Li Z, Lu H, Li Z-B
The State Key Laboratory Breeding Base of Basic Science of Stomatology (Hubei-MOST) and Key Laboratory for Oral Biomedical Engineering of the Ministry of Education, School and Hospital of Stomatology, Wuhan University, Wuhan, China; Department of Oral and Maxillofacial Surgery, School and Hospital of Stomatology, Wuhan University, Wuhan, China.
The State Key Laboratory Breeding Base of Basic Science of Stomatology (Hubei-MOST) and Key Laboratory for Oral Biomedical Engineering of the Ministry of Education, School and Hospital of Stomatology, Wuhan University, Wuhan, China; Department of Oral and Maxillofacial Surgery, School and Hospital of Stomatology, Wuhan University, Wuhan, China.
Int J Oral Maxillofac Surg. 2014 Dec;43(12):1477-83. doi: 10.1016/j.ijom.2014.05.015. Epub 2014 Jun 12.
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.
下颌骨发育畸形是最常见的颅面畸形之一，与髁突生长异常密切相关。在本研究中，研究了PI3K/Akt信号通路在髁突软骨细胞增殖和肥大分化调控中的作用。采用免疫组织化学染色法研究PI3K和p-Akt在大鼠髁突软骨中的表达。在抑制PI3K/Akt时，培养大鼠髁突软骨细胞以研究软骨细胞增殖和肥大分化。此外，在抑制PI3K/Akt时，进行大鼠下颌髁突的器官培养以评估髁突软骨生长。髁突软骨中发现有PI3K阳性细胞和显示胞质染色的p-Akt阳性细胞。抑制PI3K/Akt时，大鼠髁突软骨细胞培养中观察到细胞增殖减少；然而，肥大分化水平增加。实验组髁突软骨增殖区厚度小于对照组（P = 0.00185），但肥大区大于对照组（P = 0.01048）。PI3K/Akt信号通路对髁突软骨细胞增殖和肥大分化产生相反影响，这些数据表明PI3K/Akt是髁突软骨发育中一种潜在的细胞内调节信号通路。
