Transcriptional Analysis Reveals Key Genes in the Pathogenesis of Nifedipine-Induced Gingival Overgrowth

Background. Nifedipine-induced gingival overgrowth (NGO) is a multifactorial pathogenesis with increased extracellular matrix including collagen and glycans, inflammatory cytokines, and phenotype changes of fibroblasts. However, the molecular etiology of NGO is not well understood. The objective of...

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Main Authors: Yanqin Ju, Lijuan Huang, Shuwei Wang, Shouliang Zhao
Format: Article
Language:English
Published: Wiley 2020-01-01
Series:Analytical Cellular Pathology
Online Access:http://dx.doi.org/10.1155/2020/6128341
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author Yanqin Ju
Lijuan Huang
Shuwei Wang
Shouliang Zhao
author_facet Yanqin Ju
Lijuan Huang
Shuwei Wang
Shouliang Zhao
author_sort Yanqin Ju
collection DOAJ
description Background. Nifedipine-induced gingival overgrowth (NGO) is a multifactorial pathogenesis with increased extracellular matrix including collagen and glycans, inflammatory cytokines, and phenotype changes of fibroblasts. However, the molecular etiology of NGO is not well understood. The objective of this study is to investigate the key genes in the pathogenesis of NGO. Methods. In this study, we examined the proliferation and migration abilities of fibroblasts derived from patients with chronic periodontitis, nifedipine nonresponder gingival overgrowth, gingival overgrowth caused by nifedipine, and healthy normal gingiva. We conducted RNA-Seq on these four groups of fibroblasts and analysed the differentially expressed genes (DEGs). Results. Fibroblasts derived from NGO patients had higher proliferation and migration abilities than those of the other groups. Protein-protein interaction network analysis indicated that TGFB2, ITGA8, ITGA11, FGF5, PLA2G4D, PLA2G2F, PTGS1, CSF1, LPAR1, CCL3, and NKX3-1 are involved in the development of NGO. These factors are related to the arachidonic acid metabolism and PI3K/AKT signaling pathways. Conclusion. Transcriptional gene expression analysis identified a number of DEGs that might be functionally related to gingival overgrowth induced by nifedipine. Our study provides important information on the molecular mechanism underlying nifedipine-induced gingival overgrowth.
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spelling doaj-art-4f0f10fb6df04c37bb3a776aa528cc7c2025-08-20T03:36:32ZengWileyAnalytical Cellular Pathology2210-71772210-71852020-01-01202010.1155/2020/61283416128341Transcriptional Analysis Reveals Key Genes in the Pathogenesis of Nifedipine-Induced Gingival OvergrowthYanqin Ju0Lijuan Huang1Shuwei Wang2Shouliang Zhao3Department of Stomatology, Huashan Hospital, Fudan University, Shanghai 200040, ChinaDepartment of Stomatology, Huashan Hospital, Fudan University, Shanghai 200040, ChinaShanghai Jiading District Dental Center, Shanghai 201800, ChinaDepartment of Stomatology, Huashan Hospital, Fudan University, Shanghai 200040, ChinaBackground. Nifedipine-induced gingival overgrowth (NGO) is a multifactorial pathogenesis with increased extracellular matrix including collagen and glycans, inflammatory cytokines, and phenotype changes of fibroblasts. However, the molecular etiology of NGO is not well understood. The objective of this study is to investigate the key genes in the pathogenesis of NGO. Methods. In this study, we examined the proliferation and migration abilities of fibroblasts derived from patients with chronic periodontitis, nifedipine nonresponder gingival overgrowth, gingival overgrowth caused by nifedipine, and healthy normal gingiva. We conducted RNA-Seq on these four groups of fibroblasts and analysed the differentially expressed genes (DEGs). Results. Fibroblasts derived from NGO patients had higher proliferation and migration abilities than those of the other groups. Protein-protein interaction network analysis indicated that TGFB2, ITGA8, ITGA11, FGF5, PLA2G4D, PLA2G2F, PTGS1, CSF1, LPAR1, CCL3, and NKX3-1 are involved in the development of NGO. These factors are related to the arachidonic acid metabolism and PI3K/AKT signaling pathways. Conclusion. Transcriptional gene expression analysis identified a number of DEGs that might be functionally related to gingival overgrowth induced by nifedipine. Our study provides important information on the molecular mechanism underlying nifedipine-induced gingival overgrowth.http://dx.doi.org/10.1155/2020/6128341
spellingShingle Yanqin Ju
Lijuan Huang
Shuwei Wang
Shouliang Zhao
Transcriptional Analysis Reveals Key Genes in the Pathogenesis of Nifedipine-Induced Gingival Overgrowth
Analytical Cellular Pathology
title Transcriptional Analysis Reveals Key Genes in the Pathogenesis of Nifedipine-Induced Gingival Overgrowth
title_full Transcriptional Analysis Reveals Key Genes in the Pathogenesis of Nifedipine-Induced Gingival Overgrowth
title_fullStr Transcriptional Analysis Reveals Key Genes in the Pathogenesis of Nifedipine-Induced Gingival Overgrowth
title_full_unstemmed Transcriptional Analysis Reveals Key Genes in the Pathogenesis of Nifedipine-Induced Gingival Overgrowth
title_short Transcriptional Analysis Reveals Key Genes in the Pathogenesis of Nifedipine-Induced Gingival Overgrowth
title_sort transcriptional analysis reveals key genes in the pathogenesis of nifedipine induced gingival overgrowth
url http://dx.doi.org/10.1155/2020/6128341
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AT lijuanhuang transcriptionalanalysisrevealskeygenesinthepathogenesisofnifedipineinducedgingivalovergrowth
AT shuweiwang transcriptionalanalysisrevealskeygenesinthepathogenesisofnifedipineinducedgingivalovergrowth
AT shouliangzhao transcriptionalanalysisrevealskeygenesinthepathogenesisofnifedipineinducedgingivalovergrowth