Expression Analysis of the Stem Cell Marker <i>Pw1/Peg3</i> Reveals a CD34 Negative Progenitor Population in the Hair Follicle

Besson, V.; Kyryachenko, Sergiy; Janich, Peggy; Benitah, Salvador Aznar; Marazzi, Giovanna; Sassoon, David

doi:10.1002/stem.2540

Cited by 8 publications

(6 citation statements)

References 56 publications

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“…The observation of a relatively higher expression of Sox2 in P1 for SKMSCs matches the positive PW1+ results after isolation. In previous studies on skin, the expression of PW1/Peg3 in adult dermis was associated with hair follicle formation[47]. This finding suggests that the dermis-derived stem/progenitor cells, which meet the minimal criteria for MSC characterization, may possibly display a higher potential to form hair follicles in vitro .…”

Section: Discussionmentioning

confidence: 76%

“…Another surface marker examined in this study was the PW1. A recent study based on the mouse model demonstrated that a population of PW1-positive endothelial cells showed an increased ability to proliferate and regenerate and arrange blood vessels[29]; moreover, PW1 expression was also associated with the differentiation of hair follicle cells in vivo [47]. PW1 with the co-expression of PDGFRα was characteristic for myogenic precursor cells induced for adipogenic differentiation[27].…”

Section: Discussionmentioning

confidence: 99%

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Similarities and differences between mesenchymal stem/progenitor cells derived from various human tissues

Kozlowska

Krawczenko

Futoma

et al. 2019

WJSC

147

113

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BACKGROUND Mesenchymal stromal/stem cells (MSCs) constitute a promising tool in regenerative medicine and can be isolated from different human tissues. However, their biological properties are still not fully characterized. Whereas MSCs from different tissue exhibit many common characteristics, their biological activity and some markers are different and depend on their tissue of origin. Understanding the factors that underlie MSC biology should constitute important points for consideration for researchers interested in clinical MSC application. AIM To characterize the biological activity of MSCs during longterm culture isolated from: bone marrow (BM-MSCs), adipose tissue (AT-MSCs), skeletal muscles (SM-MSCs), and skin (SK-MSCs). METHODS MSCs were isolated from the tissues, cultured for 10 passages, and assessed for: phenotype with immunofluorescence and flow cytometry, multipotency with differentiation capacity for osteo-, chondro-, and adipogenesis, stemness markers with qPCR for mRNA for Sox2 and Oct4, and genetic stability for p53 and c-Myc; 27 bioactive factors were screened using the multiplex ELISA array, and spontaneous fusion involving a co-culture of SM-MSCs with BM-MSCs or AT-MSCs stained with PKH26 (red) or PKH67 (green) was performed. RESULTS All MSCs showed the basic MSC phenotype; however, their expression decreased during the follow-up period, as confirmed by fluorescence intensity. The examined MSCs express CD146 marker associated with proangiogenic properties; however their expression decreased in AT-MSCs and SM-MSCs, but was maintained in BM-MSCs. In contrast, in SK-MSCs CD146 expression increased in late passages. All MSCs, except BM-MSCs, expressed PW1, a marker associated with differentiation capacity and apoptosis. BM-MSCs and AT-MSCs expressed stemness markers Sox2 and Oct4 in long-term culture. All MSCs showed a stable p53 and c-Myc expression. BM-MSCs and AT-MSCs maintained their differentiation capacity during the follow-up period. In contrast, SK-MSCs and SM-MSCs had a limited ability to differentiate into adipocytes. BM-MSCs and AT-MSCs revealed similarities in phenotype maintenance, capacity for multilineage differentiation, and secretion of bioactive factors. Because AT-MSCs fused with SM-MSCs as effectively as BM-MSCs, AT-MSCs may constitute an alternative source for BM-MSCs. CONCLUSION Long-term culture affects the biological activity of MSCs obtained from various tissues. The source of MSCs and number of passages are important considerations in regenerative medicine.

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Section: Discussionmentioning

confidence: 76%

Section: Discussionmentioning

confidence: 99%

Similarities and differences between mesenchymal stem/progenitor cells derived from various human tissues

Kozlowska

Krawczenko

Futoma

et al. 2019

WJSC

147

113

View full text Add to dashboard Cite

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“…We have shown that Pw1 is specifically expressed in a wide range of adult stem cells 11 . Furthermore, it has been recently reported that Pw1 regulates adult mesoangioblast competence and that PW1 expressing cells correspond to competent and self-renewing cells 11 , 67 , 68 . In skeletal muscle, Pw1 expression is confined to two progenitor cell populations: satellite cells and interstitial cells (PICs) 12 , 13 .…”

Section: Discussionmentioning

confidence: 99%

The imprinted gene Pw1/Peg3 regulates skeletal muscle growth, satellite cell metabolic state, and self-renewal

