Angiopoietin-like protein 2 is a positive regulator of osteoblast differentiation.
Takano A., Fukuda T., Shinjo T., Iwashita M., Matsuzaki E., Yamamichi K.
Animal Study, published in Metabolism (2017) — 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
- Metabolism (2017)
- Country
- United States
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 28285646
- DOI
- 10.1016/j.metabol.2017.01.006
Abstract (original English)
Several studies have reported that angiopoietin-like protein 2 (Angptl2) is expressed abundantly in adipocytes and is associated with adipose tissue inflammation. In the present study, we found that osteoblasts and mesenchymal stem cells also expressed Angptl2 at high levels. The aim of this study was to understand the role of Angptl2 in osteoblastic cell differentiation. Angptl2 expression was examined during osteoblast and adipocyte differentiation. The role of Angptl2 on cell differentiation and associated signaling was analyzed by gene knockdown using Angptl2 small interfering ribonucleic acid (siRNA). Angptl2 was highly expressed in MC3T3-E1 cells, ST2 cells and primary osteoblasts, but not in RAW264 cells. Inhibition of Angptl2 expression using siRNA markedly inhibited alkaline phosphatase (ALP) expression and osteoblastic differentiation in MC3T3-E1, ST2 cells and primary osteoblasts. Angptl2 siRNA also inhibited adipocyte differentiation in ST2 cells. Treatment of MC3T3-E1 cells with Angptl2 siRNA led to the down-regulation of the activities of several cell signaling pathways, including extracellular signal-regulated kinase (ERK), Jun amino-terminal kinase (JNK), Akt, and nuclear factor kappa B (NF-κB) signals. It also down-regulated the expression of Osterix, but not that of runt-related transcription factor 2 (Runx2), suggesting that Angptl2 is a positive activator of
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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