Transglutaminase-2 Regulation by Arecoline in Gingival Fibroblasts

被引:27
作者
Thangjam, G. S. [1 ]
Agarwal, P. [1 ]
Khan, I. [1 ]
Verma, U. P. [2 ]
Balapure, A. K. [3 ]
Rao, S. G. [4 ]
Kondaiah, P. [1 ]
机构
[1] Indian Inst Sci, Dept Mol Reprod Dev & Genet, Bangalore 560012, Karnataka, India
[2] CSM Med Univ, Fac Dent Sci, Dept Periodont, Lucknow 226003, Uttar Pradesh, India
[3] Cent Drug Res Inst, Tissue & Cell Culture Unit, Lucknow 226001, Uttar Pradesh, India
[4] RV Dent Coll & Hosp, Dept Oral & Maxillofacial Surg, Bangalore 560078, Karnataka, India
关键词
arecoline; muscarinic acetylcholine receptor; oral submucous fibrosis; transglutaminase-2; ORAL SUBMUCOUS FIBROSIS; BUCCAL MUCOSAL FIBROBLASTS; TISSUE INHIBITOR; GENE-EXPRESSION; RECEPTOR; METALLOPROTEINASE-1; PATHOGENESIS; EXCITES; CELLS;
D O I
10.1177/0022034508329633
中图分类号
R78 [口腔科学];
学科分类号
1003 ;
摘要
Transglutaminase-2 (TGM-2) stabilizes extracellular matrix (ECM) proteins by cross-linking and has been implicated in several fibrotic disorders. Arecoline present in betel quid has been proposed as one of the causative factors for oral submucous fibrosis (OSMF). Hence, we hypothesize that arecoline may regulate TGM-2 and may have a role in the pathogenesis of OSMF. The expression of TGM-2 was studied in OSMF tissues by real-time RT-PCR analysis, and significant overexpression was observed in most OSMF tissues (P = 0.0112) compared with normal tissues. Arecoline induced TGM-2 mRNA and protein expression as well as TGM-2 activity in human gingival fibroblast cells. The addition of methocramine hemihydrate (M-2 muscarinic acetylcholine receptor selective antagonist) or 8'-bromo-cAMP abolished arecoline-mediated TGM-2 induction, suggesting a role for M-2 muscarinic acid receptor and a repressor role for cAMP. Our study provides evidence for TGM-2 overexpression in OSMF and its regulation by arecoline in oral fibroblasts.
引用
收藏
页码:170 / 175
页数:6
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