<i>Thy1</i>
            (CD90) expression is regulated by DNA methylation during adipogenesis

Flores, E'Lissa M; Woeller, Collynn F.; Falsetta, Megan L.; Susiarjo, Martha; Phipps, Richard P.

doi:10.1096/fj.201801481r

Cited by 8 publications

(4 citation statements)

References 62 publications

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“…The expression of CD90 gradually decreases during adipogenesis, and mature adipocytes express almost no CD90. The reduction of CD90 expression by siRNA treatment in MSCs has been shown to enhance MSC adipogenic differentiation [47], whereas methylation inhibitor treatment to maintain CD90 expression during adipogenic differentiation reduces adipocyte formation [48]. This finding is consistent with the characteristics presented by our NRLM-MSCs from both clinical patients and commercial MSCs.…”

Section: Discussionsupporting

confidence: 87%

The superiority of conditioned medium derived from rapidly expanded mesenchymal stem cells for neural repair

et al. 2019

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AbstractsBackgroundSpinal cord injury (SCI) is a complex and severe neurological condition. Mesenchymal stem cells (MSCs) and their secreted factors show promising potential for regenerative medicine. Many studies have investigated MSC expansion efficacy of all kinds of culture medium formulations, such as growth factor-supplemented or xeno-free medium. However, very few studies have focused on the potential of human MSC (hMSC) culture medium formulations for injured spinal cord repair. In this study, we investigated the effect of hMSC-conditioned medium supplemented with bFGF, EGF, and patient plasma, namely, neural regeneration laboratory medium (NRLM), on SCI in vitro and in vivo.MethodsCommercial and patient bone marrow hMSCs were obtained for cultivation in standard medium and NRLM separately. Several characteristics, including CD marker expression, differentiation, and growth curves, were compared between MSCs cultured in standard medium and NRLM. Additionally, we investigated the effect of the conditioned medium (referred to as NRLM-CM) on neural repair, including inflammation inhibition, neurite regeneration, and spinal cord injury (SCI), and used a coculture system to detect the neural repair function of NRLM-MSCs.ResultsCompared to standard culture medium, NRLM-CM had superior in inflammation reduction and neurite regeneration effects in vitro and improved functional restoration in SCI rats in vivo. In comparison with standard culture medium MSCs, NRLM-MSCs proliferated faster regardless of the age of the donor. NRLM-MSCs also showed increased adipose differentiative potential and reduced CD90 expression. Both types of hMSC CM effectively enhanced injured neurite outgrowth and protected against H2O2 toxicity in spinal cord neuron cultures. Cytokine arrays performed in hMSC-CM further revealed the presence of at least 120 proteins. Among these proteins, 6 demonstrated significantly increased expression in NRLM-CM: adiponectin (Acrp30), angiogenin (ANG), HGF, NAP-2, uPAR, and IGFBP2.ConclusionsThe NRLM culture system provides rapid expansion effects and functional hMSCs. The superiority of the derived conditioned medium on neural repair shows potential for future clinical applications.

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Section: Discussionsupporting

confidence: 87%

The superiority of conditioned medium derived from rapidly expanded mesenchymal stem cells for neural repair

et al. 2019

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“…However, different from the inhibitory effect of ectopic CD90 on the adipogenesis of 3T3-L1 cells, which influenced the whole process of adipogenic differentiation [69], we revealed an unrecognized role of CD90 in promoting mitotic clonal expansion, which influenced the early phase of adipogenic differentiation of ADSCs. Notably, although CD90 on S-ADSCs contributed to their proliferation and mitotic clonal expansion, a gradual loss of CD90 was observed during the process of adipogenic differentiation, which was consistent with the change of CD90 expression in differentiating 3T3-L1 cells [69, 70]. These data indicate that CD90 may play essential roles in maintaining the stemness of ADSCs, which determines their capacities for self-renewal and initiation of adipogenic differentiation in response to metabolic demands.…”

