内皮素-1及其受体ET(A)和ET(B)与药物性牙龈增生的关系

Endothelin-1 and its receptors ET(A) and ET(B) in drug-induced gingival overgrowth.

作者信息

Tamilselvan S, Raju Surya Narayana, Loganathan D, Kamatchiammal S, Abraham Georgie, Suresh R

机构信息

Department of Periodontics, Sri Ramachandra Dental College and Hospital, Sri Ramachandra Medical College and Research Institute, Deemed University, Porur, Chennai, Tamilnadu, India.

出版信息

J Periodontol. 2007 Feb;78(2):290-5. doi: 10.1902/jop.2007.060172.

Abstract

BACKGROUND

The purpose of this study was to study the expression of endothelin-1 (ET-1) and its receptors ETA and ETB in normal human gingiva and cyclosporin-induced gingival fibroblasts.

METHODS

Gingival samples were collected from eight normal healthy individuals, eight patients with periodontitis, and eight patients with cyclosporin A (CsA)-induced gingival overgrowth. Total RNA was extracted from tissue samples, and reverse transcriptase-polymerase chain reaction was performed for ET-1, ETA, and ETB. ET-1 protein was estimated from the tissues by enzyme-linked immunosorbent assay. The expression of ET-1 and its receptors was also examined in gingival fibroblast cells treated with CsA.

RESULTS

ET-1 mRNA expression was significantly higher in patients with CsA-induced gingival overgrowth (P <0.001) than in patients with periodontitis and the controls. ETA mRNA was expressed more than the ETB in all examined samples. In human gingival fibroblasts, ET-1 expression was increased with CsA incorporation compared to controls (P <0.001).

CONCLUSION

These results suggest that CsA can modulate the expression of ET-1 in gingival fibroblasts and CsA-induced gingival overgrowth.

摘要

背景

本研究旨在探讨内皮素-1(ET-1)及其受体ETA和ETB在正常人类牙龈及环孢素诱导的牙龈成纤维细胞中的表达情况。

方法

从8名正常健康个体、8名牙周炎患者以及8名环孢素A(CsA)诱导的牙龈增生患者中采集牙龈样本。从组织样本中提取总RNA,并对ET-1、ETA和ETB进行逆转录聚合酶链反应。通过酶联免疫吸附测定法从组织中估计ET-1蛋白。还用CsA处理牙龈成纤维细胞,检测ET-1及其受体的表达。

结果

CsA诱导的牙龈增生患者中ET-1 mRNA表达显著高于牙周炎患者和对照组(P<0.001)。在所有检测样本中,ETA mRNA的表达多于ETB。在人牙龈成纤维细胞中,与对照组相比,加入CsA后ET-1表达增加(P<0.001)。

结论

这些结果表明,CsA可调节牙龈成纤维细胞中ET-1的表达以及CsA诱导的牙龈增生。

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