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1.
Arch Oral Biol ; 69: 47-62, 2016 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-27236646

RESUMO

OBJECTIVE: This study has two aims: 1. Validate a non-invasive malocclusion model of mouse temporomandibular joint (TMJ) osteoarthritis (OA) that we developed and 2. Confirm role of inflammation in TMJ OA by comparing the disease in the presence and absence of the receptor for advanced glycation end products (RAGE). DESIGN: The malocclusion procedure was performed on eight week old mice, either wild type (WT) or without RAGE. RESULTS: We observed TMJ OA at two weeks post-misalignment/malocclusion. The modified Mankin score used for the semi-quantitative assessment of OA showed an overall significantly higher score in mice with malocclusion compared to control mice at all times points (2, 4, 6 and 8 weeks). Mice with malocclusion showed a decrease in body weight by the first week after misalignment but returned to normal weight for their ages during the following weeks. The RAGE knock out (KO) mice had statistically lower modified Mankin scores compared to WT mice of the same age. The RAGE KO mice had statistically lower levels of Mmp-13 and HtrA1 but higher Tgf-ß1, as measured by immunohistochemistry, compared to WT mice at eight weeks post malocclusion. CONCLUSIONS: We demonstrate an inexpensive, efficient, highly reproducible and non-invasive model of mouse TMJ OA. The mechanical nature of the malocclusion resembles the natural development of TMJ OA in humans, making this an ideal model in future studies that aim to elucidate the pathogenesis of the disease leading to the discovery of a treatment. The RAGE plays a role in mouse TMJ OA.


Assuntos
Má Oclusão/patologia , Osteoartrite/patologia , Receptor para Produtos Finais de Glicação Avançada/metabolismo , Articulação Temporomandibular/patologia , Animais , Mau Alinhamento Ósseo , Cartilagem Articular/patologia , Condrócitos/patologia , Modelos Animais de Doenças , Produtos Finais de Glicação Avançada/metabolismo , Serina Peptidase 1 de Requerimento de Alta Temperatura A , Imuno-Histoquímica , Má Oclusão/fisiopatologia , Metaloproteinase 13 da Matriz/metabolismo , Camundongos , Camundongos Endogâmicos C57BL , Camundongos Knockout , Fios Ortodônticos , Osteoartrite/fisiopatologia , Serina Endopeptidases/metabolismo , Transtornos da Articulação Temporomandibular/patologia , Fator de Crescimento Transformador beta1/metabolismo
2.
Biochem Genet ; 16(7-8): 831-53, 1978 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-728070

RESUMO

Inheritance of gliadin components unique to three different varieties of common wheat (Triticum aestivum L.) was studied in F1 and F2 seeds of intervarietal crosses using protein patterns obtained by polyacrylamide gel electrophoresis in aluminum lactate buffer (pH 3.2). The patterns of F1 seeds of the crosses Cheyenne X Justin and INIA 66R X Justin evidenced all the bands present in the patterns of the parents; band intensities reflected gene dosage levels dependent on whether the contributing parent was maternal or paternal in accordance with the triploid nature of endosperm tissue. Most of the gliadin components examined segregated in accordance with control by a single dominant gene, but in two instances single bands in the one-dimensional electrophoretic patterns segregated in the F2 as expected if controlled by two genes. A method of two-dimensional electrophoresis was developed that resolved these apparently single bands into two components each, which could segregate independently. Linkage analysis provided evidence of codominant alleles and closely linked genes coding for gliadin protein components in both coupling and repulsion situations. The gliadin protein components seem to be coded for by clusters of genes located on chromosomes of homoeologous groups 1 and 6 in hexaploid wheats.


Assuntos
Gliadina/genética , Proteínas de Plantas/genética , Plantas/genética , Alumínio , Cruzamentos Genéticos , Eletroforese , Triticum/genética
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