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下颌髁突软骨发育过程中Smad信号成员的时空表达

Spatial and temporal expression of Smad signaling members during the development of mandibular condylar cartilage.

作者信息

Xiao Di, Wang Ru, Hu Jing, Quan Huixin

机构信息

Department of Stomatology, The First Affiliated Hospital of Dalian Medical University, Dalian, Liaoning 116023, P.R. China.

State Key Laboratory of Oral Diseases and Department of Oral and Maxillofacial Surgery, West China Hospital of Stomatology, Sichuan University, Chengdu, Sichuan 610041, P.R. China.

出版信息

Exp Ther Med. 2017 Nov;14(5):4967-4971. doi: 10.3892/etm.2017.5186. Epub 2017 Sep 22.

Abstract

The present study aimed to explore the underlying developmental mechanism of mothers against decapentaplegic homolog (Smad) signaling in the development of mandibular condylar cartilage. To achieve this, the expression levels of Smad2, 3, 4 and 7, and phosphorylated Smad2/3 were investigated at different time points in developing mandibular condylar cartilage. Mandibular condyles from C57BL/6J mice were dissected at the prenatal and postnatal stages. Serial sections were made and the distributions of Smad proteins were examined using immunohistochemical techniques intermittently between day 14.5 of gestation and postnatal day 7. All Smad proteins examined in the present study were expressed in the condylar blastema and during early chondrogenesis. At the postnatal stage, Smad2 and 4 were localized in proliferative and mineralized hypertrophic chondrocytes. Smad3 and 7 were expressed in proliferative and hypertrophic chondrocytes, including pre-hypertrophic and mineralized hypertrophic chondrocytes. Later, positive immunoreactivity of Smad3 reduced at postnatal day 7. A similar expression pattern to Smad3 was observed for p-Smad2/3, but p-Smad2/3 was located in the nuclei of proliferative chondrocytes. These results suggest that Smad signaling members are involved in the development of mandibular condylar cartilage. In addition, the spatial and temporal expression of these Smads indicate that Smad signaling is involved in regulating the differentiation of chondrocytes and endochondral ossification, in order to maintain normal chondrogenesis and morphogenesis of mandibular condylar cartilage.

摘要

本研究旨在探讨母亲抗十号染色体缺失的磷酸酶和张力蛋白同源物(Smad)信号通路在下颌髁突软骨发育中的潜在机制。为此,研究了Smad2、3、4和7以及磷酸化Smad2/3在发育中的下颌髁突软骨不同时间点的表达水平。在产前和产后阶段解剖C57BL/6J小鼠的下颌髁突。制作连续切片,并在妊娠第14.5天至出生后第7天期间,间断地使用免疫组织化学技术检查Smad蛋白的分布。本研究中检测的所有Smad蛋白均在髁突芽基和软骨形成早期表达。在出生后阶段,Smad2和4定位于增殖性和矿化肥大软骨细胞。Smad3和7在增殖性和肥大软骨细胞中表达,包括前肥大和矿化肥大软骨细胞。随后,出生后第7天Smad3的阳性免疫反应性降低。p-Smad2/3观察到与Smad3相似的表达模式,但p-Smad2/3位于增殖性软骨细胞的细胞核中。这些结果表明Smad信号成员参与了下颌髁突软骨的发育。此外,这些Smad蛋白的时空表达表明Smad信号通路参与调节软骨细胞的分化和软骨内骨化,以维持下颌髁突软骨的正常软骨形成和形态发生。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5cab/5704254/fa95265099c7/etm-14-05-4967-g00.jpg

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