Adventitial SCA-1 + Progenitor Cell Gene Sequencing Reveals the Mechanisms of Cell Migration in Response to Hyperlipidemia

Kokkinopoulos, Ioannis; Wong, Man Sau; Potter, Claire M.F.; Xie, Yao; Yu, Baoqi; Warren, Derek; Nowak, Witold; Bras, Alexandra Le; Ni, Zhichao; Zhou, Chao; Ruan, Xiongzhong; Karamariti, Eirini; Hu, Yanhua; Zhang, Li; Xu, Qingbo

doi:10.1016/j.stemcr.2017.06.011

Cited by 35 publications

(28 citation statements)

References 65 publications

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“… 119 In addition, apolipoprotein E–deficient (ApoE −/− ) mice, which model atherosclerosis, have elevated numbers of Sca-1 + cells in the aortic endothelium. 120 Hu et al 26 demonstrated that adventitia-resident vascular progenitor cells express Sca-1 and that these cells contributed to atherosclerosis via migration and differentiation into SMCs. Among other studies, the work of Yu et al 121 further supported the notion that resident Sca-1 + cells contribute to neointima formation, which may increase plaque burden.…”

Section: Vascular Resident Stem Cells In Adultsmentioning

confidence: 99%

Role of Resident Stem Cells in Vessel Formation and Arteriosclerosis

Zhang

Bhaloo

Chen

et al. 2018

Circulation Research

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108

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Vascular, resident stem cells are present in all 3 layers of the vessel wall; they play a role in vascular formation under physiological conditions and in remodeling in pathological situations. Throughout development and adult early life, resident stem cells participate in vessel formation through vasculogenesis and angiogenesis. In adults, the vascular stem cells are mostly quiescent in their niches but can be activated in response to injury and participate in endothelial repair and smooth muscle cell accumulation to form neointima. However, delineation of the characteristics and of the migration and differentiation behaviors of these stem cells is an area of ongoing investigation. A set of genetic mouse models for cell lineage tracing has been developed to specifically address the nature of these cells and both migration and differentiation processes during physiological angiogenesis and in vascular diseases. This review summarizes the current knowledge on resident stem cells, which has become more defined and refined in vascular biology research, thus contributing to the development of new potential therapeutic strategies to promote endothelial regeneration and ameliorate vascular disease development.

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Section: Vascular Resident Stem Cells In Adultsmentioning

confidence: 99%

Role of Resident Stem Cells in Vessel Formation and Arteriosclerosis

Zhang

Bhaloo

Chen

et al. 2018

Circulation Research

Self Cite

108

View full text Add to dashboard Cite

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Section: Discussionmentioning

confidence: 68%

Homocysteine Promotes Migration of Adventitial Fibroblasts via Angiotensin II type 1 Receptor Activation to Aggravate Atherosclerosis

Zhu¹,

Hao²,

Li³

et al. 2020

Preprint

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BackgroundHyperhomocysteinemia (HHcy) is an independent risk factor for atherosclerosis. However, the mechanisms of HHcy-induced arteriosclerosis are largely unknown. Objective:To clarify the effect of Hcy on adventitial fibroblasts (AFs) and its relation with angiotensin II type 1 receptor (AT1R).Method:The apolipoprotein E gene-deficient mice (Apoe−/−) were used as the murine model for atherosclerosis. HHcy was induced and treated by feeding them 1.5% methionine and telmisartan (gavage 10 mg/kg/d) for 12 weeks, respectively. The AFs and HEK293A cells transfected with the AT1R plasmid were used to investigate the interaction between Hcy and AT1R. All data were expressed as mean ± SEM. The data were analyzed by one-way ANOVA or repeated measurement ANOVA.Results:HHcy aggravated the plaque area of the aortic root and increased the expression of IL-6, MCP-1, and the macrophage marker Mac3 in the plaque and adventitia of the aorta, whereas telmisartan improved this effect. Hyperhomocysteinemia induced the occurrence of the AFs marker protein ER-TR7 in the plaque and the entire layer of the aorta, whereas telmisartan also improved this effect, indicating that hyperhomocysteinemia induced AFs migration and that AT1R mediated this process. Hcy increased the production of AFs H2O2, ROS, and IL-6 of AFs, indicating that Hcy activated the oxidative stress and inflammatory reactions, which may induce cell migration. The subsequent scratch and transwell experiments confirmed that Hcy induced the AFs migration and that telmisartan inhibited this effect. Hcy increased the expression of AFs AT1R and the phosphorylation levels of PKC and ERK1/2 in the AF and HEK293A cells transfected with the AT1R plasmid, whereas telmisartan inhibited this effect, indicating that Hcy activated AT1R intracellular signaling pathway.Conclusion:Hcy promoted adventitial inflammation, induced AFs migration, and aggravated atherosclerosis by activating AT1R.

