Anti-fibrotic effect of adipose-derived mesenchymal stem cell conditioned medium in muscle fibrosis.
Oki K., Yoshihara S., Urushihata N., Ghazizadeh M.
Animal Study, published in Eur Rev Med Pharmacol Sci (2021) — summary generated from the PubMed abstract.
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.
- Study type
- Animal Study
- Journal
- Eur Rev Med Pharmacol Sci (2021)
- Country
- Italy
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 34355367
- DOI
- 10.26355/eurrev_202108_26452
Abstract (original English)
Recent investigations have demonstrated that the administration of MSC in mouse model of diseases provided beneficial effects. On the other hand, human adipose-derived MSC condition medium (ADSC-CM) is reported as containing beneficial secreted factors, but its role in muscle fibrosis has not been identified. The aim of this study was to investigate the inhibitory effects of MSC-CM in muscle fibrosis in vitro using the C2C12 murine muscle, myoblast cell line. C2C12 cells were cultured overnight in 0.1% albumin-Dulbecco's Modifies Eagle's Medium (DMEM). The cells were then pre-incubated in ADSC-CM for 20 min, treated with 2.5-10 ng/mL human TGFβ1 for 8-72 hours and analyzed using RT-qPCR, Western blot and immunofluorescent staining. Treatment with 20% ADSC-CM for 3 days suppressed αSMA protein expression in TGFβ1 treated C2C12 cells. ADSC-CM stimulated the proliferation of C2C12 cells in a dose-dependent manner. Furthermore, TGFβ1 induced Acta2/αSMA mRNA expression which was inhibited by ADSC-CM treatment for 8 hours. Decorin, one of the dermatan sulfate proteoglycans and an endogenous inhibitor of TGFβ1, was expressed in ADSC-CM, but not in TGFβ1 pre-incubated ADSC-CM. Our studies provide useful information for establishing anti-fibrotic mechanism(s) of ADSC-CM, thus facilitating potential application to prevent muscle fibrosis.
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
- • This is preclinical work; animal or laboratory results cannot be applied to humans.
Evidence level
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
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