 1 (VCAM-1), neutrophil gelatinase-associated lipocalin (NGAL) and regulated on activation, normal T cell expressed and secreted (RANTES) proteins in the culture supernatant as determined by multianalyte profiling technology. Together they form a network of interaction. Conclusions: These results show that a prolonged RPM-exposure of ECs induced TS and MCS formation. The factors VEGF, NGAL, IL-6, IL-8, MCP-1, VCAM-1, ICAM-1, fibronectin and RANTES seem to be affected when gravity is omitted.

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“…My studies demonstrate that the constitutively active form of MK2 (MK2EE) in ECs induced 0.4-to 7-fold and 2.4-to 3.4-fold upregulations of CCL5 and IL-6 mRNA, respectively, indicating the relative contribution of MK2-mediated stabilization of CCL5 mRNA in ECs to the upregulation observed when kaposin B was expressed, was small. KS lesions are characterized by chronic inflammation and neoangiogenesis; CCL5 is a potent mediator of both processes (69)(70)(71)(72). The importance of CCL5 in KS pathogenesis is underscored by the fact that both CCL5 and the cognate receptor CCR5 are upregulated in KS but not normal skin (73).…”

Section: Figmentioning

confidence: 99%

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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RANTES/CCL5-induced pro-angiogenic effects depend on CCR1, CCR5 and glycosaminoglycans

Cited by 92 publications

References 47 publications

Resveratrol Counteracts Inflammation in Human M1 and M2 Macrophages upon Challenge with 7-Oxo-Cholesterol: Potential Therapeutic Implications in Atherosclerosis

Resveratrol Counteracts Inflammation in Human M1 and M2 Macrophages upon Challenge with 7-Oxo-Cholesterol: Potential Therapeutic Implications in Atherosclerosis

Key Proteins Involved in Spheroid Formation and Angiogenesis in Endothelial Cells After Long-Term Exposure to Simulated Microgravity

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

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