In mammals, the midportion of the soft tissue of Meckel's cartilage at the degenerating stage forms a ligament known as the sphenomandibular ligament. To clarify the mechanism of formation of this ligament by Meckel's cartilage in mouse, we examined the effects of epidermal growth factor (EGF) on the chondrocytes in terms of the proliferation and differentiation of cells and calcification of the matrix in vivo and in vitro. The effects of EGF were examined by immunohistochemical staining, with EGF-soaked beads, by electron microscopy, and by general histochemical analysis of proteoglycans and calcification. Analysis of labeling with bromodeoxyuridine (BrdU) and the rate of cell growth revealed that EGF enhanced DNA synthesis and the proliferation of Meckel's chondrocytes. Histological findings in organ culture and in cell culture, with and without the application of EGF-soaked beads, revealed that EGF inhibited the differentiation of cells to chondrocytes and induced phenotypic changes in fibroblastic cells. The inhibition of alkaline phosphatase activity that resulted from exposure to EGF was accompanied by prolonged calcification of the matrix. Whole-mount staining revealed that subcutaneous injection of EGF enhanced the disappearance of Meckel's cartilage. Our results suggest a possible mechanism whereby the midportion of Meckel's cartilage remains uncalcified and is rapidly transformed into the sphenomandibular ligament.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1007/s004410100354 | DOI Listing |
J Dent Res
December 2024
Division of Developmental Biology, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio, USA.
Both the upper and lower jaws develop from cranial neural crest cells (CNCCs) populating the first pharyngeal arch in all gnathostomes. Previous studies showed that the Edn1/Ednra-Dlx5/Dlx6-Hand2 signaling pathway is necessary for lower jaw formation and that ectopic expression of or throughout the CNCCs partly transformed the upper jaw to lower jaw structures, but the molecular mechanisms regulating upper jaw development remain unclear. Here we show that the basic helix-loop-helix transcription factor Twist1 is required for upper jaw development.
View Article and Find Full Text PDFbioRxiv
October 2024
Department of Anatomy, Physiology, and Cell Biology, University of California, Davis, Davis, CA, USA.
Our lab has identified that transcripts and proteins of the cyclooxygenase (COX-1 and COX-2) isoenzymes are expressed during the early stages of vertebrate embryonic development, and that global COX-1/2 inhibition disrupts neural crest (NC) cell maturation in (axolotl) embryos, with intriguing implications for tissue regeneration and healing. NC cells are embryonic stem cells that differentiate into various adult tissues including craniofacial cartilage, bone, and neurons in the peripheral and enteric nervous systems. Naproxen (NPX), a common non-steroidal anti-inflammatory drug (NSAID) used to relieve pain and inflammation, exerts its effects through COX-1 and COX-2 inhibition.
View Article and Find Full Text PDFJ Anat
February 2025
Department of Biosciences, Universidade Federal de São Paulo (UNIFESP), Santos, São Paulo, Brazil.
When developing, the mandible presents great plasticity and contains condensed mesenchymal cells that develops into Meckel's cartilage, of which the anterior part forms the mandibular symphysis. Mandible human development studies focus on investigating whether the beginning of mandibular fusion in fetal period is related to symphysis ossification and the tensions imposed on it, considering that tongue movements, mouth opening, and closing can be seen in fetuses. This research analyses tissue modifications during human mandibular symphysis growth using light and scanning electron microscopy to relate them to its functional structure.
View Article and Find Full Text PDFComp Biochem Physiol C Toxicol Pharmacol
January 2025
College of Animal Science and Technology, Yangzhou University, Yangzhou 225009, China. Electronic address:
Sci Rep
August 2024
Department of Molecular Biology and Genetics, Aarhus University, Universitetsbyen 81, 8000, Aarhus C, Denmark.
Insulin-like growth factor (IGF) signaling is required for proper growth and skeletal development in vertebrates. Consequently, its dysregulation may lead to abnormalities of growth or skeletal structures. IGF is involved in the regulation of cell proliferation and differentiation of chondrocytes.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!