NGFI-B targets mitochondria and induces cardiomyocyte apoptosis in restraint-stressed rats by mediating energy metabolism disorder

Wang, Xinxing; Liu, Xiaohua; Kong, Ruirui; Zhan, Rui; Wang, Xiaoming; Xue, Lixiang; Gong, Jicheng; Duan, Meng; Wang, Liqun; Wu, Lei; Lei, Qian

doi:10.1007/s12192-009-0116-y

Cited by 13 publications

(7 citation statements)

References 43 publications

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“…Mitochondria are vital for maintaining the physiological function of cardiomyocytes [44] – [46] . Many stimuli can cause the mitochondrial MPTP to open [47] , with a subsequent series of cytological effects that includes a loss of mitochondrial transmembrane potentials, uncoupling of the respiratory chain, leakage of mitochondrial Ca 2+ , excess generation of ROS [48] , [49] , release of resident mitochondrial proteins such as the apoptosis initiating factor cytochrome c and release of a second mitochondria-derived activator of caspase [50] . These effects indicate that mitochondrial damage be a key step leading to myocardial death.…”

Section: Discussionmentioning

confidence: 99%

A Neuroendocrine Mechanism of Co-Morbidity of Depression-Like Behavior and Myocardial Injury in Rats

Wang

Liu²,

Wu³

et al. 2014

PLoS ONE

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Depression is generally a recurrent psychiatric disorder. Evidence shows that depression and cardiovascular diseases are common comorbid conditions, but the specific pathological mechanisms remain unclear. The purpose of this study is to determine the effects of depression induced by chronic unpredictable mild stress (CUMS) on myocardial injury and to further elucidate the biological mechanism of depression. Rats were used as a model. The CUMS procedure lasted for a total of 8 weeks. After 4 weeks of CUMS, treated rats exhibited a reduced sucrose preference and changes in scores on an open field test, body weight and content of 5-HT in the brain as compared with the values of these variables in controls. These changes indicated depression-like changes in CUMS rats and demonstrated the feasibility of the depression model. In addition, pathological changes in the myocardium and increased cardiomyocyte apoptosis demonstrated that myocardial injury had occurred after 6 weeks of CUMS and had increased significantly by the end of 8 weeks of CUMS. Plasma serotonin (5-HT), norepinephrine (NE) and epinephrine (E), all depression-related neuroendocrine factors, were measured by HPLC-ECD techniques, and the content of plasma corticosterone (GC) was evaluated by an I125–cortisol radioactivity immunoassay in control and CUMS rats. The results indicated that 5-HT had decreased, whereas NE, E and GC had increased in CUMS rats, and these factors might be associated with depression-induced myocardial injury. The effects of 5-HT, NE and GC on the survival rate of cultured cardiomyocytes were determined using an orthogonal design. The results showed that 5-HT was a more important factor affecting cell survival than GC or NE. The results suggested that normal blood levels of 5-HT had a cytoprotective effect. The neuroendocrine disorders characterized by decreased 5-HT combined with increased GC and NE mediated the occurrence of depression-induced myocardial injury.

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Section: Discussionmentioning

confidence: 99%

A Neuroendocrine Mechanism of Co-Morbidity of Depression-Like Behavior and Myocardial Injury in Rats

Wang

Liu²,

Wu³

et al. 2014

PLoS ONE

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“…We previously demonstrated that the stressful condition used in this dry eye model, an immobilized rat on a swing board in the presence of a continuous desiccated air blower, causes a decrease in tear secretion capacity accompanied an increased volume of secretory vesicles and loss of the intracellular cell structure, which indicates a dysfunction in the secretory system [7] . Exposure to stress is known to exacerbate the energy status of various organs, resulting in the loss of mitochondrial function [36] , [37] , [38] . In the present study, we showed a decrease in ATP levels and mitochondria content in the LG, in addition to lacrimal dysfunction.…”

