Impact of 60-GHz millimeter waves and corresponding heat effect on endoplasmic reticulum stress sensor gene expression

2014 ◽  
Vol 35 (6) ◽  
pp. 444-451 ◽  
Author(s):  
Catherine Le Quément ◽  
Christophe Nicolas Nicolaz ◽  
Denis Habauzit ◽  
Maxim Zhadobov ◽  
Ronan Sauleau ◽  
...  
Keyword(s):  
Gene Expression ◽  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Millimeter Waves ◽  
Heat Effect ◽  
60 Ghz ◽  
Stress Sensor

scholarly journals Endoplasmic Reticulum Stress Stimulates Heme Oxygenase-1 Gene Expression in Vascular Smooth Muscle

2004 ◽  
Vol 280 (2) ◽  
pp. 872-877 ◽  
Author(s):  
Xiao-ming Liu ◽  
Kelly J. Peyton ◽  
Diana Ensenat ◽  
Hong Wang ◽  
Andrew I. Schafer ◽  
...  
Keyword(s):  
Gene Expression ◽  
Endoplasmic Reticulum ◽  
Smooth Muscle ◽  
Endoplasmic Reticulum Stress ◽  
Vascular Smooth Muscle ◽  
Heme Oxygenase ◽  
Heme Oxygenase 1

scholarly journals Endoplasmic Reticulum Stress is Involved in DFMO Attenuating Isoproterenol-Induced Cardiac Hypertrophy in Rats

2016 ◽  
Vol 38 (4) ◽  
pp. 1553-1562 ◽  
Author(s):  
Yan Lin ◽  
Xiaojie Zhang ◽  
Wei Xiao ◽  
Bo Li ◽  
Jun Wang ◽  
...  
Keyword(s):  
Gene Expression ◽  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Cardiac Hypertrophy ◽  
Western Blot ◽  
Blot Analysis ◽  
Western Blot Analysis ◽  
Cardiac Fibrosis ◽  
Regulation Of Gene Expression ◽  
Tunel Staining

Background/Aims: Studies performed in experimental animals have shown that polyamines contribute to several physiological and pathological processes, including cardiac hypertrophy. This involves an increase in ornithine decarboxylase (ODC) activity and intracellular polyamines associated with regulation of gene expression. Difluoromethylornithine (DFMO), an irreversible inhibitor of ODC, has attracted considerable interest for its antiproliferative role, which it exerts through inhibition of the polyamine pathway and cell turnover. Whether DFMO attenuates cardiac hypertrophy through endoplasmic reticulum stress (ERS) is unclear. Methods: Myocardial hypertrophy was simulated by isoproterenol (ISO). Polyamine depletion was achieved using DFMO. Hypertrophy was estimated using the heart/body index and atrial natriuretic peptide (ANP) gene expression. Cardiac fibrosis and apoptosis were measured by Masson and TUNEL staining. Expression of ODC and spermidine/spermine N1-acetyltransferase (SSAT) were analyzed via real-time PCR and Western blot analysis. Protein expression of ERS and apoptosis factors were analyzed using Western blot analysis. Results: DFMO treatments significantly attenuated hypertrophy and apoptosis induced by ISO in cardiomyocytes. DFMO down-regulated the expression of ODC, glucose-regulated protein 78 (GRP78), C/EBP homologous protein (CHOP), cleaved caspase-12, and Bax and up-regulated the expression of SSAT and Bcl-2. Finally, these changes were partially reversed by the addition of exogenous putrescine. Conclusion: The data presented here suggest that polyamine depletion could inhibit cardiac hypertrophy and apoptosis, which is closely related to the ERS pathway.

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