Meckel's chondrocytes, derived from the ectomesenchyme, have the potential to transform into other phenotypes. In this study, we transplanted cell pellets of Meckel's chondrocytes into isogenic mouse spleens and analyzed their phenotypic transformation into osteogenic cells using histological and immunohistochemical methods. With the increasing duration of transplantation, chondrocytes were incorporated into splenic tissues and formed a von Kossa-positive calcified matrix containing calcium and phosphoric acid, similar to that of intact bone. Type I, II, and X collagens, and the bone-marker proteins osteocalcin, osteopontin, osteonectin, and bone morphogenetic protein-2 (BMP-2) were immunolocalized in the matrix formed by the transplanted chondrocytes. Osteopontin and osteonectin were detected in the calcified matrix at earlier stages than osteocalcin and BMP-2. Type II collagen was expressed during the first week of transplantation, and type X collagen-positive cells appeared scattered during the initial stage of calcification, these collagens being later replaced by type I collagen formed by osteocyte-like cells. Electron microscopic observations revealed that chondrocytes surrounded by the calcified matrix transformed into spindle-shaped osteocytic cells accompanying the formation of bone-type thick-banded collagen fibrils. These results suggest that phenotypic switching of Meckel's chondrocytes can occur under in vivo conditions at a cellular morphological level.
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http://dx.doi.org/10.1679/aohc.72.1 | DOI Listing |
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.
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August 2024
Institute of Zoology and Evolutionary Research, Friedrich-Schiller-University, Jena, Germany.
Several studies describe the development of the chondrocranium of vertebrates. The details in these studies vary a lot, which makes it hard to compare developmental patterns and identify evolutionary trends. Therefore, we aim to close this gap for anurans, which is the largest order of amphibians.
View Article and Find Full Text PDFJCI Insight
July 2024
Division of Genetics, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA.
Craniofacial dysmorphisms are among the most common birth defects. Proteasome mutations frequently result in craniofacial dysmorphisms, including lower jaw malformations; however, the underlying mechanisms are unknown. Here, we used a zebrafish proteasome subunit β 1 (psmb1) mutant to define the cellular mechanisms underlying proteasome mutation-induced craniofacial dysmorphisms.
View Article and Find Full Text PDFDev Dyn
January 2025
Department of Developmental Biology, Institute of Experimental Medicine, Czech Academy of Sciences, Prague, Czech Republic.
Background: Meis family of transcription factors operates in Pbx-Meis-Hox regulatory network controlling development of various tissues including eye, limbs, heart, hindbrain or craniofacial skeletal elements originating from the neural crest. Although studies in mouse provide abundant information about Meis factors function in embryogenesis, little is known about their role in zebrafish.
Results: We generated zebrafish lines carrying null mutations in meis1a, meis1b, meis2a, and meis2b genes.
Am J Undergrad Res
June 2023
Department of Biological Sciences, University of Texas at El Paso, El Paso, TX.
ZNF143 is a sequence-specific DNA binding protein that regulates the expression of protein-coding genes and small RNA molecules. In humans, ZNF143 interacts with HCFC1, a transcriptional cofactor, to regulate the expression of downstream target genes, including , which encodes an enzyme involved in cobalamin () metabolism. Mutations in or cause an inborn error of cobalamin metabolism characterized by abnormal metabolism, intellectual disability, seizures, and mild to moderate craniofacial abnormalities.
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