跨膜蛋白119在转化生长因子-β对小鼠骨细胞影响中的作用

Ayaka Yamada, Naoyuki Kawao, Yuya Mizukami, Hiroshi Kaji
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摘要

转化生长因子-β (TGF-β)是一种局部生长因子,对骨重塑至关重要;当在骨组织中使用时,它会刺激骨形成。另一方面,跨膜蛋白119 (Tmem119)是与TGF-β信号分子Smad3相关的成骨细胞骨形成的关键因子。然而,Tmem119在TGF-β介导的成骨细胞和破骨细胞作用中的作用尚不清楚。在野生型和Tmem119缺陷小鼠的成骨细胞、脂肪组织源性基质细胞和骨髓细胞中,检测Tmem119在TGF-β介导的成骨细胞分化、骨基质蛋白表达和破骨细胞形成中的功能。Tmem119缺乏显著逆转了TGF-β诱导的小鼠成骨细胞I型胶原和基质gla蛋白(MGP)的表达,但不影响TGF-β抑制的小鼠脂肪组织源性基质细胞碱性磷酸酶活性,即使TGF-β可以抑制小鼠成骨细胞碱性磷酸酶(ALP)活性,而不考虑Tmem119缺乏。Tmem119缺乏显著降低小鼠骨髓细胞破骨细胞形成和活化t细胞核因子-胞浆1 (NFATc1) mRNA水平。Tmem119参与调节I型胶原和MGP表达以及TGF-β诱导的破骨细胞形成,但不影响TGF-β抑制的小鼠细胞成骨细胞分化。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Roles of Transmembrane Protein 119 in the Effects of Transforming Growth Factor-β on Mouse Bone Cells.

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 differentiation in mouse cells.

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