Section: Discussionmentioning

confidence: 99%

Oral Administration of Royal Jelly Restores Tear Secretion Capacity in Rat Blink-Suppressed Dry Eye Model by Modulating Lacrimal Gland Function

et al. 2014

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Tears are secreted from the lacrimal gland (LG), a dysfunction in which induces dry eye, resulting in ocular discomfort and visual impairment. Honey bee products are used as a nutritional source in daily life and medicine; however, little is known about their effects on dry eye. The aim of the present study was to investigate the effects of honey bee products on tear secretion capacity in dry eye. We selected raw honey, propolis, royal jelly (RJ), pollen, or larva from commercially available honey bee products. Tear secretion capacity was evaluated following the oral administration of each honey bee product in a rat blink-suppressed dry eye model. Changes in tear secretion, LG ATP content, and LG mitochondrial levels were measured. RJ restored the tear secretion capacity and decrease in LG ATP content and mitochondrial levels to the largest extent. Royal jelly can be used as a preventative intervention for dry eye by managing tear secretion capacity in the LG.

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“…Because restraint is considered to be a non-specific stressor, the animal model of restraint stress is often used to study the influence of stress on physiological functions and pathological processes. In a previous study, we observed cardiovascular function disruption and pathological alterations in the electrocardiograms of chronically restraint-stressed rats (Wang et al 2009). Cardiomyocyte damage is considered to be an important cellular basis for stress-induced cardiovascular injury and disease (Liu et al 2004).…”

Section: Discussionmentioning

confidence: 89%

HSP70 inhibits stress-induced cardiomyocyte apoptosis by competitively binding to FAF1

Gao¹,

Liu²,

Huang³

et al. 2015

Cell Stress and Chaperones

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Stress-induced cardiomyocyte apoptosis plays an important role in the pathogenesis of a variety of cardiovascular diseases. Our early studies showed that HSP70 effectively inhibited apoptosis, but the underlying mechanism remained unclear. Fas-associated factor 1 (FAF1) is a member of the Fas death-inducing signaling complex (Fas-DISC) that acts upstream of caspase-8. We investigated the interactions among FAF1, HSP70, and FAS in stressed cardiomyocytes to elucidate the protective mechanism of HSP70. FAS and caspase-3/8 activity was higher in cardiomyocytes undergoing stress-induced apoptosis in restraint-stressed rats compared with cardiomyocytes in non-stressed rats, which indicated that the Fas signaling pathway was activated after restraint stress. Geranylgeranylacetone (GGA) induced an increase in HSP70 expression, which reduced stress-induced apoptosis. Additionally, overexpression of HSP70 via transfection with the pEGFP-rHSP70 plasmid attenuated norepinephrine (NE)-induced apoptosis. FAF1 expression increased during stressinduced apoptosis, and overexpression of FAF1 exacerbated NE-induced apoptosis. We also found that HSP70 interacted with FAF1. Overexpression of HSP70 inhibited the binding of FAF1 to FAS in H9C2 cells, which indicated that HSP70 suppressed NE-induced apoptosis by competitively binding to FAF1. An N-terminal deletion mutant of HSP70 (HSP70-△N) was unable to interact with FAF1. After HSP70-△N was transfected into H9C2 cells, the cells were unable to attenuate the NE-induced increases in caspase-8 and apoptosis. These results indicate that the 1-120 sequence of HSP70 binds to FAF1, which alters the interactions between FAS and FAF1 and inhibits the activation of the Fas signaling pathway and apoptosis.

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NGFI-B targets mitochondria and induces cardiomyocyte apoptosis in restraint-stressed rats by mediating energy metabolism disorder

Cited by 13 publications

References 43 publications

A Neuroendocrine Mechanism of Co-Morbidity of Depression-Like Behavior and Myocardial Injury in Rats

A Neuroendocrine Mechanism of Co-Morbidity of Depression-Like Behavior and Myocardial Injury in Rats

Oral Administration of Royal Jelly Restores Tear Secretion Capacity in Rat Blink-Suppressed Dry Eye Model by Modulating Lacrimal Gland Function

HSP70 inhibits stress-induced cardiomyocyte apoptosis by competitively binding to FAF1

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