Fibroblast Growth Factor 2 High Molecular Weight Isoforms in Dentoalveolar Mineralization.
Fibroblast Growth Factor 2 High Molecular Weight Isoforms in Dentoalveolar Mineralization.
复制标题
成纤维细胞生长因子2在牙道肺泡矿化中高分子量同工型。
DOI：
10.1007/s00223-021-00888-3
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发表时间：
2022-01
影响因子：
4.2
通讯作者：
Hurley MM
中科院分区：
文献类型：
--
作者：
Millington G;Joseph J;Xiao L;Vijaykumar A;Mina M;Hurley MM
在成骨细胞和成牙本质细胞系(HMWTg)中高表达人高分子量成纤维细胞生长因子2(HMWFGF2)亚型的转基因小鼠表现出牙本质和牙槽骨矿化减少，牙髓腔扩大，成纤维细胞生长因子23(FGF23)增加。我们检测了HMWTg小鼠的牙槽骨和牙本质矿化缺陷是否由FGF23表达增加所致，以及FGF23中和抗体是否可以挽救低矿化表型。HMWTg和VectorTg对照组小鼠从出生后第21天开始皮下注射FGF23中和抗体，每周2次，共6周。由于骨化三醇(1，25D)具有促进骨矿化的直接作用，我们还确定了1，25D是否对牙本质缺陷和牙槽骨矿化有保护作用。因此，HMWTg小鼠每天皮下注射1，25d或同时注射FGF23中和抗体6周。结果表明，HMWTg组小鼠牙本质前增厚，牙槽骨矿化减少，牙髓腔增大。FGF23中和抗体和1，25D单药治疗可部分修复HMWTg小鼠牙本质矿化缺陷和髓室扩大表型。单纯1，25D不足以挽救牙槽骨的矿化。有趣的是，用FGF23中和抗体和1.25D治疗的HMWTg小鼠进一步挽救了扩大的牙髓腔大小，以及牙本质和牙槽骨矿化缺陷。我们认为HMWTg小鼠牙本质和牙槽骨矿化缺陷可能是由于FGF23表达增加所致。我们的结果表明，HMWFGF2在牙槽骨矿化中具有新的作用。
Transgenic mice overexpressing human high molecular weight fibroblast growth factor 2 (HMWFGF2) isoforms in osteoblast and odontoblast lineages (HMWTg) exhibit decreased dentin and alveolar bone mineralization, enlarged pulp chamber, and increased fibroblast growth factor 23 (FGF23). We examined if the alveolar bone and dentin mineralization defects in HMWTg mice resulted from increased FGF23 expression and whether an FGF23 neutralizing antibody could rescue the hypomineralization phenotype. HMWTg and VectorTg control mice were given subcutaneous injections of FGF23 neutralizing antibody twice/week starting at postnatal day 21 for 6 weeks. Since Calcitriol (1,25D) have direct effects in promoting bone mineralization, we also determined if 1,25D protects against the defective dentin and alveolar bone mineralization. Therefore, HMWTg mice were given subcutaneous injections of 1,25D daily or concomitantly with FGF23 neutralizing antibody for 6 weeks. Our results showed that HMWTg mice displayed thickened predentin, alveolar bone hypomineralization and enlarged pulp chambers. FGF23 neutralizing antibody and 1,25D monotherapy partially rescued the dentin mineralization defects and the enlarged pulp chamber phenotype in HMWTg mice. 1,25D alone was not sufficient to rescue the alveolar bone hypomineralization. Interestingly, HMWTg mice treated with both FGF23 neutralizing antibody and 1.25D further rescued the enlarged pulp chamber size, and dentin and alveolar bone mineralization defects. We conclude that the dentin and alveolar bone mineralization defects in HMWTg mice might result from increased FGF23 expression. Our results show a novel role of HMWFGF2 on dentoalveolar mineralization.
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影响因子：
33.6
作者：
Martin A;David V;Quarles LD
通讯作者：
Quarles LD
影响因子：
6.2
作者：
Carpenter, Thomas O.;Imel, Erik A.;Holm, Ingrid A.;de Beur, Suzanne M. Jan;Insogna, Karl L.
通讯作者：
Insogna, Karl L.
影响因子：
4.3
作者：
Fong H;Chu EY;Tompkins KA;Foster BL;Sitara D;Lanske B;Somerman MJ
通讯作者：
Somerman MJ
影响因子：
3.3
作者：
Ribeiro, T. R.;Costa, F. W. G.;Fonteles, C. S. R.
通讯作者：
Fonteles, C. S. R.
影响因子：
5.6
作者：
Ma, Xin;Dang, Xitong;Kardami, Elissavet
通讯作者：
Kardami, Elissavet