Section: Discussionsupporting

confidence: 66%

CD90 serves as differential modulator of subcutaneous and visceral adipose-derived stem cells by regulating AKT activation that influences adipose tissue and metabolic homeostasis

et al. 2019

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BackgroundWhite adipose tissue includes subcutaneous and visceral adipose tissue (SAT and VAT) with different metabolic features. SAT protects from metabolic disorders, while VAT promotes them. The proliferative and adipogenic potentials of adipose-derived stem cells (ADSCs) are critical for maintaining adipose tissue homeostasis through driving adipocyte hyperplasia and inhibiting pathological hypertrophy. However, it remains to be elucidated the critical molecules that regulate different potentials of subcutaneous and visceral ADSCs (S-ADSCs, V-ADSCs) and mediate distinct metabolic properties of SAT and VAT. CD90 is a glycosylphosphatidylinositol-anchored protein on various cells, which is also expressed on ADSCs. However, its expression patterns and differential regulation on S-ADSCs and V-ADSCs remain unclear.MethodsS-ADSCs and V-ADSCs were detected for CD90 expression. Proliferation, colony formation, cell cycle, mitotic clonal expansion, and adipogenic differentiation were assayed in S-ADSCs, V-ADSCs, or CD90-silenced S-ADSCs. Glucose tolerance test and adipocyte hypertrophy were examined in mice after silencing of CD90 in SAT. CD90 expression and its association with CyclinD1 and Leptin were analyzed in adipose tissue from mice and humans. Regulation of AKT by CD90 was detected using a co-transfection system.ResultsCompared with V-ADSCs, S-ADSCs expressed high level of CD90 and showed increases in proliferation, mitotic clonal expansion, and adipogenic differentiation, together with AKT activation and G1-S phase transition. CD90 silencing inhibited AKT activation and S phase entry, thereby curbing proliferation and mitotic clonal expansion of S-ADSCs. In vivo CD90 silencing in SAT inhibited S-ADSC proliferation, which caused adipocyte hypertrophy and glucose intolerance in mice. Furthermore, CD90 was highly expressed in SAT rather than in VAT in human and mouse, which had positive correlation with CyclinD1 but negative correlation with Leptin. CD90 promoted AKT activation through recruiting its pleckstrin homology domain to plasma membrane.ConclusionsCD90 is differentially expressed on S-ADSCs and V-ADSCs, and plays critical roles in ADSC proliferation, mitotic clonal expansion, and hemostasis of adipose tissue and metabolism. These findings identify CD90 as a crucial modulator of S-ADSCs and V-ADSCs to mediate distinct metabolic features of SAT and VAT, thus proposing CD90 as a valuable biomarker or target for evaluating ADSC potentials, monitoring or treating obesity-associated metabolic disorders.

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“…A different study which used shRNAs to silence Thy-1 expression in MSCs showed increased adipogenic and osteogenic differentiation, indicating that Thy-1 functions as a differentiation obstacle ( Moraes, Sibov et al, 2016 ). Thy-1 expression is itself decreased during adipogenesis via epigenetic silencing ( Flores, Woeller et al, 2019 ). Thy-1 inhibits adipogenesis in preadipocytes via inhibition of Fyn and PPARγ ( Woeller, O'Loughlin et al, 2015 ).…”

Section: Thy-1–integrin Interaction In Pathophysiologymentioning

confidence: 99%

Thy-1-Integrin Interactions in cis and Trans Mediate Distinctive Signaling

Leyton

Hagood

et al. 2022

Front. Cell Dev. Biol.

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Thy-1 is a cell surface glycosylphosphatidylinositol (GPI)-anchored glycoprotein that bears a broad mosaic of biological roles across various cell types. Thy-1 displays strong physiological and pathological implications in development, cancer, immunity, and tissue fibrosis. Quite uniquely, Thy-1 is capable of mediating integrin-related signaling through direct trans- and cis-interaction with integrins. Both interaction types have shown distinctive roles, even when interacting with the same type of integrin, where binding in trans or in cis often yields divergent signaling events. In this review, we will revisit recent progress and discoveries of Thy-1–integrin interactions in trans and in cis, highlight their pathophysiological consequences and explore other potential binding partners of Thy-1 within the integrin regulation/signaling paradigm.

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Thy1 (CD90) expression is regulated by DNA methylation during adipogenesis

Cited by 8 publications

References 62 publications

The superiority of conditioned medium derived from rapidly expanded mesenchymal stem cells for neural repair

The superiority of conditioned medium derived from rapidly expanded mesenchymal stem cells for neural repair

CD90 serves as differential modulator of subcutaneous and visceral adipose-derived stem cells by regulating AKT activation that influences adipose tissue and metabolic homeostasis

Thy-1-Integrin Interactions in cis and Trans Mediate Distinctive Signaling

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