{"title":"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","authors":"Ayaka Yamada, Naoyuki Kawao, Yuya Mizukami, Hiroshi Kaji","doi":"10.1055/a-2555-4543","DOIUrl":null,"url":null,"abstract":"<p><p>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.</p>","PeriodicalId":94001,"journal":{"name":"Experimental and clinical endocrinology & diabetes : official journal, German Society of Endocrinology [and] German Diabetes Association","volume":" ","pages":"246-252"},"PeriodicalIF":0.0000,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Roles of Transmembrane Protein 119 in the Effects of Transforming Growth Factor-β on Mouse Bone Cells.\",\"authors\":\"Ayaka Yamada, Naoyuki Kawao, Yuya Mizukami, Hiroshi Kaji\",\"doi\":\"10.1055/a-2555-4543\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>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.</p>\",\"PeriodicalId\":94001,\"journal\":{\"name\":\"Experimental and clinical endocrinology & diabetes : official journal, German Society of Endocrinology [and] German Diabetes Association\",\"volume\":\" \",\"pages\":\"246-252\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2025-05-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Experimental and clinical endocrinology & diabetes : official journal, German Society of Endocrinology [and] German Diabetes Association\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.1055/a-2555-4543\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2025/4/29 0:00:00\",\"PubModel\":\"Epub\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Experimental and clinical endocrinology & diabetes : official journal, German Society of Endocrinology [and] German Diabetes Association","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1055/a-2555-4543","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2025/4/29 0:00:00","PubModel":"Epub","JCR":"","JCRName":"","Score":null,"Total":0}
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.