scholarly journals Susceptibilities of p53 Knockout and rasH2 Transgenic Mice to Urethane-Induced Lung Carcinogenesis are Inherited from their Original Strains

2005 ◽  
Vol 33 (2) ◽  
pp. 267-271 ◽  
Author(s):  
Masakazu Ozaki ◽  
Keisuke Ozaki ◽  
Tomoyuki Watanabe ◽  
Satoshi Uwagawa ◽  
Yasuyoshi Okuno ◽  
...  
Keyword(s):  
Gene Knockout ◽  
P53 Gene ◽  
Lung Tumors ◽  
Peliosis Hepatis ◽  
Original Strain ◽  
Lung Carcinogenesis ◽  
Ras Gene ◽  
Experimental Conditions ◽  
Gene Knockout Mice ◽  
Rash2 Mice

In the present study, susceptibility of CB6F1 mice carrying the human prototype c-Ha- ras gene (rasH2 mice) and p53 gene knockout mice ( p53 (+/−) mice) to urethane-induced lung carcinogenesis was compared under the same experimental conditions. Both strains were administered 500 ppm urethane in their drinking water for 3 weeks. At week 26, lung adenocarcinomas and adenomas were observed in 53% and 100% of rasH2 mice, respectively, and lung adenomas were observed in 67% of rasH2 littermate (non-Tg) mice. However, lung tumors were not observed in either p53 (+/−) or p53 (+/+) mice. Peliosis hepatis and hepatic hemangiomas were observed in 27% and 67% of p53 (+/−) mice, but only in 6.7% and 6.7% of the rasH2 animals, respectively. Under the same experimental conditions, BALB/c mice, the strain of origin of the rasH2 mice, developed lung adenomas at an incidence of 93%, whereas none of the C57BL/6 original strain for p53 (+/−) mice developed lung tumors. Peliosis hepatis was observed in 40% of the C57BL/6 mice, but not in BALB/c mice; hepatic and splenic hemangiomas were not observed in these animals. These results indicate that organ susceptibility of rasH2 and p53 (+/−) mice is inherited from their strains of origin, the rasH2 and BALB/c lines being much more sensitive to the induction of pulmonary carcinogenesis.

Detrimental implication of B1 receptors in myocardial ischemia: evidence from pharmacological blockade and gene knockout mice

2002 ◽  
Vol 2 (6) ◽  
pp. 815-822 ◽  
Author(s):  
Caroline Lagneux ◽  
Michael Bader ◽  
João B. Pesquero ◽  
Pierre Demenge ◽  
Christophe Ribuot
Keyword(s):  
Myocardial Ischemia ◽  
Knockout Mice ◽  
Gene Knockout ◽  
B1 Receptors ◽  
Gene Knockout Mice ◽  
Pharmacological Blockade

Enhanced antinociceptive effects of morphine in histamine H2 receptor gene knockout mice

2006 ◽  
Vol 51 (3) ◽  
pp. 612-622 ◽  
Author(s):  
Jalal Izadi Mobarakeh ◽  
Kazuhiro Takahashi ◽  
Shinobu Sakurada ◽  
Atsuo Kuramasu ◽  
Kazuhiko Yanai
Keyword(s):  
Knockout Mice ◽  
Gene Knockout ◽  
Receptor Gene ◽  
Histamine H2 Receptor ◽  
H2 Receptor ◽  
Antinociceptive Effects ◽  
Gene Knockout Mice

scholarly journals Increased glycosphingolipid levels in serum and aortae of apolipoprotein E gene knockout mice

2002 ◽  
Vol 43 (2) ◽  
pp. 205-214 ◽  
Author(s):  
Brett Garner ◽  
David A. Priestman ◽  
Roland Stocker ◽  
David J. Harvey ◽  
Terry D. Butters ◽  
...  
Keyword(s):  
Apolipoprotein E ◽  
Knockout Mice ◽  
Gene Knockout ◽  
E Gene ◽  
Apolipoprotein E Gene ◽  
Gene Knockout Mice

scholarly journals The Alopecia Areata Phenotype Is Induced by the Water Avoidance Stress Test In cchcr1-Deficient Mice

Biomedicines ◽  
2021 ◽  
Vol 9 (7) ◽  
pp. 840
Author(s):  
Qiaofeng Zhao ◽  
Satoshi Koyama ◽  
Nagisa Yoshihara ◽  
Atsushi Takagi ◽  
Etsuko Komiyama ◽  
...  
Keyword(s):  
Alopecia Areata ◽  
Gene Knockout ◽  
Stress Test ◽  
Coiled Coil ◽  
Risk Haplotype ◽  
Gene Expression Microarray ◽  
Wild Type ◽  
Gene Knockout Mice ◽  
Deficient Mice ◽  
Gene Expression Microarray Analysis

We recently discovered a nonsynonymous variant in the coiled-coil alpha-helical rod protein 1 (CCHCR1) gene within the alopecia areata (AA) risk haplotype. We also reported that the engineered mice with this risk allele exhibited. To investigate more about the involvement of the CCHCR1 gene in AA pathogenesis, we developed an AA model using C57BL/6N cchcr1 gene knockout mice. In this study, mice (6–8 weeks) were divided into two groups: cchcr1−/− mice and wild-type (WT) littermates. Both groups were subjected to a water avoidance stress (WAS) test. Eight weeks after the WAS test, 25% of cchcr1−/− mice exhibited non-inflammatory foci of alopecia on the dorsal skin. On the other hand, none of wild-type littermates cause hair loss. The foci resembled human AA in terms of gross morphology, trichoscopic findings and histological findings. Additionally, gene expression microarray analysis of cchcr1−/− mice revealed abnormalities of hair related genes compared to the control. Our results strongly suggest that CCHCR1 is associated with AA pathogenesis and that cchcr1−/− mice are a good model for investigating AA.

