Roles of Transmembrane Protein 119 in the Effects of Transforming Growth Factor-β on Mouse Bone Cells.
Yamada A., Kawao N., Mizukami Y., Kaji H.
Animal Study, published in Exp Clin Endocrinol Diabetes (2025) — 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
- Exp Clin Endocrinol Diabetes (2025)
- Country
- Germany
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 40300647
- DOI
- 10.1055/a-2555-4543
Abstract (original English)
Transforming growth factor-β (TGF-β), a local growth factor, is essential for bone remodeling; when administered in bone tissues, it stimulates bone formation. On the other hand, transmembrane protein 119 (Tmem119) is a crucial factor for osteoblastic bone formation related to the TGF-β signaling molecule, Smad3. However, the role of Tmem119 in TGF-β-mediated effects on osteoblasts and osteoclasts remains unclear.The function of Tmem119 in TGF-β-mediated effects was examined for osteoblastic differentiation, bone matrix protein expression, and osteoclast formation in mouse osteoblasts, adipose tissue-derived stromal cells, and bone marrow cells from wild-type and Tmem119-deficient mice. Tmem119 deficiency significantly reversed the TGF-β-induced expressions of type I collagen and matrix-Gla protein (MGP) in mouse osteoblasts but did not affect TGF-β-suppressed alkaline phosphatase activity in mouse adipose tissue-derived stromal cells, even when TGF-β could suppress alkaline phosphatase (ALP) activity in mouse osteoblasts regardless of Tmem119 deficiency. Tmem119 deficiency significantly reduced osteoclast formation and Nuclear factor of activated T-cells, cytoplasmic 1 (NFATc1) mRNA levels in mouse bone marrow cells.Tmem119 is involved in regulating type I collagen and MGP expressions and TGF-β-induced osteoclast formation, but does not affect TGF-β-suppressed osteoblastic dif
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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