Localization and Expression of Hsp27 and αB-Crystallin in Rat Primary Myocardial Cells during Heat Stress In Vitro

Tang, Shu; Rehana, B; Liu, Zhijun; Zhang, Miao; Islam, Asimul; Adam, Abdelnasir; Hartung, J.; Bao, Endong

doi:10.1371/journal.pone.0069066

Cited by 26 publications

(27 citation statements)

References 47 publications

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“…These enzymes are generally designated as cardiomyocyte damage-related enzymes and further regarded as important indicators for judging acute myocardial injury (Amani et al 2013;Chen et al 2013;Chon et al 2013;Wu et al 2013), especially CK-MB (Zeren et al 2013). In addition to these enzymes, cytopathological changes like swollen in size, uneven staining in the cytoplasm and vacuolar degeneration were clearly identified in a lot of researches (Chen et al 2015;Tang et al 2013). According to these myocardial cell damage markers, it is clearly to find that overexpressed HspB1 by ASA was accompanied with relatively slight heat stress injury in myocardial cells, while severe cell damage appeared when ASA was not involved and the HspB1 level In the ASA-HS group and the ASA group, HspB1 concentration almost kept two orders of magnitude higher than the HS group in which the only HspB1 inducer was high temperature…”

Section: Discussionmentioning

confidence: 99%

“…Such injuries will change the permeability of the myocardial cell membrane and cause the release of a series of enzymes such as creatine kinase-MB (CK-MB) and lactate dehydrogenase (LDH) (Saravanan et al 2013). Increases of these myocardial cell damage-related enzymes have been clearly detected after heat stress (Tang et al 2013;Yan et al 2009). Moreover, heat stress exposure leads to obvious pathological changes.…”

Section: Introductionmentioning

confidence: 99%

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In vitro evaluation of aspirin-induced HspB1 against heat stress damage in chicken myocardial cells

Zhang

et al. 2016

Cell Stress and Chaperones

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To understand the potential association of heat stress resistance with HspB1 induction by aspirin (ASA) in chicken myocardial cells, variations of HspB1 expression and heat stressed-induced damage of myocardial cells after ASA administration were studied in primary cultured myocardial cells. Cytopathological lesions as well as damage-related enzymes, such as creatine kinase-MB (CK-MB) and lactate dehydrogenase (LDH), indicated the considerable protective ability of ASA pre-treatment against acute heat stress. Immunostaining assays showed that heat stress caused HspB1 to relocate into the nucleus, while ASA did not. ELISA analysis, revealed that HspB1 expression induced by ASA averaged 45.62-fold higher than that of the control. These results indicated that the acute heat-stressed injuries were accompanied by comparatively lower HspB1 expression caused by heat stress in vitro. ASA pretreatment induced a level of HspB1 presumed to be sufficient to protect myocardial cells from acute heat stress in the extracorporal model, although more detailed mechanisms will require further investigation.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

In vitro evaluation of aspirin-induced HspB1 against heat stress damage in chicken myocardial cells

Zhang

et al. 2016

Cell Stress and Chaperones

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“…The damages caused by heat stress to breeding industries have been explained in our previous works, especially the considerable economic loss on poultry breeding (Wu et al 2015(Wu et al , 2016. Previous research also has revealed that acute HS leads to cardiac dysfunction and other forms of myocardial cell damage (Tang et al 2013), and these effects are responsible for sudden infant death in animals and even in humans after HS exposure (Gathiram et al 1987(Gathiram et al , 1988Rai and Ambwany 1980).…”

Section: Introductionmentioning

confidence: 92%

“…HS exposure increases the permeability of myocardial cells, causing a series of enzymes such as isoenzyme creatine kinase-MB (CK-MB) and lactate dehydrogenase (LDH) to be released from the myocardial cells (Ma et al 2013;Xue et al 2015). These enzymes are categorized as myocardial cell damage-related enzymes and are widely used as markers of myocardial cell injury (Saravanan et al 2013;Tang et al 2013;Wu et al 2015). In addition to these enzymes, histopathological or cytopathological damages are also commonly observed in myocardial cells after HS; for example, the cells may be swollen in size, show uneven matrix staining in the cytoplasm, appear shrunken and dull-stained in the nucleus, or exhibit acute degeneration (Tang et al 2013;Wu et al 2015).…”

