The Expression of Semaphorin 7A in Human Periapical Lesions
The Expression of Semaphorin 7A in Human Periapical Lesions
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信号蛋白7A在人根尖周病变中的表达
DOI：
10.1016/j.joen.2021.06.005
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发表时间：
2021
期刊：
影响因子：
--
通讯作者：
Dingming Huang
中科院分区：
文献类型：
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作者：
Yao Song;Liu Wang;Jiatong Li;Fan Yang;Yuxuan Gao;Dongzhe Song;Jianxun Sun;Ling Ye;Lan Zhang;Dingming Huang
脑信号蛋白7A（Semaphorin 7A，SEMA 7A）是一种膜结合或分泌蛋白，在炎症、神经退化和肿瘤进展中发挥多种功能。根尖周病是由细菌引起的慢性感染性疾病。然而，SEMA 7A在人类根尖周病变中的参与仍不清楚。本研究旨在探讨SEMA 7A在人根尖周病变中的表达及其与基质金属蛋白酶（MMP）-1和MMP-3在根尖周炎进展过程中的潜在相关性。分别提取总RNA和蛋白质进行实时定量PCR和Western blot分析。另外，6个健康样本和27个根尖周病变样本被固定、脱水并包埋用于进一步的组织学和免疫化学分析。通过平均积分光密度定量SEMA 7A的表达。免疫荧光法检测SEMA 7A/MMP-1和SEMA 7A/MMP-3在根尖周病变组织中的共定位。结果与正常对照组相比，根尖周病变组织中SEMA 7A的mRNA和蛋白表达均显著上调。MMP-1、MMP-3和炎性细胞因子在根尖周病变中的表达明显高于健康组。SEMA 7A在根尖肉芽肿组和根尖囊肿组中的表达均高于正常组（P<0.01）。结论SEMA 7A在根尖周炎中表达上调，可能参与了根尖周病变组织的破坏和免疫细胞的浸润。
IntroductionSemaphorin 7A (SEMA7A) is a membrane-bound or secretory protein exerting multiple functions in the regulation of inflammation, neural degradation, and cancer progression. Human periapical lesions are chronic and infectious diseases mainly caused by bacteria. However, the involvement of SEMA7A in human periapical lesions is still unclear. This study aimed to explore the expression of SEMA7A in human periapical lesions accompanied by the potential association of SEMA7A with matrix metalloproteinase (MMP)-1 and MMP-3 during the progression of apical periodontitis.MethodsSamples of periapical lesions and healthy controls were collected. Total RNA and protein were extracted respectively for quantitative real-time polymerase chain reaction and Western blot analysis. Additionally, 6 healthy samples and 27 periapical lesion samples were fixed, dehydrated, and embedded for further histologic and immunochemical analysis. The expression of SEMA7A was quantified by average integrated optical density. Immunofluorescence analysis was conducted to explore the colocalization of SEMA7A/MMP-1 and SEMA7A/MMP-3.ResultsCompared with healthy controls, the messenger RNA and protein expression of SEMA7A was markedly up-regulated in periapical lesions. A stronger expression of MMP-1, MMP-3, and inflammatory cytokines was exhibited in periapical lesions than in healthy groups. An increasing expression of SEMA7A can be observed in both the periapical granuloma group and the radicular cyst group compared with the normal group (P< .01). Immunofluorescence results showed the colocalization of SEMA7A with both MMP-1 and MMP-3 in vascular vessels and extracellular matrix.ConclusionsSEMA7A was up-regulated in periapical periodontitis and might be involved in the tissue destruction and infiltration of immune cells in periapical lesions.