Effects of oestrogen on sarcoplasmic reticulum Ca2+-ATPase activity and gene expression in genioglossus in chronic intermittent hypoxia rat

2009 ◽  
Vol 54 (4) ◽  
pp. 322-328 ◽  
Author(s):  
Yue-Hua Liu ◽  
Wen Li ◽  
Wei-Hua Song
Keyword(s):  
Gene Expression ◽  
Sarcoplasmic Reticulum ◽  
Atpase Activity ◽  
Intermittent Hypoxia ◽  
Chronic Intermittent Hypoxia

Invited Review: Oxygen sensing during intermittent hypoxia: cellular and molecular mechanisms

2001 ◽  
Vol 90 (5) ◽  
pp. 1986-1994 ◽  
Author(s):  
Nanduri R. Prabhakar
Keyword(s):  
Gene Expression ◽  
Cell Cultures ◽  
Carotid Body ◽  
Intermittent Hypoxia ◽  
Oxygen Sensing ◽  
Regulation Of Gene Expression ◽  
Chronic Intermittent Hypoxia ◽  
Carotid Body Chemoreceptors ◽  
Sustained Hypoxia

To the majority of the population, recurrent episodes of hypoxia are more likely encountered in life than sustained hypoxia. Until recently, much of the information on the long-term effects of intermittent hypoxia has come from studies on human subjects experiencing chronic recurrent apneas. Recent development of animal models of intermittent hypoxia and techniques for exposing cell cultures to alternating cycles of hypoxia have led to new information on the effects of episodic hypoxia on oxygen-sensing mechanisms in the carotid body chemoreceptors and regulation of gene expression. The purpose of this review is to highlight some recent studies on the effects of intermittent hypoxia on oxygen sensing at the carotid bodies and regulation of gene expression. In a rodent model, chronic intermittent hypoxia selectively enhances hypoxic sensitivity of the carotid body chemoreceptors. More interestingly, chronic intermittent hypoxia also induces a novel form of plasticity in the carotid body, leading to long-term facilitation in the sensory discharge. Studies on cell cultures reveal that intermittent hypoxia is more potent in activating activator protein-1 and hypoxia-inducible factor-1 transcription factors than sustained hypoxia. Moreover, some evidence suggests that intermittent hypoxia utilizes intracellular signaling pathways distinct from sustained hypoxia. Reactive oxygen species generated during the reoxygenation phase of intermittent hypoxia might play a key role in the effects of intermittent hypoxia on carotid body function and gene expression. Global gene profile analysis in cell cultures suggests that certain genes are selectively affected by intermittent hypoxia, some upregulated and some downregulated. It is suggested that, in intact animals, coordinated gene regulation of gene expression might be critical for eliciting phenotypic changes in the cardiorespiratory systems in response to intermittent hypoxia. It is hoped that future studies will unravel new mechanisms that are unique to intermittent hypoxia that may lead to a better understanding of the changes in the cardiorespiratory systems and new therapies for diseases associated with chronic recurrent episodes of hypoxia.

Chronic intermittent hypoxia upregulates genes of lipid biosynthesis in obese mice

2005 ◽  
Vol 99 (5) ◽  
pp. 1643-1648 ◽  
Author(s):  
Jianguo Li ◽  
Dmitry N. Grigoryev ◽  
Shui Qing Ye ◽  
Laura Thorne ◽  
Alan R. Schwartz ◽  
...  
Keyword(s):  
Gene Expression ◽  
Fatty Acid ◽  
Fatty Liver ◽  
Real Time ◽  
Real Time Pcr ◽  
Intermittent Hypoxia ◽  
Fatty Acid Biosynthesis ◽  
Lipid Biosynthesis ◽  
Chronic Intermittent Hypoxia ◽  
Acid Biosynthesis

Obstructive sleep apnea (OSA), a condition tightly linked to obesity, leads to chronic intermittent hypoxia (CIH) during sleep. There is emerging evidence that OSA is independently associated with insulin resistance and fatty liver disease, suggesting that OSA may affect hepatic lipid metabolism. To test this hypothesis, leptin-deficient obese ( ob/ob) mice were exposed to CIH during the light phase (9 AM–9 PM) for 12 wk. Liver lipid content and gene expression profile in the liver (Affymetrix 430 GeneChip with real-time PCR validation) were determined on completion of the exposure. CIH caused a 30% increase in triglyceride and phospholipid liver content ( P < 0.05), whereas liver cholesterol content was unchanged. Gene expression analysis showed that CIH upregulated multiple genes controlling 1) cholesterol and fatty acid biosynthesis [malic enzyme and acetyl coenzyme A (CoA) synthetase], 2) predominantly fatty acid biosynthesis (acetyl-CoA carboxylase and stearoyl-CoA desaturases 1 and 2), and 3) triglyceride and phospholipid biosynthesis (mitochondrial glycerol-3-phosphate acyltransferase). A majority of overexpressed genes were transcriptionally regulated by sterol regulatory element-binding protein (SREBP) 1, a master regulator of lipogenesis. A 2.8-fold increase in SREBP-1 gene expression in CIH was confirmed by real-time PCR ( P = 0.001). Expression of major genes of cholesterol biosynthesis, SREBP-2 and 3-hydroxy-3-methylglutaryl-CoA reductase, was unchanged. In conclusion, we have shown that CIH may exacerbate preexisting fatty liver of obesity via upregulation of the pathways of lipid biosynthesis in the liver.

