PDGFRb+ mesenchymal cells, but not NG2+ mural cells, contribute to cardiac fat

Jiang, Zhen; Feng, Teng; Lu, Zuliang; Wei, Yuanxin; Meng, Jufeng; Lin, Chao-Po; Zhou, Bin; Liu, Chen; Zhang, Hui

doi:10.1016/j.celrep.2021.108697

Cited by 15 publications

(19 citation statements)

References 87 publications

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“…Since there is extensive evidence that Ng2 is highly expressed by pericytes (Ozerdem et al, 2001;Ozerdem and Stallcup, 2004;Armulik et al, 2011;Ieronimakis et al, 2013), the identification of Ng2+ perivascular cells arising from distinct fibroblast lineages reveals a previously unrecognized relationship between fibroblasts and pericytes during skin development. Adventitial fibroblasts and pericytes are both present in the adventitia layer of the blood vessel wall separated by the basal lamina (Kuwabara and Tallquist, 2017;Riew et al, 2018;Tinajero and Gotlieb, 2020) and share expression of several markers including Pdgfrα, Pdgfrβ, Nestin, Vimentin and Col1A1 (Lin et al, 2008;Riew et al, 2018;Jiang et al, 2021). However, adventitial fibroblasts do not express Ng2 (Ieronimakis et al, 2013;Jiang et al, 2021) and although pericytes and fibroblasts are both reported to differentiate into adipocytes (Tang et al, 2008;Cattaneo et al, 2020) we did not observe Ng2 progenitor derived adipocytes in the DWAT skin layer.…”

Section: Discussionmentioning

confidence: 54%

“…Adventitial fibroblasts and pericytes are both present in the adventitia layer of the blood vessel wall separated by the basal lamina (Kuwabara and Tallquist, 2017;Riew et al, 2018;Tinajero and Gotlieb, 2020) and share expression of several markers including Pdgfrα, Pdgfrβ, Nestin, Vimentin and Col1A1 (Lin et al, 2008;Riew et al, 2018;Jiang et al, 2021). However, adventitial fibroblasts do not express Ng2 (Ieronimakis et al, 2013;Jiang et al, 2021) and although pericytes and fibroblasts are both reported to differentiate into adipocytes (Tang et al, 2008;Cattaneo et al, 2020) we did not observe Ng2 progenitor derived adipocytes in the DWAT skin layer. Co-expression of Ng2 and Pdgfrα by blood vessel associated cells at E12.5 suggests that some Ng2+ pericytes originate from the Pdgfrα+ multipotent fibroblast progenitor described previously (Driskell et al, 2013).…”

Section: Discussionmentioning

confidence: 54%

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Distinct Fibroblast Lineages Give Rise to NG2+ Pericyte Populations in Mouse Skin Development and Repair

Goss

Rognoni

Salameti

et al. 2021

Front. Cell Dev. Biol.

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We have examined the developmental origins of Ng2+ perivascular cell populations that adhere to the basement membrane of blood vessels, and their contribution to wound healing. Neural/glial antigen 2 (Ng2) labeled most perivascular cells (70–80%) in developing and adult mouse back skin, a higher proportion than expressed by other pericyte markers Tbx18, Nestin and Pdgfrβ. In adult mouse back skin Ng2+ perivascular cells could be categorized into 4 populations based on whether they expressed Pdgfrα and Pdgfrβ individually or in combination or were Pdgfr-negative. Lineage tracing demonstrated that although Ng2+ cells in embryonic and neonatal back skin contributed to multiple cell types they did not give rise to interfollicular fibroblasts within the dermis. Lineage tracing of distinct fibroblast populations during skin development showed that papillary fibroblasts (Lrig1+) gave rise to Ng2+ perivascular cells in the upper dermis, whilst Ng2+ perivascular cells in the lower dermis were primarily derived from reticular Dlk1+ fibroblasts. Following wounding of adult skin, Ng2+ dermal cells only give rise to Ng2+ blood vessel associated cells and did not contribute to other fibroblast lineages. The relative abundance of Ng2+ Pdgfrβ+ perivascular populations was comparable in wounded and non-wounded skin, indicating that perivascular heterogeneity was maintained during full thickness skin repair. In the wound bed Ng2+ perivascular populations were primarily derived from Lrig1+ papillary or Dlk1+ reticular fibroblast lineages, according to the location of the regenerating blood vessels. We conclude that Ng2+ perivascular cells represent a heterogeneous lineage restricted population that is primarily recruited from the papillary or reticular fibroblast lineages during tissue regeneration.

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Section: Discussionmentioning

confidence: 54%

Section: Discussionmentioning

confidence: 54%

Distinct Fibroblast Lineages Give Rise to NG2+ Pericyte Populations in Mouse Skin Development and Repair

Goss

Rognoni

Salameti

et al. 2021

Front. Cell Dev. Biol.

