Expression Profiles of Inflammation-associated microRNAs in Periapical Lesions and Human Periodontal Ligament Fibroblasts Inflammation.

J Endod

State Key Laboratory of Oral Diseases, Department of Endodontics, West China Hospital of Stomatology, Sichuan University, Chengdu, Sichuan, China. Electronic address:

Published: December 2016

Introduction: microRNAs (miRNAs) have been identified to be closely related to inflammatory diseases. The aim of our study was to identify expression profiles of miRNAs associated with inflammation in apical periodontitis (AP) lesions and human periodontal ligament fibroblasts (HPDLFs) inflammation.

Methods: Total RNAs were extracted from 10 AP lesions, 6 control tissues, and HPDLFs using lysis buffer. Expressions of miRNAs (miR-29b, 106b, 125b, 143, 155, and 198) were detected by real-time polymerase chain reaction. The dual luciferase assay was used to test miR-155 directly targeted semaphorein3a (SEMA3A). Western Blot and the enzyme-linked immunosorbent assay were used to detect the protein expressions of SEMA3A and proinflammatory cytokines, respectively. All experiments were repeated at least 3 times. Data were analyzed using the independent sample t test.

Results: The previously mentioned miRNAs were all significantly up-regulated in AP lesions (P < .05), whereas they were not in HPDLFs inflammation, in which miR-29b, 106b, 125b, and 198 were down-regulated (P < .05) and miR-143 and 155 were unchanged (P > .05). Overexpression of miR-155 induced proinflammatory phenotype, and down-regulation reduced the other miRNAs in HPDLFs (P < .05). Moreover, miR-155 directly targeted SEMA3A, which was significantly up-regulated (increased) in acute HPDLFs inflammation and down-regulated (decreased) in AP lesions (P < .05). Knockdown of SEMA3A led to induction of the proinflammatory phenotype; down-regulation of miR-29b, 106b, 125b, 143, and 198 (P < .05); and, more importantly, up-regulation of miR-155 (P < .01).

Conclusions: Our study showed that the expression profiles of inflammation-associated miRNAs associated with inflammation in AP lesions and HPDLFs inflammation were different. miR-155 may play a crucial role in apical periodontitis progression by directly inhibiting SEMA3A.

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http://dx.doi.org/10.1016/j.joen.2016.08.013DOI Listing

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