MicroRNA-21 promotes bone reconstruction in maxillary bone defects.

Abstract:

BACKGROUND:Bone reconstruction of the maxillary bone defects is an urgent issue due to its functional and aesthetic influence. MicroRNAs (miRNAs) are a class of non-coding RNAs that function in diverse biological and pathological processes. Recently, microRNA-21 (miR-21) was reported to play significant roles in bone formation, suggesting that miR-21 can be novel biomarker and therapeutic target for bone remodelling and skeletal diseases. However, the role of miR-21 in maxillary bone defects remains unclear. OBJECTIVE AND METHODS:This study aimed to investigate the effect of miR-21 on the bone reconstruction by inducing maxillary bone defects in wild-type (WT) and miR-21 knockout (miR-21-KO) mice and explore these mice as maxillary bone defect models. RESULTS:Micro-computed tomography (micro-CT) and histochemistry showed that the miR-21-KO mice had reduced bone reformation ability compared with the WT mice. The expression levels of alkaline phosphatase (ALP) and osteocalcin (OCN) were dramatically decreased in the miR-21-KO mice. In addition, injection of miR-21 agomir intra-peritoneally into miR-21-KO mice (miR-21-KO+ agomir) following the maxillary bone defects surgery displayed a significantly enhanced bone formation -promoting ability, which indicated that miR-21 agomir could ameliorate maxillary bone defects in miR-21-KO mice in vivo. Furthermore, immunohistochemistry suggested that ALP and OCN expressions were prominently increased in miR-21-KO+ agomir mice. CONCLUSION:These findings demonstrated that miR-21 deficiency impaired bone reformation and miR-21 contributed to the bone reconstruction of the maxillary bone defects. The evidence also supported the use of WT and miR-21-KO mice as maxillary bone defect models for further research.

journal_name

J Oral Rehabil

authors

Wang H,Wang H,Li X,Zhang Z,Zhao X,Wang C,Wei F

doi

10.1111/joor.12896

subject

Has Abstract

pub_date

2020-11-01 00:00:00

pages

4-11

eissn

0305-182X

issn

1365-2842

journal_volume

47 Suppl 1

pub_type

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