scholarly journals DNA-Encoded Library-Derived DDR1 Inhibitor Prevents Fibrosis and Renal Function Loss in a Genetic Mouse Model of Alport Syndrome

2018 ◽  
Vol 14 (1) ◽  
pp. 37-49 ◽  
Author(s):  
Hans Richter ◽  
Alexander L. Satz ◽  
Marc Bedoucha ◽  
Bernd Buettelmann ◽  
Ann C. Petersen ◽  
...  
Keyword(s):  
Renal Function ◽  
Mouse Model ◽  
Alport Syndrome ◽  
Genetic Mouse Model ◽  
Function Loss

1734-P: High Dietary Fat Intake Exacerbates Insulin Resistance in a Type 2 Diabetes Genetic Mouse Model

Diabetes ◽  
2020 ◽  
Vol 69 (Supplement 1) ◽  
pp. 1734-P
Author(s):  
AUSTIN REILLY ◽  
SHIJUN YAN ◽  
ALEXA J. LONCHARICH ◽  
HONGXIA REN
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Mouse Model ◽  
Dietary Fat ◽  
Fat Intake ◽  
Dietary Fat Intake ◽  
Genetic Mouse Model

scholarly journals Carrot Supplementation Improves Blood Pressure and Reduces Aortic Root Lesions in an Atherosclerosis-Prone Genetic Mouse Model

Nutrients ◽  
2021 ◽  
Vol 13 (4) ◽  
pp. 1181
Author(s):  
Raffaella Soleti ◽  
Marine Coué ◽  
Charlotte Trenteseaux ◽  
Gregory Hilairet ◽  
Lionel Fizanne ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Mouse Model ◽  
Aortic Root ◽  
De Novo ◽  
Body Weight Gain ◽  
Density Lipoprotein ◽  
De Novo Lipogenesis ◽  
Hemodynamic Parameters ◽  
Cellular Models ◽  
Genetic Mouse Model

Epidemiological studies have shown that carrot consumption may be associated with a lower risk of developing several metabolic dysfunctions. Our group previously determined that the Bolero (Bo) carrot variety exhibited vascular and hepatic tropism using cellular models of cardiometabolic diseases. The present study evaluated the potential metabolic and cardiovascular protective effect of Bo, grown under two conditions (standard and biotic stress conditions (BoBS)), in apolipoprotein E-knockout (ApoE−/−) mice fed with high fat diet (HFD). Effects on metabolic/hemodynamic parameters and on atherosclerotic lesions have been assessed. Both Bo and BoBS decreased plasma triglyceride and expression levels of genes implicated in hepatic de novo lipogenesis and lipid oxidation. BoBS supplementation decreased body weight gain, secretion of very-low-density lipoprotein, and increased cecal propionate content. Interestingly, Bo and BoBS supplementation improved hemodynamic parameters by decreasing systolic, diastolic, and mean blood pressure. Moreover, Bo improved cardiac output. Finally, Bo and BoBS substantially reduced the aortic root lesion area. These results showed that Bo and BoBS enriched diets corrected most of the metabolic and cardiovascular disorders in an atherosclerosis-prone genetic mouse model and may therefore represent an interesting nutritional approach for the prevention of cardiovascular diseases.

scholarly journals Honokiol Prevents Non-Alcoholic Steatohepatitis-Induced Liver Cancer via EGFR Degradation through the Glucocorticoid Receptor—MIG6 Axis

Cancers ◽  
2021 ◽  
Vol 13 (7) ◽  
pp. 1515
Author(s):  
Keiichiro Okuda ◽  
Atsushi Umemura ◽  
Shiori Umemura ◽  
Seita Kataoka ◽  
Hiroyoshi Taketani ◽  
...  
Keyword(s):  
Mouse Model ◽  
Glucocorticoid Receptor ◽  
Nuclear Translocation ◽  
Growth Factor Receptor ◽  
Public Health Problem ◽  
Egfr Signaling ◽  
Alcoholic Steatohepatitis ◽  
Genetic Mouse Model ◽  
Treatment And Prevention ◽  
Egfr Expression

Non-alcoholic steatohepatitis (NASH) has become a serious public health problem associated with metabolic syndrome. The mechanisms by which NASH induces hepatocellular carcinoma (HCC) remain unknown. There are no approved drugs for treating NASH or preventing NASH-induced HCC. We used a genetic mouse model in which HCC was induced via high-fat diet feeding. This mouse model strongly resembles human NASH-induced HCC. The natural product honokiol (HNK) was tested for its preventative effects against NASH progression to HCC. Then, to clarify the mechanisms underlying HCC development, human HCC cells were treated with HNK. Human clinical specimens were also analyzed to explore this study’s clinical relevance. We found that epidermal growth factor receptor (EGFR) signaling was hyperactivated in the livers of mice with NASH and human HCC specimens. Inhibition of EGFR signaling by HNK drastically attenuated HCC development in the mouse model. Mechanistically, HNK accelerated the nuclear translocation of glucocorticoid receptor (GR) and promoted mitogen-inducible gene 6 (MIG6)/ERBB receptor feedback inhibitor 1 (ERRFI1) expression, leading to EGFR degradation and thereby resulting in robust tumor suppression. In human samples, EGFR-positive HCC tissues and their corresponding non-tumor tissues exhibited decreased ERRFI1 mRNA expression. Additionally, GR-positive non-tumor liver tissues displayed lower EGFR expression. Livers from patients with advanced NASH exhibited decreased ERRFI1 expression. EGFR degradation or inactivation represents a novel approach for NASH–HCC treatment and prevention, and the GR–MIG6 axis is a newly defined target that can be activated by HNK and related compounds.

scholarly journals Renal Function Loss After Cryoablation of Small Renal Masses in Solitary Kidneys: European Registry for Renal Cryoablation Multi-Institutional Study

2020 ◽  
Vol 34 (2) ◽  
pp. 233-239 ◽  
Author(s):  
Seshadri Sriprasad ◽  
Mohammed Aldiwani ◽  
Shiv Pandian ◽  
Tommy K. Nielsen ◽  
Mohamed Ismail ◽  
...  
Keyword(s):  
Renal Function ◽  
Small Renal Masses ◽  
Renal Masses ◽  
Function Loss ◽  
European Registry

scholarly journals sar: a genetic mouse model for human sarcosinemia generated by ethylnitrosourea mutagenesis.

1992 ◽  
Vol 89 (7) ◽  
pp. 2644-2648 ◽  
Author(s):  
C. O. Harding ◽  
P. Williams ◽  
D. M. Pflanzer ◽  
R. E. Colwell ◽  
P. W. Lyne ◽  
...  
Keyword(s):  
Mouse Model ◽  
Genetic Mouse Model

scholarly journals Metabolomic signature of the Dravet syndrome: A genetic mouse model study

Epilepsia ◽  
2021 ◽  
Author(s):  
Nina Miljanovic ◽  
Roelof Maarten van Dijk ◽  
Verena Buchecker ◽  
Heidrun Potschka
Keyword(s):  
Mouse Model ◽  
Dravet Syndrome ◽  
Genetic Mouse Model ◽  
Model Study

Schizophrenia-relevant behaviours in a genetic mouse model for Y2 deficiency

2010 ◽  
Vol 207 (2) ◽  
pp. 434-440 ◽  
Author(s):  
Tim Karl ◽  
Rose Chesworth ◽  
Liesl Duffy ◽  
Herbert Herzog
Keyword(s):  
Mouse Model ◽  
Genetic Mouse Model
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