scholarly journals Analysis of the stability of housekeeping gene expression in the left cardiac ventricle of rats submitted to chronic intermittent hypoxia

2016 ◽  
Vol 42 (3) ◽  
pp. 211-214 ◽  
Author(s):  
Guilherme Silva Julian ◽  
Renato Watanabe de Oliveira ◽  
Sergio Tufik ◽  
Jair Ribeiro Chagas
Keyword(s):  
Gene Expression ◽  
Intermittent Hypoxia ◽  
Disease Risk ◽  
Cardiovascular Disease Risk ◽  
Housekeeping Gene ◽  
Experimental Models ◽  
Chronic Intermittent Hypoxia ◽  
Obstructive Sleep ◽  
Cardiac Ventricle ◽  
The Stability

ABSTRACT Obstructive sleep apnea (OSA) has been associated with oxidative stress and various cardiovascular consequences, such as increased cardiovascular disease risk. Quantitative real-time PCR is frequently employed to assess changes in gene expression in experimental models. In this study, we analyzed the effects of chronic intermittent hypoxia (an experimental model of OSA) on housekeeping gene expression in the left cardiac ventricle of rats. Analyses via four different approaches-use of the geNorm, BestKeeper, and NormFinder algorithms; and 2−ΔCt (threshold cycle) data analysis-produced similar results: all genes were found to be suitable for use, glyceraldehyde-3-phosphate dehydrogenase and 18S being classified as the most and the least stable, respectively. The use of more than one housekeeping gene is strongly advised.

scholarly journals The effect of chronic intermittent hypoxia in cardiovascular gene expression is modulated by age in a mice model of sleep apnea

SLEEP ◽  
2021 ◽  
Author(s):  
Anabel L Castro-Grattoni ◽  
Monique Suarez-Giron ◽  
Ivan Benitez ◽  
Lourdes Tecchia ◽  
Marta Torres ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Intermittent Hypoxia ◽  
Molecular Mechanisms ◽  
Fold Increase ◽  
Fold Change ◽  
Chronic Intermittent Hypoxia ◽  
Aortic Tissue ◽  
Old Mice ◽  
Young Mice

Abstract Study objectives Chronic intermittent hypoxia (CIH) is a major determinant in OSA cardiovascular morbidity and this effect is influenced by age. The objective of the present study was to assess the differential molecular mechanisms at gene level expression involved in the cardiovascular remodeling induced by CIH according to chronological age. Methods Two-month and 18-month old mice (N=8 each) were subjected to CIH or normoxia for 8-weeks. Total mRNA was extracted from left ventricle myocardium and aortic arch, and gene expression of 46 intermediaries of aging, oxidative stress and inflammation was measured by quantitative real time PCR. Results Cardiac gene expression of Nrf2 (2.05-fold increase, p&lt;0.001), Sod2 (1.9-fold increase, p=0.035), Igf1r (1.4-fold increase, p=0.028), Mtor (1.8-fold increase, p=0.06), Foxo3 (1.5-fold increase, p=0.020), Sirt4, Sirt6, and Sirt7 (1.3-fold increase, p=0.012; 1.1-fold change, p=0.031; 1.3-fold change, p=0.029) was increased after CIH in young mice, but not in old mice. In aortic tissue, eNOS was reduced in young mice (p&lt;0.001), Nrf2 was reduced in 80% (p&lt;0.001) in young mice and in 45% (p=0.07) in old mice, as its downstream antioxidant target Sod2 (82% reduced, p&lt;0.001). IL33 Conclusions CIH effect in gene expression is organ-dependent, and is modulated by age. CIH increased transcriptional expression of genes involved in cardioprotection and cell survival in young, but not in old mice. In aortic tissue, CIH reduced gene expression related to an antioxidant response in both young and old mice, suggesting vascular oxidative stress and a pro-aging process.

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