Gene expression response of mouse lung, liver and white adipose tissue to β-carotene supplementation, knockout of Bcmo1 and sex

2011 ◽  
Vol 55 (10) ◽  
pp. 1466-1474 ◽  
Author(s):  
Yvonne G. J. van Helden ◽  
Roger W. L. Godschalk ◽  
Johannes von Lintig ◽  
Georg Lietz ◽  
Jean-Francois Landrier ◽  
...  
Cell Reports ◽  
2020 ◽  
Vol 33 (1) ◽  
pp. 108228 ◽  
Author(s):  
John M. Dean ◽  
Anyuan He ◽  
Min Tan ◽  
Jun Wang ◽  
Dongliang Lu ◽  
...  

2000 ◽  
Vol 279 (6) ◽  
pp. R2329-R2335 ◽  
Author(s):  
Paul Trayhurn ◽  
Jacqueline S. Duncan ◽  
Anne M. Wood ◽  
John H. Beattie

White adipose tissue (WAT) has been examined to determine whether the gene encoding metallothionein (MT), a low-molecular-weight stress response protein, is expressed in the tissue and whether MT may be a secretory product of adipocytes. The MT-1 gene was expressed in epididymal WAT, with MT-1 mRNA levels being similar in lean and obese ( ob/ ob) mice. MT-1 mRNA was found in each of the main adipose tissue sites (epididymal, perirenal, omental, subcutaneous), and there was no major difference between depots. Separation of adipocytes from the stromal-vascular fraction of WAT indicated that the MT gene (MT-1 and MT-2) was expressed in adipocytes themselves. Treatment of mice with zinc had no effect on MT-1 mRNA levels in WAT, despite strong induction of MT-1 expression in the liver. MT-1 gene expression in WAT was also unaltered by fasting or norepinephrine. However, administration of a β3-adrenoceptor agonist, BRL-35153A, led to a significant increase in MT-1 mRNA. On differentiation of fibroblastic preadipocytes to adipocytes in primary culture, MT was detected in the medium, suggesting that the protein may be secreted from WAT. It is concluded that WAT may be a significant site of MT production; within adipocytes, MT could play an antioxidant role in protecting fatty acids from damage.


2011 ◽  
Vol 12 (1) ◽  
pp. 136
Author(s):  
M. Saukko ◽  
E. Malo ◽  
M. Santaniemi ◽  
M. Hietaniemi ◽  
O. Ukkola ◽  
...  

2009 ◽  
Vol 296 (3) ◽  
pp. L418-L429 ◽  
Author(s):  
Eleonora Cavarra ◽  
Paolo Fardin ◽  
Silvia Fineschi ◽  
Annamaria Ricciardi ◽  
Giovanna De Cunto ◽  
...  

We have investigated the effects of cigarette smoke exposure in three different strains of mice. DBA/2 and C57BL/6J are susceptible to smoke and develop different lung changes in response to chronic exposure, whereas ICR mice are resistant to smoke and do not develop emphysema. The present study was carried out to determine early changes in the gene expression profile of mice exposed to cigarette smoke with either a susceptible or resistant phenotype. The three strains of mice were exposed to smoke from three cigarettes per day, 5 days/wk, for 4 wk. Microarray analysis was carried out on total RNA extracted from the lung using the Affymetrix platform. Cigarette smoke modulates several clusters of genes (i.e., proemphysematous, acute phase response, and cell adhesion) in smoke-sensitive DBA/2 or C57BL/6J strains, but the same genes are not altered by smoke in ICR resistant mice. Only a few genes were commonly modulated by smoke in the three strains of mice. This pattern of gene expression suggests that the response to smoke is strain-dependent and may involve different molecular signaling pathways. Real-time quantitative PCR was used to verify the pattern of modulation of selected genes and their potential biological relevance. We conclude that gene expression response to smoke is highly dependent on the mouse genetic background. We speculate that the definition of gene clusters associated, to various degrees, with mouse susceptibility or resistance to smoke may be instrumental in defining the molecular basis of the individual response to smoke-induced lung injury in humans.


Obesity ◽  
2018 ◽  
Vol 27 (1) ◽  
pp. 103-111 ◽  
Author(s):  
Candida J. Rebello ◽  
Frank L. Greenway ◽  
Frank H. Lau ◽  
Yuan Lin ◽  
Jacqueline M. Stephens ◽  
...  

2020 ◽  
Vol 267 ◽  
pp. 115483
Author(s):  
Marco Gerdol ◽  
Andrea Visintin ◽  
Sara Kaleb ◽  
Francesca Spazzali ◽  
Alberto Pallavicini ◽  
...  

2021 ◽  
Author(s):  
Phillip J Dexheimer ◽  
Mario Pujato ◽  
Krishna Roskin ◽  
Matthew T Weirauch

AbstractMotivationHuman viruses cause significant mortality, morbidity, and economic disruption worldwide. The human gene expression response to viral infection can yield important insights into the detrimental effects to the host. To date, hundreds of studies have performed genome-scale profiling of the effect of viral infection on human gene expression. However, no resource exists that aggregates human expression results across multiple studies, viruses, and tissue types.ResultsWe developed the Virus Expression Database (VExD), a comprehensive curated resource of transcriptomic studies of viral infection in human cells. We have processed all studies within VExD in a uniform manner, allowing users to easily compare human gene expression changes across conditions.Availability and ImplementationVExD is freely accessible at https://vexd.cchmc.org for all modern web browsers. An Application Programming Interface (API) for VExD is also available. The source code is available at https://github.com/pdexheimer/[email protected], [email protected]


2019 ◽  
Author(s):  
Maritere Urioistegui-Arcos ◽  
Rodrigo Aguayo-Ortiz ◽  
María del Pilar Valencia-Morales ◽  
Erika Melchy-Pérez ◽  
Yvonne Rosenstein ◽  
...  

AbstractDisruption of the enzymatic activities of the transcription factor TFIIH by Triptolide (TPL) or THZ1 could be used against cancer. Here, we used an oncogenesis model to compare the effect of TFIIH inhibitors between transformed cells and their progenitors. We report that tumour cells exhibited highly increased sensitivity to TPL or THZ1 and that the combination of both had an additive effect. TPL affects the interaction between XPB and P52, causing a reduction in the levels of XPB, P52, and P8, but not other TFIIH subunits. RNA-Seq and RNAPII-ChIP-Seq experiments showed that although the levels of many transcripts were reduced, the levels of a significant number were increased after TPL treatment, with maintained or increased RNAPII promoter occupancy. A significant number of these genes encode for factors that have been related to tumour growth and metastasis. Some of these genes were also overexpressed in response to THZ1, which depletion enhances the toxicity of TPL and are possible new targets against cancer.


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