In vivo and in vitro effects of PTH1-34 on osteogenic and adipogenic differentiation of human bone marrow-derived mesenchymal stem cells through regulating microRNA-155.
Han HS., Ju F., Geng S.
Prospective Study, published in J Cell Biochem (2018) — summary generated from the PubMed abstract.
Early human evidence such as case series or small samples is exploring possible benefits.
- 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
- Prospective Study
- Journal
- J Cell Biochem (2018)
- Country
- United States
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 29091308
- DOI
- 10.1002/jcb.26478
Abstract (original English)
This study aimed to investigate the effect of parathyroid hormone (PTH1-34) on osteogenic and adipogenic differentiation of hBMSCs by the regulation of miR-155. A total of 36 adult volunteers were selected in this study. Effects of PTH1-34 on the proliferation of hBMSCs and miR-155 expression were investigated using a MTT assay. The hBMSCs were divided into blank, PTH1-34, miR-155 mimic, miR-155 mimic negative control (NC), miR-155 inhibitor, miR-155 inhibitor NC, PTH1-34 + miR-155 mimic, PTH1-34 + miR-155 inhibitor, and NPS R-568 groups. Postmenopausal osteoporosis (PMOP) mouse models were established by ovariectomy (OVX) and divided into ten groups. The RT-qPCR and Western blotting assay were carried out to detect the expression of osteogenesis/adipogenic-related genes and miR-155, and osteogenesis/adipogenic-related proteins. PTH1-34 could promote hBMSCs proliferation and inhibit miR-155 expression in a dose-dependent manner. Compared with the blank control group, expressions of Runx2, and BSP was up-regulated in the PTH1-34 and miR-155 inhibitor groups, while expressions of miR-155, PPAR-γ, lipoprotein lipase (LPL), fatty acid binding protein 4 (Fabp4), adiponectin, and CCAAT/enhancer binding protein α (C/EBPα) were down-regulated. In the in vivo experiment, compared with the OVX group, the BMD and expressions of Runx2 and BSP was up-regulated in the PTH1-34, miR-155 inhibi
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
Evidence level
Early human evidence such as case series or small samples is exploring possible benefits.
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