Spatial and Temporal Expression of Ectodysplasin-A Signaling Pathway Members During Mandibular Condylar Development in Postnatal Mice.
Ludan XingYuan LiuJiayan WuChenyu SongBeizhan JiangPublished in: The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society (2023)
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 in vitro . 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.
Keyphrases
- signaling pathway
- poor prognosis
- computed tomography
- pi k akt
- binding protein
- epithelial mesenchymal transition
- magnetic resonance imaging
- positron emission tomography
- long non coding rna
- type diabetes
- gestational age
- induced apoptosis
- pregnant women
- cell proliferation
- high fat diet induced
- adipose tissue
- drug induced