Regulation of monocyte subset systemic levels by distinct chemokine receptors controls post-ischaemic neovascularization

Cochain, Clément; Rodero, Mathieu P; Vilar, José; Récalde, Alice; Richart, Adèle; Loinard, Céline; Zouggari, Yasmine; Guérin, Coralie L.; Duriez, Micheline; Combadière, Béhazine; Poupel, Lucie; Lévy, Bernard; Mallat, Ziad; Combadière, Christophe; Silvestre, Jean‐Sébastien

doi:10.1093/cvr/cvq153

Cited by 64 publications

(85 citation statements)

References 28 publications

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“…Murine monocytes present in blood and the major monocyte reservoirs of the bone marrow and spleen express GFP. A 7/4 expression was used to discriminate between monocyte subsets, 30 and we found that both the CD11b Figure 4B). Analysis of Ly-6C is also commonly used to differentiate between mouse monocyte subsets; accordingly, we confirmed that Ly-6C and 7/4 identify the same populations of blood monocytes and that our observations of GFP expression can be applied to the Ly-6C…”

Section: Promoter Directs Gfp Transgene Expression E35mentioning

confidence: 89%

Human CD68 promoter GFP transgenic mice allow analysis of monocyte to macrophage differentiation in vivo

Iqbal

McNeill

Kapellos

et al. 2014

Blood

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• CD68-GFP reporter mice show GFP transgene expression in both monocytes and tissue resident macrophage populations.• Adoptively transferred CD68-GFP monocytes maintain GFP expression after recruitment in an ongoing inflammatory response.The recruitment of monocytes and their differentiation into macrophages at sites of inflammation are key events in determining the outcome of the inflammatory response and initiating the return to tissue homeostasis. To study monocyte trafficking and macrophage differentiation in vivo, we have generated a novel transgenic reporter mouse expressing a green fluorescent protein (GFP) under the control of the human CD68 promoter. CD68-GFP mice express high levels of GFP in both monocyte and embryoderived tissue resident macrophages in adult animals. The human CD68 promoter drives GFP expression in all CD115 1 monocytes of adult blood, spleen, and bone marrow; we took advantage of this to directly compare the trafficking of bone marrow-derived CD68-GFP monocytes to that of CX 3 CR1 GFP monocytes in vivo using a sterile zymosan peritonitis model. Unlike CX 3 CR1 GFP monocytes, which downregulate GFP expression on differentiation into macrophages in this model, CD68-GFP monocytes retain high-level GFP expression for 72 hours after differentiation into macrophages, allowing continued cell tracking during resolution of inflammation. In summary, this novel CD68-GFP transgenic reporter mouse line represents a powerful resource for analyzing monocyte mobilization and monocyte trafficking as well as studying the fate of recruited monocytes in models of acute and chronic inflammation. (Blood. 2014;124(15):e33-e44)

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Section: Promoter Directs Gfp Transgene Expression E35mentioning

confidence: 89%

Human CD68 promoter GFP transgenic mice allow analysis of monocyte to macrophage differentiation in vivo

Iqbal

McNeill

Kapellos

et al. 2014

Blood

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“…40 By contrast, in a leg ischemia model, the transplantation of Ly6Chi monocytes, but not of Ly6Clo monocytes, leads to activation of the processes of neovascularization. 41 Two subtypes of macrophage can also be distinguished on the basis of various markers and functional criteria: the M1 population expresses the inducible NOS and proinflammatory cytokines, such as interleukin-1 and interleukin-12, whereas the M2 population produces large amounts of arginase 1, the anti-inflammatory cytokine interleukin-10 and VEGF.…”

Section: Diabetes Mellitus and Inflammation-related Pathwaysmentioning

confidence: 99%

“…The cellular response of monocytes to VEGF-A is attenuated in patients with diabetes mellitus because of a downstream signal transduction defect. 46 Mice lacking the chemokine receptor CCR2 47 or its ligand CCL2 41,48 display impaired revascularization associated with a low level of monocyte/macrophage infiltration in ischemic territories. The monocyte migration toward CCL2 is also strongly reduced in diabetic rabbits with CLI, leading to a reduced blood volume index in the region of growing collaterals.…”

Section: Diabetes Mellitus and The Inflammatory Balance In Ischemic Mmentioning

confidence: 99%

Diabetes Mellitus and Ischemic Diseases

Howangyin

Silvestre

2014

ATVB

124

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Hypoxia-Inducible Factor 1Hypoxia, at least in part through activation of the hypoxiainducible factor 1 (HIF-1) α-related pathways, controls all steps of the postischemic revascularization process. Recent studies uncover that destabilization of HIF-1 is most likely the event that transduces hyperglycemia into the loss of the cellular response to hypoxia in most diabetic complications.2 Levels of HIF-1α are decreased in biopsies from foot ulcers of patients with diabetes mellitus as compared with venous ulcers that share the same hypoxic environment but are not exposed to hyperglycemia.3 Downregulation of HIF-1 in response to hyperglycemia also seems to account for the decreased collateral growth triggered by myocardial ischemia in patients with © 2014 American Heart Association, Inc. Abstract-In patients with diabetes mellitus, the ability of ischemic tissue to synchronize the molecular and cellular events leading to restoration of tissue perfusion in response to the atherosclerotic occlusion of a patent artery is markedly impaired. As a consequence, adverse tissue remodeling and the extent of ischemic injury are intensified, leading to increased morbidity and mortality. Growing evidence from preclinical and clinical studies has implicated alterations in hypoxia-inducible factor 1 levels in the abrogation of proangiogenic pathways, including vascular endothelial growth factor A/phosphoinositide 3′ kinase/AKT/endothelial nitric oxide synthase and in the activation of antiangiogenic signals characterized by accumulation of advanced glycation end products, reactive oxygen species overproduction, and endoplasmic reticulum stress. In addition, the diabetic milieu shows a switch toward proinflammatory antiregenerative pathways. Finally, the mobilization, subsequent recruitment, and the proangiogenic potential of the different subsets of angiogenesis-promoting bone marrow-derived cells are markedly impaired in the diabetic environment. In this review, we will give an overview of the current understanding on the signaling molecules contributing to the diabetes mellitusinduced impairment of postischemic revascularization mainly in the setting of myocardial infarction or critical limb ischemia. (Arterioscler Thromb Vasc Biol. 2014;34:1126-1135.)

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“…5 Hence, numerous studies have demonstrated the importance of lymphocyte and monocyte recruitment in stimulating vessel growth and remodeling in ischemic tissue, [6][7][8][9][10][11] including Tie-2-positive myeloid cells. Indeed, the authors used Tie2Cre mouse to generate XBP1ecko animals, and it is conceivable that hematopoietic cells contribute to the XBP1-deficient phenotype.…”

Section: Article See P 1712mentioning

confidence: 99%

Vascular Endothelial Growth Factor and Angiogenesis

Silvestre

2013

Circulation

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Regulation of monocyte subset systemic levels by distinct chemokine receptors controls post-ischaemic neovascularization

Abstract: Altogether, our data demonstrate that regulation of proangiogenic Ly6C(hi) monocytes systemic levels by CCL2/CCR2 controls post-ischaemic vessel growth, whereas Ly6C(lo) monocytes have no major role in this setting.

Cited by 64 publications

References 28 publications

Human CD68 promoter GFP transgenic mice allow analysis of monocyte to macrophage differentiation in vivo

Human CD68 promoter GFP transgenic mice allow analysis of monocyte to macrophage differentiation in vivo

Diabetes Mellitus and Ischemic Diseases

Vascular Endothelial Growth Factor and Angiogenesis

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