Detection and analysis of apoptosis- and autophagy-related miRNAs of mouse vascular endothelial cells in chronic intermittent hypoxia model

Liu, Kaixiong; Chen, Gongping; Lin, Pingli; Huang, Jian-Chai; Lin, Xi Zhang; Qi, Jia-Chao; Lin, Qi‐Chang

doi:10.1016/j.lfs.2017.11.001

Cited by 43 publications

(31 citation statements)

References 19 publications

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“…Chronic intermittent hypoxia (CIH) is a novel pathophysiological hallmark of OSA [1]. A study by Liu and colleagues [10] concluded that CIH induces differential expression of miRNAs which was associated with apoptosis or autophagy-related gene expression. Previous studies also showed that CIH enhances both hippocampal and myocardial apoptosis in rat mimicking OSA, and telmisartan administration can relieve the apoptosis levels [11, 12].…”

Section: Introductionmentioning

confidence: 99%

Telmisartan attenuates kidney apoptosis and autophagy-related protein expression levels in an intermittent hypoxia mouse model

et al. 2018

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Section: Introductionmentioning

confidence: 99%

Telmisartan attenuates kidney apoptosis and autophagy-related protein expression levels in an intermittent hypoxia mouse model

et al. 2018

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“…One recent study in mice has implied that miRNA profiles can potentially be affected by IH. (21) We hypothesized that IH might additionally lead to differential miR-365 expression, which in turn contributes to the observed phenotype of increased IL-6 mRNA levels within our cell-based experiments.…”

Section: Mirna-365a Inhibition Promotes Il-6 Expression But Does Not mentioning

confidence: 97%

Intermittent hypoxia is a proinflammatory stimulus resulting in IL‐6 expression and M1 macrophage polarization

Schaefer

Mark

et al. 2017

Hepatology Communications

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The biological factors that promote inflammation or nonalcoholic steatohepatitis (NASH) in the setting of nonalcoholic fatty liver disease remain incompletely understood. Clinical studies have demonstrated an association between obstructive sleep apnea (OSA) and both inflammation and fibrosis in NASH, but the mechanism has not been identified. In this study, we use in vitro modeling to examine the impact of intermittent hypoxia on the liver. Hepatocyte, stellate cell, and macrophage cell lines were exposed to intermittent or sustained hypoxia. Candidate genes associated with inflammation, fibrosis, and lipogenesis were analyzed. Circulating cytokines were assessed in human serum of patients with nonalcoholic fatty liver disease. Intermittent hypoxia results in significant induction of interleukin (IL)‐6 expression in both hepatocytes and macrophages. The increase in IL‐6 expression was independent of hypoxia inducible factor 1 induction but appeared to be in part related to antioxidant response element and nuclear factor kappa B activation. Mature microRNA 365 (miR‐365) has been demonstrated to regulate IL‐6 expression, and we found that miR‐365 expression was decreased in the setting of intermittent hypoxia. Furthermore, macrophage cell lines showed polarization to an M1 but not M2 phenotype. Finally, we found a trend toward higher circulating levels of IL‐6 in patients with OSA and NASH. Conclusion: Intermittent hypoxia acts as a potent proinflammatory stimulus, resulting in IL‐6 induction and M1 macrophage polarization. Increased IL‐6 expression may be due to both induction of antioxidant response element and nuclear factor kappa B as well as inhibition of miR‐365 expression. Higher levels of IL‐6 were observed in human samples of patients with OSA and NASH. These findings provide biological insight into mechanisms by which obstructive sleep apnea potentiates inflammation and fibrosis in patients with fatty liver disease. (Hepatology Communications 2017;1:326–337)

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“…Despite this, many recent publications pertaining to in vitro hypoxia still implement the simplified model, which does not consider the difference between headspace and pericellular O 2 tensions. Such studies encompass various areas of hypoxic research, ranging from IH (131)(132)(133) to the tumor microenvironment (134,135) to reperfusion injury modeling. In regards to the latter, placing cells into anoxic conditions generally reflects the ischemic insult occurring in vivo (132,136).…”

Section: Downsides Of Conventional Systemsmentioning

confidence: 99%

Technical Feasibility and Physiological Relevance of Hypoxic Cell Culture Models

Pavlacky

Polàk

2020

Front. Endocrinol.

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Hypoxia is characterized as insufficient oxygen delivery to tissues and cells in the body and is prevalent in many human physiology processes and diseases. Thus, it is an attractive state to experimentally study to understand its inner mechanisms as well as to develop and test therapies against pathological conditions related to hypoxia. Animal models in vivo fail to recapitulate some of the key hallmarks of human physiology, which leads to human cell cultures; however, they are prone to bias, namely when pericellular oxygen concentration (partial pressure) does not respect oxygen dynamics in vivo. A search of the current literature on the topic revealed this was the case for many original studies pertaining to experimental models of hypoxia in vitro. Therefore, in this review, we present evidence mandating for the close control of oxygen levels in cell culture models of hypoxia. First, we discuss the basic physical laws required for understanding the oxygen dynamics in vitro, most notably the limited diffusion through a liquid medium that hampers the oxygenation of cells in conventional cultures. We then summarize up-to-date knowledge of techniques that help standardize the culture environment in a replicable fashion by increasing oxygen delivery to the cells and measuring pericellular levels. We also discuss how these tools may be applied to model both constant and intermittent hypoxia in a physiologically relevant manner, considering known values of partial pressure of tissue normoxia and hypoxia in vivo, compared to conventional cultures incubated at rigid oxygen pressure. Attention is given to the potential influence of three-dimensional tissue cultures and hypercapnia management on these models. Finally, we discuss the implications of these concepts for cell cultures, which try to emulate tissue normoxia, and conclude that the maintenance of precise oxygen levels is important in any cell culture setting.

show abstract

Detection and analysis of apoptosis- and autophagy-related miRNAs of mouse vascular endothelial cells in chronic intermittent hypoxia model

Cited by 43 publications

References 19 publications

Telmisartan attenuates kidney apoptosis and autophagy-related protein expression levels in an intermittent hypoxia mouse model

Telmisartan attenuates kidney apoptosis and autophagy-related protein expression levels in an intermittent hypoxia mouse model

Intermittent hypoxia is a proinflammatory stimulus resulting in IL‐6 expression and M1 macrophage polarization

Technical Feasibility and Physiological Relevance of Hypoxic Cell Culture Models

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