Transforming growth factor beta1 induces osteogenic differentiation of murine bone marrow stromal cells.
Zhao L., Jiang S., Hantash BM.
Animal Study, published in Tissue Eng Part A (2010) — 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
- Tissue Eng Part A (2010)
- Country
- United States
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 19769530
- DOI
- 10.1089/ten.TEA.2009.0495
Abstract (original English)
Bone marrow stromal cells (BMSCs) have been shown to contribute to regeneration of numerous mesodermal tissue types including adipose, bone, and cartilage. Recent studies have shown that BMSCs migrate into damaged bone and help facilitate effects such as fracture healing. Although bone morphogenic proteins have been shown to stimulate bone repair, their levels remain low postfracture. Peripheral blood levels of transforming growth factor beta1 (TGF-beta1), on the other hand, rise dramatically within 2 weeks postfracture. Therefore, we investigated the role of TGF-beta1 on BMSC osteogenic differentiation in vitro. Murine BMSCs were freshly isolated from femurs, fluorescence-activated cell sorted for Sca-1, cultured in Iscove's modified Dulbecco's medium, and exposed to TGF-beta1. After 14 days, real-time reverse transcriptase-polymerase chain reaction and immunohistochemical staining were performed to examine the expression of self-renewal and terminal differentiation markers. Results showed that the treatment with TGF-beta1 reduced mRNA levels of self-renewal markers (Oct4, Stella, Nanos3, and Abcg2) by twofold and increased osteoblast differentiation markers (Runx2, Opn, and Col1) up to sevenfold compared with controls. We also observed decreased mRNA levels of adipogenic markers (Pparg2 and Adn) and an increase in alkaline phosphatase activity. Transcriptional coactivator wit
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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