Reduced Dentin Matrix Protein Expression in Camurati-Engelmann Disease Transgenic Mouse Model

2015 ◽  
Vol 231 (5) ◽  
pp. 1106-1113
Author(s):  
Angela Gullard ◽  
Christina M. Croney ◽  
Xiangwei Wu ◽  
Olga Mamaeva ◽  
Philip Sohn ◽  
...  
Keyword(s):  
Mouse Model ◽  
Protein Expression ◽  
Transgenic Mouse ◽  
Matrix Protein ◽  
Transgenic Mouse Model ◽  
Dentin Matrix Protein ◽  
Dentin Matrix ◽  
Engelmann Disease

scholarly journals Periodontal Breakdown in the Dmp1 Null Mouse Model of Hypophosphatemic Rickets

2008 ◽  
Vol 87 (7) ◽  
pp. 624-629 ◽  
Author(s):  
L. Ye ◽  
S. Zhang ◽  
H. Ke ◽  
L. F. Bonewald ◽  
JQ. Feng
Keyword(s):  
Mouse Model ◽  
Matrix Protein ◽  
Alveolar Bone ◽  
Alveolar Bone Loss ◽  
Hypophosphatemic Rickets ◽  
Null Mouse ◽  
Dentin Matrix Protein ◽  
Periodontal Breakdown ◽  
Dentin Matrix ◽  
Increased Susceptibility

Dentin Matrix Protein 1 (DMP1) is highly expressed in alveolar bone and cementum, which are important components of the periodontium. Therefore, we hypothesized that Dmp1 is critical for the integrity of the periodontium, and that deletion may lead to increased susceptibility to disease. An early-onset periodontal defect was observed in the Dmp1 null mouse, a mouse model of hypophosphatemic rickets. The alveolar bone is porous, with increased proteoglycan expression. The cementum is also defective, as characterized by irregular, punctate fluorochrome labeling and elevated proteoglycan. The osteocyte and cementocyte lacuno-canalicular system of both alveolar bone and cementum is abnormal, with irregular lacunar walls and fewer canaliculi. As a consequence, there is significant interproximal alveolar bone loss, combined with detachment between the periodontal ligament (PDL) and cementum. We propose that defective alveolar bone and cementum may account for the periodontal breakdown and increased susceptibility to bacterial infection in Dmp1 null mice.

scholarly journals Mutant Prion Protein Expression Causes Motor and Memory Deficits and Abnormal Sleep Patterns in a Transgenic Mouse Model

Neuron ◽  
2008 ◽  
Vol 60 (4) ◽  
pp. 598-609 ◽  
Author(s):  
Sara Dossena ◽  
Luca Imeri ◽  
Michela Mangieri ◽  
Anna Garofoli ◽  
Loris Ferrari ◽  
...  
Keyword(s):  
Mouse Model ◽  
Protein Expression ◽  
Transgenic Mouse ◽  
Prion Protein ◽  
Memory Deficits ◽  
Transgenic Mouse Model ◽  
Sleep Patterns ◽  
Abnormal Sleep

scholarly journals Disrupted Protein Expression and Altered Proteolytic Events in Hypophosphatemic Dentin Can Be Rescued by Dentin Matrix Protein 1

2020 ◽  
Vol 11 ◽  
Author(s):  
Elizabeth Guirado ◽  
Yinghua Chen ◽  
Ryan D. Ross ◽  
Youbin Zhang ◽  
Catherine Chaussain ◽  
...  
Keyword(s):  
Protein Expression ◽  
Matrix Protein ◽  
Dentin Matrix Protein 1 ◽  
Dentin Matrix Protein ◽  
Dentin Matrix

miR-29c regulates NAV3 protein expression in a transgenic mouse model of Alzheimer׳s disease

2015 ◽  
Vol 1624 ◽  
pp. 95-102 ◽  
Author(s):  
Yuanyuan Zong ◽  
Pin Yu ◽  
Hongxia Cheng ◽  
Hailin Wang ◽  
Xiaoying Wang ◽  
...  
Keyword(s):  
Mouse Model ◽  
Protein Expression ◽  
Transgenic Mouse ◽  
Transgenic Mouse Model

scholarly journals Characterization of liver histopathology in a transgenic mouse model expressing genotype 1a hepatitis C virus core and envelope proteins 1 and 2

2005 ◽  
Vol 86 (8) ◽  
pp. 2185-2196 ◽  
Author(s):  
Turaya Naas ◽  
Masoud Ghorbani ◽  
Ikuri Alvarez-Maya ◽  
Michael Lapner ◽  
Rashmi Kothary ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Mouse Model ◽  
Protein Expression ◽  
Transgenic Mouse ◽  
Transgenic Mouse Model ◽  
Structural Proteins ◽  
Hcv Rna ◽  
Hcv Structural Proteins

Hepatitis C virus (HCV) is a major cause of chronic hepatitis and hepatocellular carcinoma worldwide. The purpose of this study was to determine how the HCV structural proteins affect the dynamic structural and functional properties of hepatocytes and measure the extra-hepatic manifestations induced by these viral proteins. A transgenic mouse model was established by expressing core, E1 and E2 proteins downstream of a CMV promoter. HCV RNA was detected using RT-PCR in transgenic mouse model tissues, such as liver, kidney, spleen and heart. Expression of the transgene was analysed by real-time PCR to quantify viral RNA in different tissues at different ages. Immunofluorescence analysis revealed the expression of core, E1 and E2 proteins predominantly in hepatocytes. Lower levels of protein expression were detected in spleen and kidneys. HCV RNA and viral protein expression increased in the liver with age. Histological analysis of liver cells demonstrated steatosis in transgenic mice older than 3 months, which was more progressed with age. Electron microscopy analysis revealed alterations in nuclei, mitochondria and endoplasmic reticulum. HCV structural proteins induce a severe hepatopathy in the transgenic mouse model. These mice became more prone to liver and lymphoid tumour development and hepatocellular carcinoma. In this model, the extra-hepatic effects of HCV, which included swelling of renal tubular cells, were mild. It is likely that the HCV structural proteins mediate some of the histological alterations in hepatocytes by interfering with lipid transport and liver metabolism.

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