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在出生后小鼠下颌髁突发育过程中,外胚层发育不良-A 信号通路成员的时空表达。

Spatial and Temporal Expression of Ectodysplasin-A Signaling Pathway Members During Mandibular Condylar Development in Postnatal Mice.

机构信息

Department of Pediatric Dentistry, Stomatological Hospital and Dental School of Tongji University, Shanghai Engineering Research Center of Tooth Restoration and Regeneration, Shanghai, China.

出版信息

J Histochem Cytochem. 2023 Nov;71(11):631-642. doi: 10.1369/00221554231201691. Epub 2023 Sep 20.

DOI:10.1369/00221554231201691
PMID:37731334
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10617443/
Abstract

A growing body of evidence emerging supported that ectodysplasin-A (EDA) signaling pathway contributed to craniofacial development. However, their expression in condyle has not been elucidated yet. This study investigated the expression patterns of EDA, EDA receptor (EDAR), and EDAR-associated death domain (EDARADD) in condyle of postnatal mice. Histological staining and micro-computed tomography (CT) scanning showed that as endochondral ossification proceeded, the thickness of chondrocyte layer decreased, and the volume of mandibular condyle increased. Osteoclasts remained active throughout the condylar development. Immunohistochemistry staining demonstrated that EDA was expressed in almost all layers during the first 2 weeks after birth. EDA shifted from the mature and hypertrophic layers to fibrous and proliferating layers at postnatal 3 weeks. As condyle matured, the distribution of EDA tended to be limited to hypertrophic layer. The distribution patterns of EDAR and EDARADD were consistent with EDA, while the level of EDAR expression was slightly lower. mRNA expression levels of EDA signaling pathway-related components increased after birth. Furthermore, we evaluated the expression of EDA using ATDC5 . EDA increased during the late stage of chondrogenesis. These findings proved that EDA signaling pathway was involved in condylar development and acted as a regulatory factor in condylar maturation and differentiation.

摘要

越来越多的证据表明,外胚层发育不良蛋白-A(EDA)信号通路参与颅面发育。然而,其在髁突中的表达尚未阐明。本研究探讨了 EDA、EDA 受体(EDAR)和 EDAR 相关死亡结构域(EDARADD)在出生后小鼠髁突中的表达模式。组织学染色和微计算机断层扫描(CT)扫描显示,随着软骨内骨化的进行,软骨细胞层的厚度减少,下颌髁突的体积增加。破骨细胞在整个髁突发育过程中保持活跃。免疫组织化学染色表明,EDA 在出生后前 2 周几乎存在于所有层中。EDA 从成熟和肥大层转移到 3 周龄时的纤维和增殖层。随着髁突的成熟,EDA 的分布趋于局限于肥大层。EDAR 和 EDARADD 的分布模式与 EDA 一致,而 EDAR 的表达水平略低。EDA 信号通路相关成分的 mRNA 表达水平在出生后增加。此外,我们使用 ATDC5 评估了 EDA 的表达。EDA 在软骨生成的晚期增加。这些发现证明 EDA 信号通路参与髁突发育,并作为髁突成熟和分化的调节因子。

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Osteoarthritis: pathogenic signaling pathways and therapeutic targets.骨关节炎:发病信号通路和治疗靶点。
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Tooth number abnormality: from bench to bedside.牙齿数目异常:从基础到临床。
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Ectodysplasin A1 Deficiency Leads to Osteopetrosis-like Changes in Bones of the Skull Associated with Diminished Osteoclastic Activity.外胚层发育不良蛋白 A1 缺陷导致颅骨骨骼出现类骨质硬化改变,与破骨细胞活性降低有关。
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Ectodysplasin A (EDA) Signaling: From Skin Appendage to Multiple Diseases.外胚层发育不全 A(EDA)信号通路:从皮肤附属器到多种疾病。
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