Section: Introductionmentioning

confidence: 99%

Aspirin-induced heat stress resistance in chicken myocardial cells can be suppressed by BAPTA-AM in vitro

Zhang

et al. 2016

Cell Stress and Chaperones

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Our recent studies have displayed the protective functions of aspirin against heat stress (HS) in chicken myocardial cells, and it may be associated with heat shock proteins (HSPs). In this study, we further investigated the potential role of HSPs in the aspirin-induced heat stress resistance. Four of the most important HSPs including HspB1 (Hsp27), Hsp60, Hsp70, and Hsp90 were induced by aspirin pretreatment and were suppressed by BAPTA-AM. When HSPs were induced by aspirin, much slighter HS injury was detected. But more serious damages were observed when HSPs were suppressed by BAPTA-AM than those cells exposed to HS without BAPTA-AM, even the myocardial cells have been treated with aspirin in prior. Comparing to other HSPs, HspB1 presented the largest increase after aspirin treatments, 86-fold higher than the baseline (the level before HS). These findings suggested that multiple HSPs participated in aspirin's anti-heat stress function but HspB1 may contribute the most. Interestingly, during the experiments, we also found that apoptosis rate as well as the oxidative stress indicators (T-SOD and MDA) was not consistently responding to heat stress injury as expected. By selecting from a series of candidates, myocardial cell damage-related enzymes (CK-MB and LDH), cytopathological tests, and necrosis rate (measured by flow cytometry assays) are believed to be reliable indicators to evaluate heat stress injury in chicken's myocardial cells and they will be used in our further investigations.

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“…The chief impact of HSF1 activation is the elevated production of HSPs whose major representative is HSP70. Small heat shock proteins induced by fever, such as HSP27, also contribute to cytoprotection [82,83].…”

Section: Anti-inflammatory Role Of Intracellular Hsp70mentioning

confidence: 99%

Physiological regulation of the heat shock response by glutamine: implications for chronic low-grade inflammatory diseases in age-related conditions

Leite

Cruzat

Krause

et al. 2016

Nutrire

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Aging is an intricate process modulated by different molecular and cellular events, such as genome instability, epigenetic and transcriptional changes, molecular damage, cell death and senescence, inflammation, and metabolic dysfunction. Particularly, protein quality control (chaperone systems) tends to be negatively affected by aging, thus leading to cellular senescence in metabolic tissues and, as a consequence, to the increasing dissemination of inflammation throughout the body. The heat shock (HS) response and its associated expression of the 70 kDa family of heat shock proteins (HSP70), which are anti-inflammatory molecular chaperones, are found to be markedly decreased during muscle inactivity and aging, while evidence supports the loss of HSP70 as a key mechanism which may drive muscle atrophy, contractile dysfunction, and reduced regenerative capacity. In addition, abnormal stress response is linked with higher incidence of neurodegenerative diseases as well as low-grade inflammatory diseases that are associated with physical inactivity and obesity. Therefore, strategies to increase or, at least, to maintain the levels of HSP70, and its accompanying HS response to stress, are key to reduce biological cell dysfunctions that occur in aging. In this sense, physical exercise is of note as it is the most powerful inducer of the HS response, comparable only to heat stress and fever-like conditions. On the other hand, the amino acid L-glutamine, whose production within the skeletal muscle and liberation into the blood stream is dependent on muscle activity, is a potentializer of HSP70 expression and HS response, particularly via its entering in hexosamine biosynthetic pathway (HBP). Herein, we discuss the collaborative role of glutamine (and its donors/precursors) and physical exercise (mostly responsible for glutamine release into the circulation) as potential tools to increase HSP70 expression and the HS response in the elderly.

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Localization and Expression of Hsp27 and αB-Crystallin in Rat Primary Myocardial Cells during Heat Stress In Vitro

Cited by 26 publications

References 47 publications

In vitro evaluation of aspirin-induced HspB1 against heat stress damage in chicken myocardial cells

In vitro evaluation of aspirin-induced HspB1 against heat stress damage in chicken myocardial cells

Aspirin-induced heat stress resistance in chicken myocardial cells can be suppressed by BAPTA-AM in vitro

Physiological regulation of the heat shock response by glutamine: implications for chronic low-grade inflammatory diseases in age-related conditions

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