Isolation and characterization of peritoneal microvascular pericytes

Tang, Lei; Shi, Jun; Yu, Manshu; Shan, Yun; Juan, Zhao; Sheng, Maoyin

doi:10.1002/2211-5463.13386

Cited by 4 publications

(3 citation statements)

References 29 publications

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“…Mural cells were isolated and cultured following a modified version of the protocol previously published 50 . Briefly, the mice were euthanised by i.p.…”

Section: Isolation and Primary Culture Of Mural Cells And In Vitro St...mentioning

confidence: 99%

Sympathetic neuron derived NPY protects from obesity by sustaining the mural progenitors of thermogenic adipocytes

Zhu,

Yao,

Gallo-Ferraz

et al. 2024

Preprint

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Neuropeptide Y (NPY) is secreted by sympathetic nerves1,2, but its direct impact on thermogenic adipocytes is unknown. Here we uncover the mechanism by which peripheral NPY protects from obesity. Our imaging of cleared murine brown and white adipose tissue (BAT and WAT) established that NPY+ sympathetic axons are only a minority that mostly maps to the peri-vasculature; our analysis of single-cell RNA-sequencing datasets identifies mural cells as the main NPY-responsive cells in adipose tissues. We show that NPY sustains mural cells, which are known to be a source of beige cells in both BAT and WAT3-5 and that NPY facilitates the differentiation to thermogenic adipocytes. We found that diet-induced obesity leads to neuropathy of NPY+ axons and concomitant depletion of the mural cell pool of beige fat progenitors. This defect is replicated in conditional knockout (cKO) mice with NPY specifically abrogated from sympathetic neurons. These cKO mice have whitened iBAT with reduced thermogenic ability and lower energy expenditure even before the onset of obesity; they develop adult-onset obesity on a regular chow diet and are more susceptible to diet-induced obesity without increasing food consumption. Our results indicate that relative to central NPY, peripheral NPY produced by the sympathetic nerves has the opposite effect on body weight homeostasis by sustaining the proliferation of the mural cell progenitors of thermogenic adipocytes.

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“…Mural cells were isolated and cultured following a modified version of the protocol previously published 50 . Briefly, the mice were euthanised by i.p.…”

Section: Isolation and Primary Culture Of Mural Cells And In Vitro St...mentioning

confidence: 99%

Sympathetic neuron derived NPY protects from obesity by sustaining the mural progenitors of thermogenic adipocytes

Zhu,

Yao,

Gallo-Ferraz

et al. 2024

Preprint

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“…During angiogenesis, the exchange of cytokines occurs between pericytes and endothelial cells. PDGF-BB, PDGF-DD, endothelin-1 (ET-1), and TGF-β—produced by endothelial cells—act as the primary catalysts for pericyte activation, which results in pericyte damage and stimulates the transition of pericytes into a myofibroblast phenotype ( Tang L. et al, 2022 ). As the marker of differentiated myofibroblasts, α-SMA is an important indicator of PMT.…”

Section: Intercellular Communicationmentioning

confidence: 99%

Intercellular communication in peritoneal dialysis

Sheng,

Shan,

Dai

et al. 2024

Front. Physiol.

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Long-term peritoneal dialysis (PD) causes structural and functional alterations of the peritoneal membrane. Peritoneal deterioration and fibrosis are multicellular and multimolecular processes. Under stimulation by deleterious factors such as non-biocompatibility of PD solution, various cells in the abdominal cavity show differing characteristics, such as the secretion of different cytokines, varying protein expression levels, and transdifferentiation into other cells. In this review, we discuss the role of various cells in the abdominal cavity and their interactions in the pathogenesis of PD. An in-depth understanding of intercellular communication and inter-organ communication in PD will lead to a better understanding of the pathogenesis of this disease, enabling the development of novel therapeutic targets.

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“…The ECs can be isolated from the human umbilical vein, [28][29][30][31][32] cord blood, 33 lung, 34 or liver. 26 The pericytes can be derived from the brain, 29,30 lung, 23 and mesenteric tissue 35 or be replaced by other types of cells, such as mesenchymal stem cells 36 or lung fibroblasts. 33,37 The use of different cellular sources in these models poses a significant challenge to mimicking organ-specific microvessels due to vascular heterogeneity.…”

mentioning

confidence: 99%

Extracellular Matrix Stiffness Regulates Microvascular Stability by Controlling Endothelial Paracrine Signaling to Determine Pericyte Fate

Yu,

Leng,

Song

et al. 2023

ATVB

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BACKGROUND: The differentiation of pericytes into myofibroblasts causes microvascular degeneration, ECM (extracellular matrix) accumulation, and tissue stiffening, characteristics of fibrotic diseases. It is unclear how pericyte-myofibroblast differentiation is regulated in the microvascular environment. Our previous study established a novel 2-dimensional platform for coculturing microvascular endothelial cells (ECs) and pericytes derived from the same tissue. This study investigated how ECM stiffness regulated microvascular ECs, pericytes, and their interactions. METHODS: Primary microvessels were cultured in the tubular microvascular growth medium on 2-dimensional stiff substrates. Stiff ECM was prepared by incubating ECM solution in regular culture dishes for 1 hour followed by PBS wash. Soft ECM with Young modulus of ≈6 kPa was used unless otherwise noted. Bone grafts were prepared from the rat skull. Immunostaining, RNA sequencing, qRT-PCR, Western blotting, and knockdown experiments were performed on the cells. RESULTS: Primary microvascular pericytes differentiated into myofibroblasts (NG2 + αSMA + ) on stiff ECM, even with the TGFβ (transforming growth factor beta) signaling inhibitor A83-01. Soft ECM and A83-01 cooperatively maintained microvascular stability while inhibiting pericyte-myofibroblast differentiation (NG2 + αSMA −/low ). We thus defined 2 pericyte subpopulations: primary (NG2 + αSMA −/low ) and activated (NG2 + αSMA + ) pericytes. Soft ECM promoted microvascular regeneration and inhibited fibrosis in bone graft transplantation in vivo. As integrins are the major mechanosensor, we performed qRT-PCR screening of integrin family members and found Itgb1 (integrin β1) was the major subunit downregulated by soft ECM and A83-01 treatment. Knocking down Itgb1 suppressed myofibroblast differentiation on stiff ECM. Interestingly, ITGB1 phosphorylation (Y783) was mainly located on microvascular ECs on stiff ECM, which promoted EC secretion of paracrine factors, including CTGF (connective tissue growth factor), to induce pericyte-myofibroblast differentiation. CTGF knockdown or monoclonal antibody treatment partially reduced myofibroblast differentiation, implying the participation of multiple pathways in fibrosis formation. CONCLUSIONS: ECM stiffness and TGFβ signaling cooperatively regulate microvascular stability and pericyte-myofibroblast differentiation. Stiff ECM promotes EC ITGB1 phosphorylation (Y783) and CTGF secretion, which induces pericyte-myofibroblast differentiation.

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Isolation and characterization of peritoneal microvascular pericytes

Cited by 4 publications

References 29 publications

Sympathetic neuron derived NPY protects from obesity by sustaining the mural progenitors of thermogenic adipocytes

Sympathetic neuron derived NPY protects from obesity by sustaining the mural progenitors of thermogenic adipocytes

Intercellular communication in peritoneal dialysis

Extracellular Matrix Stiffness Regulates Microvascular Stability by Controlling Endothelial Paracrine Signaling to Determine Pericyte Fate

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