Expression of hypoxia-induced semaphorin 7A correlates with the severity of inflammation and osteoclastogenesis in experimentally induced periapical lesions
Expression of hypoxia-induced semaphorin 7A correlates with the severity of inflammation and osteoclastogenesis in experimentally induced periapical lesions
复制标题
缺氧诱导的信号蛋白 7A 的表达与实验诱导的根尖周病变中炎症和破骨细胞生成的严重程度相关。
DOI:
10.1016/j.archoralbio.2016.10.032
复制
发表时间:
2017-03-01
影响因子:
3
通讯作者:
Bian, Zhuan
中科院分区:
文献类型:
--
作者:
He, Miao;Bian, Zhuan
Objective: While hypoxia and inflammation are intimately linked, the effects of inflammatory hypoxia on the pathogenesis of periapical lesions remain largely unknown. The aim of this study was to examine hypoxia during the progression of experimentally induced rat periapical lesions, and to derive correlations between hypoxia-induced Semaphorin 7A (Sema7a) expression, severity of inflammation, and osteoclastogenesis in the lesions.Design: Periapical lesions were developed after mandibular first molar pulp exposure in forty Sprague-Dawley rats. The animals were randomly divided into four groups and sacrificed at 0, 7, 14, and 28 days after pulpal exposure. The bilateral mandibles containing the first molar were obtained and routinely prepared for histological, immunohistochemical, enzyme histochemical analyses and quantitative polymerase chain reaction detecting Sema7a mRNA expression. Data were analysed by one-way analysis of variance and the Pearson's correlation and linear tendency test.Results: Periapical tissues become hypoxic during the development of experimentally induced periapical lesions, with steadily increasing numbers of HIF-l alpha-positive cells that positively correlate with the expression of Sema7a mRNA in the lesions. Furthermore, significant positive correlates were derived for the expression of Sema7a and the degree of inflammatory infiltration and osteoclast number, respectively.Conclusions: Hypoxia-induced Sema7a participates in the pathogenesis of periapical lesions, providing a novel therapeutic target for the treatment of this inflammatory disease in the future. (C) 2016 Elsevier Ltd. All rights reserved.