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首页> 外文期刊>The Journal of Musculoskeletal and Neuronal Interactions >Osteocytic connexin 43 is not required for the increase in bone mass induced by intermittent PTH administration in male mice
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Osteocytic connexin 43 is not required for the increase in bone mass induced by intermittent PTH administration in male mice

机译：雄性小鼠间歇性PTH给药所引起的骨量增加不需要骨质连接蛋白43

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Objective: To investigate whether osteocytic connexin 43 (Cx43) is required for the bone response to intermittent PTH administra- tion, and whether the connexin is involved in maintaining the bone matrix. Methods: Human PTH(1-34) was injected to adult male mice expressing (Cx43 fl/fl ) or not osteocytic Cx43 (Cx43 fl/fl ;DMP1-8kb-Cre) daily (100 μg/kg/d) for 14 days. Results: Cx43 fl/fl ;DMP1- 8kb-Cre mice have no difference in body weight and BMD from 1 to 4 months of age. Intermittent PTH administration increased BMD and BV/TV and induced a similar increase in type I collagen, alkaline phosphatase, runx2, osteocalcin, and bone sialoprotein expres- sion in mice from both genotypes. On the other hand, osteocytic deletion of Cx43 did not alter mRNA levels of glycosaminoglycans, proteoglycans, collagens and osteoblast-related genes. In addition, expression of collagens assessed by immunohistochemistry was not affected by deleting osteocytic Cx43. However, PTH administration increased type II collagen only in Cx43 fl/fl control mice, whereas hormone increased type I collagen expression only in Cx43 fl/fl ;DMP1-8kb-Cre mice. Furthermore, PTH increased maturity of collagen fibers in control, but not in Cx43-deficient mice. Conclusion: Expression of Cx43 in osteocytes is dispensable for bone anabolism induced by intermittent PTH administration; but it can modulate, at least in part, the effect of PTH on the bone matrix environment.
机译：目的：研究是否需要骨质连接蛋白43（Cx43）来应对间歇性PTH给药的骨反应，以及连接蛋白是否参与维持骨基质。方法：每天向表达（Cx43 fl / fl）或不表达骨钙蛋白Cx43（Cx43 fl / fl; DMP1-8kb-Cre）（100μg/ kg / d）的成年雄性小鼠注射人PTH（1-34），持续14天。结果：Cx43 fl / fl; DMP1-8kb-Cre小鼠在1-4个月大时体重和BMD无差异。间歇性施用PTH会增加两种基因型小鼠的BMD和BV / TV，并引起I型胶原蛋白，碱性磷酸酶，runx2，骨钙蛋白和骨唾液蛋白表达的相似增加。另一方面，Cx43的骨细胞缺失并没有改变糖胺聚糖，蛋白聚糖，胶原蛋白和成骨细胞相关基因的mRNA水平。另外，通过免疫组织化学评估的胶原蛋白的表达不受缺失骨细胞Cx43的影响。但是，仅在Cx43 fl / fl对照小鼠中施用PTH会增加II型胶原蛋白，而激素仅在Cx43 fl / fl; DMP1-8kb-Cre小鼠中会增加I型胶原蛋白表达。此外，在对照中，PTH增加了胶原纤维的成熟度，但在Cx43缺陷型小鼠中却没有。结论：Cx43在骨细胞中的表达对于间歇性PTH诱导的骨合成代谢是必不可少的。但它可以至少部分地调节PTH对骨基质环境的影响。

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