ABSTRACT
We cloned a novel mouse cDNA, Mcpr1 (mouse cleft palate-related gene 1), between retinoic acid (RA)-treated murine embryonic palatal and control shelves by improved subtractive hybridization. Its transcript was identified by Northern blotting. The open reading frame encodes 132 amino acids and shows almost no identity to other genetic products. Mcpr1 expression could be detected extensively in adult mouse tissues and during murine embryonic development. It was identified to be significantly stimulated by RA in murine palatal shelves at embryonic day 12 and in palatal mesenchymal cells in vitro. We demonstrate that MCPR1 protein was localized primarily in the cytoplasm and could be synthesized and secreted by transfected COS-7 cells. Both the secretory and recombinant proteins of Mcpr1 inhibited proliferation of murine embryonic palatal mesenchymal cells and impeded the progression from the G1 to S phase in the cell cycle. The cells were prone to apoptosis after exposure to glutathione S-transferase-MCPR1. Furthermore, knockdown of MCPR1 protein levels by antisense oligodeoxynucleotides promoted progression of cells from the G1 to S phase and completely abolished the RA-induced block of the cell cycle from the G1 to S phase. These findings suggest that Mcpr1 might function as one of the RA-up-regulated genes involved in inhibiting cell proliferation during palatogenesis and RA-induced cleft palate by regulating proliferation and apoptosis of embryonic palatal mesenchymal cells and might even play a role in the development of many other organs.
Subject(s)
Adaptor Proteins, Signal Transducing/genetics , Cell Proliferation , Cleft Palate/genetics , Mesenchymal Stem Cells/pathology , Palate/abnormalities , Adaptor Proteins, Signal Transducing/physiology , Animals , Apoptosis , Blotting, Northern , Cleft Palate/chemically induced , Cleft Palate/pathology , Cloning, Molecular , Female , Gene Library , Glutathione Transferase/genetics , Glutathione Transferase/metabolism , Male , Mice , Mice, Inbred C57BL , Molecular Sequence Data , Oligodeoxyribonucleotides, Antisense/pharmacology , Palate/drug effects , Palate/embryology , Recombinant Fusion Proteins/genetics , Recombinant Fusion Proteins/metabolism , Subtraction Technique , Tretinoin/toxicityABSTRACT
PURPOSE: To explore the significance of genetic factor in the pathogenesis of skeletal angle III malocclusion. METHODS: A case-control study of 96 probands, 200 controls and their relatives was performed and the data were analyzed with genetic epidemiologic methods. SPSS11.5 software package was used for Chi-square test. RESULTS: The prevalence rates of skeletal angle III malocclusion in the first-degree relatives and second-degree relatives in the proband group were 9.00% and 1.88%,respectively,which were higher than that in the first-degree relatives in the control group(0.96%). The heritability in the first-degree relatives was 0.74+/-0.092.The results of segregation analysis didn't suggest that skeletal angle III malocclusion followed a pattern of autosomal recessive inheritance. CONCLUSION: Skeletal angle III malocclusion has characteristics of polygenetic disease. Genetic factor might play an important role in the pathogenesis of skeletal angle III malocclusion.
Subject(s)
Malocclusion, Angle Class III/epidemiology , Malocclusion, Angle Class III/genetics , Quantitative Trait, Heritable , Case-Control Studies , Chi-Square Distribution , Humans , Malocclusion/epidemiology , Malocclusion/genetics , PrevalenceABSTRACT
PURPOSE: To study histological changes under the conditions of orthodontic rapid tooth movement through distraction osteogenesis of the periodental ligament on dogs. METHODS: The experiment was carried out in 6 dogs, the left side of jaws of each one was set as test or control side, and the other side was control or test side. On the control side, the first premolar was moved using traditional methods while the third premolar as anchor, on the test side, using self-made distraction device. The periodental tissue of tooth moved were extracted at the end of the test, some of decalcified sections were stained with hematoxylin and eosin and others with modified Mallory's trichrome staining method, being examined by LM. RESULTS: Decalcified sections stained with hematoxylin and eosin showed the bone formed actively, and there were a large number of fibroblasts and osteoblasts as well as abundant vascularity. The modified Mallory's trichrome staining method showed the newly formed bone very clearly and distinctly. CONCLUSIONS: There was no difference in quality but in quantity on the histological reactions in tension side of the tooth moved by traditional method and by distraction osteogenesis through the peridental ligament and periodontal membrane, the latter could induce higher activity of histological synthesization than the former.
