Comparative Analysis of αB-Crystallin Expression in Heat-Stressed Myocardial Cells In Vivo and In Vitro

Tang, Shu; Lv, Yingjun; Chen, Hongbo; Adam, Abdelnasir; Cheng, Yanfen; Hartung, J.; Bao, Endong

doi:10.1371/journal.pone.0086937

Cited by 17 publications

(23 citation statements)

References 57 publications

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“…Our previous research confirmed short term exposure to heat stress (1 h) induced detectable levels of enzymes related to heart damage, such as AST, CK and CKMB, in both the serum of rat blood and supernatant of rat myocardial cells938. Furthermore, pathological lesions, mainly due to necrosis, were observed in the rat myocardium after 40 min of heat stress in vivo , accompanied by lower CryAB expression, indicating CryAB may play an important role to protect the mammalian heart against heat stress21. In the present research, we investigated the expression profile of CryAB in the chicken myocardium using in vivo and in vitro models of heat stress lasting up to 24 h. Furthermore, we assessed the ability of ASA to protect the myocardium during heat stress, as it has been identified that the drug may protect the heart from heat stress by inducing Hsp90 and HspB1 expression39.…”

Section: Discussionsupporting

confidence: 65%

“…Interestingly, these experiments clearly indicated that overexpression of Hsp90 protected against a number of stimuli1920. Our other studies21 indicated overexpression of Hsp70 exerted a protective effect against heat stress2223. Therefore, these studies indicate the individual Hsps exert specific protective effects and their functions should be assessed separately.…”

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confidence: 70%

“…It is now believed that the pleotropic functions of CryAB are the result of its diverse interactions with a wide variety of different proteins31. In our previous research, we investigated CryAB expression and localization, and demonstrated it plays a protective role against heat stress in rat myocardial cells in vivo and in vitro 21. However, the function of CryAB remains poorly explored compared to other members of the sHsp family.…”

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confidence: 99%

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Aspirin upregulates αB-Crystallin to protect the myocardium against heat stress in broiler chickens

Tang

Yin

Song

et al. 2016

Sci Rep

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We established in vivo and in vitro models to investigate the role of αB-Crystallin (CryAB) and assess the ability of aspirin (ASA) to protect the myocardium during prolonged heat stress. Thirty-day-old chickens were divided into three groups (n = 90): heat stress (HS, 40±1 °C); ASA(−)HS(+), 1 mg/kg ASA orally 2 h before heat stress; and ASA(+)HS(−), pretreated with aspirin, no heat stress (25 °C). Hearts were excised after 0, 1, 2, 3, 5, 7, 10, 15 and 24 h. Heat stress increased body temperature, though the ASA(−)HS(+) group had significantly higher temperatures than the ASA(+)HS(+) group at all time points. Compared to ASA(+)HS(+), the ASA(−)HS(+) group displayed increased sensitivity to heat stress. Pathological analysis revealed the ASA (+)HS(+) myocardium showed less severe changes (narrowed, chaotic fibers; fewer necrotic cells) than the ASA(−)HS(+) group (bleeding and extensive cell death). In vitro, ASA-pretreatment significantly increased primary chicken myocardial cell survival during heat stress. ELISAs indicated ASA induced CryAB in vivo to protect against heat stress-induced myocardial damage, but ASA did not induce CryAB in primary chicken myocardial cells. The mechanisms by which ASA induces the expression of CryAB in vivo and protects the myocardium during heat stress merit further research.

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Section: Discussionsupporting

confidence: 65%

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confidence: 70%

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confidence: 99%

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Aspirin upregulates αB-Crystallin to protect the myocardium against heat stress in broiler chickens

Tang

Yin

Song

et al. 2016

Sci Rep

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“…This therefore indicated that H9c2 cells and myocardial cells were protected from damage, particularly at the beginning of heat stress. These results were comparable with the findings of previous studies (32,33). It has been reported that increased levels of AST and LDH were associated with heart disease (34), the proposed mechanism of this is thought to be due to external stresses that may damage myocardial cell membranes, leading to the release of CK into the supernatant in vitro (35).…”

Section: Discussionsupporting

confidence: 91%

Localization and expression of heat shock protein 70 with rat myocardial cell damage induced by heat stress in vitro and in vivo

Chen

Adam

Cheng

et al. 2014

Molecular Medicine Reports

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The aim of the present study was to investigate the association between heat shock protein (Hsp) 70 expression kinetics and heat stress‑induced damage to rat myocardial cells in vitro and in vivo. The results showed that the activity of heart injury‑associated enzymes, including aspartate aminotransferase and creatine kinase, significantly increased and myocardial cells developed acute histopathological lesions; this therefore suggested that heat stress altered the integrity of myocardial cells in vitro and in vivo. Levels of Hsp70 in vitro decreased following the initiation of heat stress and then steadily increased until heat stress ceased at 100 min; however, in vivo studies demonstrated a gradual increase in Hsp70 levels in the heart cells of rats from the initiation of heat stress, followed by a sharp decline at 100 min. These results indicated that the cells sustained different degrees of injury in vivo compared with those sustained in vitro, this may be due to different regulatory mechanisms in the two environments. Intracytoplasmic Hsp70 signaling was significantly reduced at 60 min in vitro, compared with that of the in vivo study, indicating that Hsp70 consumption may have exceeded its production prior to 60 min of heat stress, and following 60 min the cells produced sufficient Hsp70 protein for their protection against heat stress. Hsp70‑positive signals in the cytoplasm of heart cells in vivo were more prominent in the intact areas compared with those of the degenerated areas and the density of Hsp70‑positive signals was significantly reduced following 60 min of heat stress. In conclusion, comprehensive comparisons of enzymes, cell morphology and Hsp70 levels indicated that decreased levels of Hsp70 were associated with the reduced protective effect on myocardial cells in vitro and in vivo.

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“…In addition to the expression of myocardial cell damage-related enzymes and pathological changes, which have been validated by previous studies in our laboratory (Tang et al 2013(Tang et al , 2014Wu et al 2015), oxidative stress factors like SOD and MDA (Altan et al 2003;Paul et al 2009) along with the rates of apoptosis and necrosis (Green 2011;Masri and Chandrashekhar 2008) have also been suggested to respond to HS. However, in the present study, the oxidative stress indicators and apoptosis rate did not accurately reflect the myocardial cell damage.…”

Section: Discussionsupporting

confidence: 59%

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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Comparative Analysis of αB-Crystallin Expression in Heat-Stressed Myocardial Cells In Vivo and In Vitro

Cited by 17 publications

References 57 publications

Aspirin upregulates αB-Crystallin to protect the myocardium against heat stress in broiler chickens

Aspirin upregulates αB-Crystallin to protect the myocardium against heat stress in broiler chickens

Localization and expression of heat shock protein 70 with rat myocardial cell damage induced by heat stress in vitro and in vivo

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

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