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“…Third, PV-ADSCs lack unique markers, thus difficult to track in vivo . PDGFRA/PDGFRB may be potential markers for PV-ADSCs mentioned in the latest two publications 25,26 , but it is still under debate. Therefore, there is no definite conclusion whether PV-ADSCs themselves would truly participate in neointimal formation in vivo .…”

Section: Discussionmentioning

confidence: 99%

MGP Regulates Perivascular Adipose-Derived Stem Cells Differentiation Toward Smooth Muscle Cells Via BMP2/SMAD Pathway Enhancing Neointimal Formation

Liu

Chen

et al. 2022

Cell Transplant

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Perivascular adipose-derived stem cells (PV-ADSCs) could differentiate into smooth muscle cells (SMCs), participating in vascular remodeling. However, its underlying mechanism is not well explored. Our previous single-cell RNA-sequencing dataset identified a unique expression of matrix Gla protein (MGP) in PV-ADSCs compared with subcutaneous ADSCs. MGP involves in regulating SMC behaviors in vascular calcification and atherosclerosis. In this study, we investigated MGP’s role in PV-ADSCs differentiation toward SMCs in vitro and in vascular remodeling in vivo. PV-ADSCs were isolated from perivascular regions of mouse aortas. Quantitative reverse transcription–polymerase chain reaction (qRT-PCR), Western blot, and immunofluorescence confirmed higher MGP expression in PV-ADSCs. The MGP secretion increased along PV-ADSCs differentiation toward SMCs in response to transforming growth factor–beta 1 (TGF-β1). Lentivirus knockdown of MGP markedly promoted the bone morphogenetic protein 2 (BMP2) expression and phosphorylation of SMAD1/5/8 in PV-ADSCs, subsequently inhibiting its differentiation toward SMCs. Such inhibition could be partially reversed by further application of BMP2 inhibitors. On the contrary, exogenous MGP inhibited BMP2 expression and SMAD1/5/8 phosphorylation in PV-ADSCs, thereby promoting its differentiation toward SMCs. Transplantation of cultured PV-ADSCs, which was pretreated by MGP knockdown, in mouse femoral artery guide-wire injury model significantly alleviated neointimal hyperplasia. In conclusion, MGP promoted the differentiation of PV-ADSCs toward SMCs through BMP2/SMAD-mediated signaling pathway. This study offers a supplement to the society of perivascular tissues and PV-ADSCs.

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“…To examine the contribution of fibroblasts, pericytes, and SMCs to intramyocardial adipocytes in mice, our recent study took advantage of various genetic tools to target and trace these cell populations [31]. Lineage tracing of fibroblasts using Pdgfra‐DreER and Col1a2‐2A‐CreER mouse lines showed that a small number of intramyocardial adipocytes were derived from fibroblasts during postnatal heart development and in heart homeostasis [31]. PDGFRb was considered to be a pericyte marker, and most of intramyocardial adipocytes were progenies of PDGFRb + cells in the mouse hearts [31].…”

Section: Both Pdgfra++ and Pdgfrb++ Cells But Not Ng2++ Pericytes Con...mentioning

confidence: 99%

Functions and origins of cardiac fat

Jiang

Tang

et al. 2022

The FEBS Journal

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Triglyceride droplets can be stored within cardiac adipocytes (CAs) and cardiomyocytes in the heart. Cardiac adipocytes reside in three distinct regions: pericardial, epicardial, and intramyocardial adipose tissues. In healthy individuals, cardiac adipose tissues modulate cardiovascular functions and energy partitioning, which are, thus, protective. However, ectopic deposition of cardiac adipose tissues turns them into adverse lipotoxic, prothrombotic, and pro‐inflammatory tissues with local and systemic contribution to the development of cardiovascular disorders. Accumulation of triglyceride droplets in cardiomyocytes may lead to lipotoxic injury of cardiomyocytes and contribute to the development of cardiac hypertrophy and dysfunction. Here, we summarize the roles of CAs and myocardial triglyceride droplets under physiological and pathological conditions and review the cellular sources of CAs in heart development and diseases. Understanding the functions and cellular origins of cardiac fat will provide clues for future studies on pathophysiological processes and treatment of cardiovascular diseases.

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PDGFRb+ mesenchymal cells, but not NG2+ mural cells, contribute to cardiac fat

Cited by 15 publications

References 87 publications

Distinct Fibroblast Lineages Give Rise to NG2+ Pericyte Populations in Mouse Skin Development and Repair

Distinct Fibroblast Lineages Give Rise to NG2+ Pericyte Populations in Mouse Skin Development and Repair

MGP Regulates Perivascular Adipose-Derived Stem Cells Differentiation Toward Smooth Muscle Cells Via BMP2/SMAD Pathway Enhancing Neointimal Formation

Functions and origins of cardiac fat

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