Serotonin2A/C receptors mediate the aggressive phenotype of TLX gene knockout mice

2013 ◽  
Vol 256 ◽  
pp. 354-361 ◽  
Author(s):  
Pablo Juárez ◽  
Maria G. Valdovinos ◽  
Michael E. May ◽  
Blair P. Lloyd ◽  
Maria H. Couppis ◽  
...  
Keyword(s):  
Knockout Mice ◽  
Gene Knockout ◽  
Aggressive Phenotype ◽  
Gene Knockout Mice

scholarly journals Age-Dependent Defects of Regulatory B Cells in Wiskott-Aldrich Syndrome Gene Knockout Mice

PLoS ONE ◽  
2015 ◽  
Vol 10 (10) ◽  
pp. e0139729 ◽  
Author(s):  
Tadafumi Yokoyama ◽  
Ayumi Yoshizaki ◽  
Karen L. Simon ◽  
Martha R. Kirby ◽  
Stacie M. Anderson ◽  
...  
Keyword(s):  
B Cells ◽  
Knockout Mice ◽  
Gene Knockout ◽  
Regulatory B Cells ◽  
Wiskott Aldrich Syndrome ◽  
Age Dependent ◽  
Gene Knockout Mice

scholarly journals NNK-Induced Lung Tumors: A Review of Animal Model

2011 ◽  
Vol 2011 ◽  
pp. 1-8 ◽  
Author(s):  
Hua-Chuan Zheng ◽  
Yasuo Takano
Keyword(s):  
Lung Cancer ◽  
Animal Model ◽  
Animal Models ◽  
Molecular Mechanisms ◽  
Expression Profiles ◽  
Genetic Mutation ◽  
Lung Tumors ◽  
Chemotherapeutic Agents ◽  
Signal Pathways ◽  
Lung Carcinogenesis

The incidence of lung adenocarcinoma has been remarkably increasing in recent years due to the introduction of filter cigarettes and secondary-hand smoking because the people are more exposed to higher amounts of nitrogen oxides, especially 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone(NNK), which is widely applied in animal model of lung tumors. In NNK-induced lung tumors, genetic mutation, chromosome instability, gene methylation, and activation of oncogenes have been found so as to disrupt the expression profiles of some proteins or enzymes in various cellular signal pathways. Transgenic animal with specific alteration of lung cancer-related molecules have also been introduced to clarify the molecular mechanisms of NNK in the pathogenesis and development of lung tumors. Based on these animal models, many antioxidant ingredients and antitumor chemotherapeutic agents have been proved to suppress the NNK-induced lung carcinogenesis. In the future, it is necessary to delineate the most potent biomarkers of NNK-induced lung tumorigenesis, and to develop efficient methods to fight against NNK-associated lung cancer using animal models.

scholarly journals Selective expression of TLQP-21 and other VGF peptides in gastric neuroendocrine cells and modulation by feeding

2010 ◽  
Vol 207 (3) ◽  
pp. 329-341 ◽  
Author(s):  
Carla Brancia ◽  
Cristina Cocco ◽  
Filomena D'Amato ◽  
Barbara Noli ◽  
Fabrizio Sanna ◽  
...  
Keyword(s):  
Gene Knockout ◽  
Cell Types ◽  
Neuroendocrine Cells ◽  
Mucosal Cell ◽  
Clear Cut ◽  
Ecl Cell ◽  
C Terminus ◽  
Gene Knockout Mice ◽  
Definition Of ◽  
Fasted Rats

Although vgf gene knockout mice are hypermetabolic, administration of the VGF peptide TLQP-21 itself increased energy consumption. Agonist–antagonist roles are thus suggested for different VGF peptides, and the definition of their tissue heterogeneity is mandatory. We studied the rat stomach using antisera to C- or N-terminal sequences of known or predicted VGF peptides in immunohistochemistry and ELISA. TLQP (rat VGF556–565) peptide/s were most abundant (162±11 pmol/g, mean±s.e.m.) and were brightly immunostained in enterochromaffin-like (ECL) cells and somatostatin cells. A peptide co-eluting with TLQP-21 was revealed in HPLC of gastric and hypothalamic extracts, while the extended TLQP-62 form was restricted to the hypothalamus. Novel PGH (rat VGF422–430) peptide/s were revealed in ghrelin cells, mostly corresponding to low MW forms (0.8–1.5 kDa), while VGF C-terminus peptides were confined to neurons. VGF mRNA was present in the above gastric endocrine cell types, and was prominent in chief cells, in parallel with low-intensity staining for further cleaved products from the C-terminal region of VGF (HVLL peptides: VGF605–614). In swine stomach, a comparable profile of VGF peptides was revealed by immunohistochemistry. When fed and fasted rats were studied, a clear-cut, selective decrease on fasting was observed for TLQP peptides only (162±11 vs 74±5.3 pmol/g, fed versus fasted rats, mean±s.e.m., P<0.00001). In conclusion, specific VGF peptides appear to be widely represented in different gastric endocrine and other mucosal cell populations. The selective modulation of TLQP peptides suggests their involvement in peripheral neuro-endocrine mechanisms related to feeding responses and/or ECL cell regulation.

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