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Adipose-derived stem cells contribute to vascular remodeling via Clec11a+ subpopulation

ABSTRACT: Adipose-derived stem cells contribute to vascular remodeling via Clec11a+ subpopulation

PROVIDER: PRJNA722988 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14274252_1.fastq.gz	Fastqsanger.gz
	SRR14274252_2.fastq.gz	Fastqsanger.gz
	SRR14274253_1.fastq.gz	Fastqsanger.gz
	SRR14274253_2.fastq.gz	Fastqsanger.gz
	SRR14274254_1.fastq.gz	Fastqsanger.gz

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Adipose-derived stem cells contribute to vascular remodeling via Clec11a+ subpopulation

Project description:Recent researches identified the existence of adipose derived stem cells (ADSCs) in adipose tissue. Perivascular ADSCs (PV-ADSCs) locate around vasculatures and can differentiate into vascular lineages. However, the detailed cellular heterogeneity within PV-ADSCs has not been investigated. Therefore, we performed single-cell profiling of subcutaneous (S-) and perivascular (PV-) ADSCs from wild-type and obese mice. After referring to the clustering strategies from other ADSCs’ single-cell data, we provided a more comprehensive picture and trajectory, especially for PV-ADSCs. Both single-cell analysis and in vitro experiments revealed that S-ADSCs from obese mice had impaired abilities of cell migration and proliferation compared to wild-type S-ADSCs. PV-ADSCs have distinctively intrinsic properties. We uncovered 4 subpopulations of PV-ADSCs including Dpp4+, Col4a2+, Clec11a+ and Sult1e1+ cells. Notably, the differentiative function of PV-ADSCs towards vascular lineages was mainly attributed to the existence of Clec11a+ subpopulation, which highly expressed Mgp. The present study provided an integrative view of the ADSCs’ variance from the perspective of origins and obesity.

2022-02-23 | GSE172336 | GEO

Pericytes contribute to pulmonary vascular remodeling via HIF2α signaling

Project description:Pericytes contribute to pulmonary vascular remodeling via HIF2α signaling

| PRJNA873093 | ENA

Pericytes contribute to pulmonary vascular remodeling via HIF2α signaling [lung]

Project description:Pericytes contribute to pulmonary vascular remodeling via HIF2α signaling [lung]

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Beiging of perivascular adipose tissue regulates its inflammation and vascular remodeling

Project description:Although inflammation plays critical roles in the development of atherosclerosis, its regulatory mechanisms remain incompletely understood. Perivascular adipose tissue (PVAT) has been reported to undergo inflammatory changes in response to vascular injury. Here, we showed that vascular injury induced the beiging (brown adipose tissue-like phenotype change) of PVAT, which fine-tunes inflammatory response and thus vascular remodeling as a protective mechanism. In a mouse model of endovascular injury, macrophages accumulated in PVAT, causing beiging phenotype change. Inhibition of PVAT beiging by genetically silencing PRDM16, a key regulator to beiging, exacerbated inflammation and vascular remodeling following injury. Conversely, activation of PVAT beiging attenuated inflammation and pathological vascular remodeling. Single-cell RNA sequencing revealed that beige adipocytes abundantly expressed neuregulin 4 (Nrg4) which critically regulated alternative macrophage activation. Importantly, significant beiging was observed in the diseased aortic PVAT in patients with acute aortic dissection. Taken together, vascular injury induced the beiging of adjacent PVAT with macrophage accumulation, where NRG4 secreted from the beige PVAT facilitated alternative activation of macrophages, leading to the resolution of vascular inflammation. Our study demonstrated the pivotal roles of PVAT in vascular inflammation and remodeling and will open a new avenue for treating atherosclerosis.

2022-06-21 | GSE206399 | GEO

Obesity drives depot-specific vascular remodeling in white adipose tissue

Project description:Obesity drives depot-specific vascular remodeling in white adipose tissue

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Beiging of perivascular adipose tissue regulates its inflammation and vascular remodeling

Project description:Beiging of perivascular adipose tissue regulates its inflammation and vascular remodeling

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GLI1+ cells contribute to vascular remodeling in hypoxia- and cigarette smokeinduced pulmonary hypertension

Project description:GLI1+ cells contribute to vascular remodeling in hypoxia- and cigarette smokeinduced pulmonary hypertension

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Pericytes contribute to pulmonary vascular remodeling via HIF2α signaling [lung]

Project description:Vascular remodeling is the process of structural alteration and cell rearrangement of blood vessels in response to injury and is the cause of many of the world's most afflicted cardiovascular conditions, including pulmonary arterial hypertension(PAH). Many studies have focused on the effects of vascular endothelial cells and smooth muscle cells(SMCs) during vascular remodeling, but pericytes, an indispensable cell population residing largely in capillaries, are ignored in this maladaptive process. Here we report that hypoxia-inducible factor 2α(HIF2α) expression is increased in human PAH patient lung tissues and HIF2α overexpressed pericytes result in greater contractility and an impaired endothelial-pericyte interaction. Using single-cell RNAseq and hypoxia-induced pulmonary hypertension(PH) models, we show HIF2α as a major molecular regulator for pericytes’ transformation into SMC-like cells. HIF2α overexpression in pericyte-selective mice exacerbate PH and right ventricular hypertrophy. Temporal cellular lineage tracing shows that HIF2α overexpressing reporter NG2+ cells (pericyte-selective) relocate from capillaries to arterioles and co-express SMA. This novel insight into the potential role of NG2+ pericytes in pulmonary vascular remodeling via HIF2α signaling suggests a potential drug target for PH.

2023-12-11 | GSE249461 | GEO

GLI1+ cells contribute to vascular remodeling in hypoxia- and cigarette smoke-induced pulmonary hypertension

Project description:GLI1+ cells contribute to vascular remodeling in hypoxia- and cigarette smoke-induced pulmonary hypertension

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Obesity drives depot-specific vascular remodeling in white adipose tissue

Project description:Obesity-driven pathological expansion of white adipose tissue (WAT) is a key driver of endothelial dysfunction. Contrary to this paradigm, early vascular alterations associated with over nutrition also exacerbate AT dysfunction. To dissect this complex cause and consequence relationship, here we perform a single-cell transcriptomics screen to generate a detailed landscape of endothelial heterogeneity and vascular alterations in murine model of obesity. Given the differences in ontogeny and function of distinct WAT depots, we demarcate key differences in subcutaneous and visceral WAT vasculature. In addition to descriptive taxonomy, we perform in-depth validation and characterization of our in silico data. We identify a sWAT specific fenestrated endothelial cell subtype, which is drastically reduced in obese conditions. This reduction was associated with a decrease in VEGFA expressing perivascular cells. The novel endothelial subtypes provide a basis for future research and new directions for therapeutic interventions.

2023-05-26 | E-MTAB-12855 | biostudies-arrayexpress

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