Correra

Ollitrault

Valente

et al. 2018

Sci Rep

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Pw1/Peg3 is an imprinted gene expressed from the paternally inherited allele. Several imprinted genes, including Pw1/Peg3, have been shown to regulate overall body size and play a role in adult stem cells. Pw1/Peg3 is expressed in muscle stem cells (satellite cells) as well as a progenitor subset of muscle interstitial cells (PICs) in adult skeletal muscle. We therefore examined the impact of loss-of-function of Pw1/Peg3 during skeletal muscle growth and in muscle stem cell behavior. We found that constitutive loss of Pw1/Peg3 function leads to a reduced muscle mass and myofiber number. In newborn mice, the reduction in fiber number is increased in homozygous mutants as compared to the deletion of only the paternal Pw1/Peg3 allele, indicating that the maternal allele is developmentally functional. Constitutive and a satellite cell-specific deletion of Pw1/Peg3, revealed impaired muscle regeneration and a reduced capacity of satellite cells for self-renewal. RNA sequencing analyses revealed a deregulation of genes that control mitochondrial function. Consistent with these observations, Pw1/Peg3 mutant satellite cells displayed increased mitochondrial activity coupled with accelerated proliferation and differentiation. Our data show that Pw1/Peg3 regulates muscle fiber number determination during fetal development in a gene-dosage manner and regulates satellite cell metabolism in the adult.

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“…The transgenic PW1 reporter mouse model has facilitated the identification of PW1 + cells and demonstrated the importance of PW1 as a pan-tissue stem cell marker 19,20,[26][27][28] . Herein, we used this model to specifically isolate cardiac PW1 + cells and adopt a multi-omic unbiased approach to further decipher the cell surface membranome of these cells.…”

Section: Discussionmentioning

confidence: 99%

Anti-integrin αv therapy improves cardiac fibrosis after myocardial infarction by blunting cardiac PW1+ stromal cells

Bouvet

Claude

Roux

et al. 2020

Sci Rep

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There is currently no therapy to limit the development of cardiac fibrosis and consequent heart failure. We have recently shown that cardiac fibrosis post-myocardial infarction (MI) can be regulated by resident cardiac cells with a fibrogenic signature and identified by the expression of PW1 (Peg3). Here we identify αV-integrin (CD51) as an essential regulator of cardiac PW1 + cells fibrogenic behavior. We used transcriptomic and proteomic approaches to identify specific cell-surface markers for cardiac PW1 + cells and found that αV-integrin (CD51) was expressed in almost all cardiac PW1 + cells (93% ± 1%), predominantly as the αVβ1 complex. αV-integrin is a subunit member of the integrin family of cell adhesion receptors and was found to activate complex of latent transforming growth factor beta (TGFβ at the surface of cardiac PW1 + cells. Pharmacological inhibition of αV-integrin reduced the profibrotic action of cardiac PW1 + CD51 + cells and was associated with improved cardiac function and animal survival following MI coupled with a reduced infarct size and fibrotic lesion. These data identify a targetable pathway that regulates cardiac fibrosis in response to an ischemic injury and demonstrate that pharmacological inhibition of αV-integrin could reduce pathological outcomes following cardiac ischemia. Heart failure (HF) remains a leading cause of mortality and hospitalization worldwide and represents a heavy financial burden on health care systems 1-6. Current pharmacological treatments limit the peripheral consequences of cardiac dysfunction, but therapeutic approaches that impact primary adverse cardiac remodeling at the myocardial level are limited. While the etiology of HF is diverse, HF is typically associated with a range of physiological and morphological changes including fibrosis within the myocardium 7-9. Cardiac fibrosis is characterized with the excessive production and deposition of extracellular matrix (ECM) proteins within the myocardium that results in normal tissue architecture disruption, reduced tissue compliance, and mechanical and electrical dysfunction, consequently leading to HF 10,11. The mechanisms underlying cardiac fibrosis are incompletely understood, thereby impeding the development of effective anti-fibrotic therapeutics to complement the current therapies for HF 9,11,12. Activated cardiac fibroblasts are essential for the production of ECM proteins that accumulate during cardiac fibrosis; however, recent studies have established that cardiac fibroblasts represent a heterogeneous cell population 10-14. The exact nature of activated fibroblasts and consequently the sources of cardiac fibrosis remain unclear 9,12. Different mechanisms underlying fibrosis have been reported including the activation and

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Expression Analysis of the Stem Cell Marker Pw1/Peg3 Reveals a CD34 Negative Progenitor Population in the Hair Follicle

Cited by 8 publications

References 56 publications

Similarities and differences between mesenchymal stem/progenitor cells derived from various human tissues

Similarities and differences between mesenchymal stem/progenitor cells derived from various human tissues

The imprinted gene Pw1/Peg3 regulates skeletal muscle growth, satellite cell metabolic state, and self-renewal

Anti-integrin αv therapy improves cardiac fibrosis after myocardial infarction by blunting cardiac PW1+ stromal cells

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