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“…Furthermore, lipid loading increased adventitial metalloproteinase-9 levels to promote cell migration. 30 Intriguingly, we found that HHcy induced AFs migration and invasion in vitro and in vivo. Telmisartan also inhibited the migration and invasion of broblasts induced by HHcy (Figs.…”

Section: Discussionmentioning

confidence: 68%

Homocysteine promotes migration of adventitial fibroblasts via Angiotensin II type 1 receptor activation to aggravate atherosclerosis

Zhu

Hao

et al. 2020

Preprint

View full text Add to dashboard Cite

Background: Hyperhomocysteinemia (HHcy) is an independent risk factor for atherosclerosis. However, the mechanisms of HHcy-induced arteriosclerosis are largely unknown. Objective: To clarify the effect of Hcy on adventitial fibroblasts (AFs) and its relation with angiotensin II type 1 receptor (AT1R). Method: The apolipoprotein E gene-deficient mice (Apoe−/−) were used as the murine model for atherosclerosis. HHcy was induced and treated by feeding them 1.5% methionine and telmisartan (gavage 10 mg/kg/d) for 12 weeks, respectively. The AFs and HEK293A cells transfected with the AT1R plasmid were used to investigate the interaction between Hcy and AT1R. All data were expressed as mean ± SEM. The data were analyzed by one-way ANOVA or repeated measurement ANOVA. Results: HHcy aggravated the plaque area of the aortic root and increased the expression of IL-6, MCP-1, and the macrophage marker Mac3 in the plaque and adventitia of the aorta, whereas telmisartan improved this effect. Hyperhomocysteinemia induced the occurrence of the AFs marker protein ER-TR7 in the plaque and the entire layer of the aorta, whereas telmisartan also improved this effect, indicating that hyperhomocysteinemia induced AFs migration and that AT1R mediated this process. Hcy increased the production of AFs H 2 O 2 , ROS, and IL-6 of AFs, indicating that Hcy activated the oxidative stress and inflammatory reactions, which may induce cell migration. The subsequent scratch and transwell experiments confirmed that Hcy induced the AFs migration and that telmisartan inhibited this effect. Hcy increased the expression of AFs AT1R and the phosphorylation levels of PKC and ERK1/2 in the AF and HEK293A cells transfected with the AT1R plasmid, whereas telmisartan inhibited this effect, indicating that Hcy activated AT1R intracellular signaling pathway. Conclusion: Hcy promoted adventitial inflammation, induced AFs migration, and aggravated atherosclerosis by activating AT1R.

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Adventitial SCA-1 + Progenitor Cell Gene Sequencing Reveals the Mechanisms of Cell Migration in Response to Hyperlipidemia

Cited by 35 publications

References 65 publications

Role of Resident Stem Cells in Vessel Formation and Arteriosclerosis

Role of Resident Stem Cells in Vessel Formation and Arteriosclerosis

Homocysteine Promotes Migration of Adventitial Fibroblasts via Angiotensin II type 1 Receptor Activation to Aggravate Atherosclerosis

Homocysteine promotes migration of adventitial fibroblasts via Angiotensin II type 1 receptor activation to aggravate atherosclerosis

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