Literature DB >> 24929453

The PI3K/Akt signalling pathway may play an internal role related to abnormal condylar growth: a preliminary study.

Z Li1, H Lu1, Z-B Li2.   

Abstract

Developmental deformity of the mandible is one of the most common craniofacial malformations and is closely related to abnormal condylar growth. In this study, the role of PI3K/Akt signalling in the regulation of chondrocyte proliferation and hypertrophic differentiation in the condylar cartilage was studied. Immunohistochemical staining was used to investigate the expression of PI3K and p-Akt in the rat condyle cartilage. Rat condylar chondrocytes were cultured for the investigation of chondrocyte proliferation and hypertrophic differentiation when PI3K/Akt was inhibited. In addition, organ culture of the rat mandibular condyle was performed to evaluate the condyle cartilage growth while PI3K/Akt was inhibited. PI3K-positive cells and p-Akt-positive cells showing cytoplasmic staining were found to be present in the condylar cartilage. Reduced cell proliferation was observed in the culture of rat condylar chondrocytes when PI3K/Akt was inhibited; however, the hypertrophic differentiation level was increased. The proliferative zone thickness of condylar cartilage in the experimental group was less than that in the control group (P=0.00185), but the hypertrophic zone was greater than that in the control group (P=0.01048). PI3K/Akt signalling exerts opposite influences on chondrocyte proliferation and hypertrophic differentiation of the condylar cartilage, and these data suggest that PI3K/Akt is a potential intracellular regulation signal pathway in condylar cartilage development.
Copyright © 2014 International Association of Oral and Maxillofacial Surgeons. Published by Elsevier Ltd. All rights reserved.

Entities:  

Keywords:  PI3K/Akt; chondrocyte; condyle cartilage; differentiation.; proliferation

Mesh:

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Year:  2014        PMID: 24929453     DOI: 10.1016/j.ijom.2014.05.015

Source DB:  PubMed          Journal:  Int J Oral Maxillofac Surg        ISSN: 0901-5027            Impact factor:   2.789


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