2011
DOI: 10.1016/j.rvsc.2010.06.028
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Variation in the expression of Hsp27, αB-crystallin mRNA and protein in heart and liver of pigs exposed to different transport times

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Cited by 8 publications
(7 citation statements)
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“…In contrast, the transcription of both hsp27 mRNA and αB-crystallin mRNA showed a dramatic and similar increase from the onset of heat stress (according to the results of qPCR). This suggests that sHsp expression was delayed or overtaxed due to rapid consumption of both sHsps at the onset of heat stress, since they are required for myocardial cell balance in response to stress [6]. It has been reported that overexpression of mutant αB-crystallin (R120G) in the heart can lead to cardiomyocyte death, dilation, and heart failure [50], suggesting that even molecular chaperones like Hsps need to be in a relatively stable state to play a protective role in vivo and in vitro.…”
Section: Discussionmentioning
confidence: 99%
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“…In contrast, the transcription of both hsp27 mRNA and αB-crystallin mRNA showed a dramatic and similar increase from the onset of heat stress (according to the results of qPCR). This suggests that sHsp expression was delayed or overtaxed due to rapid consumption of both sHsps at the onset of heat stress, since they are required for myocardial cell balance in response to stress [6]. It has been reported that overexpression of mutant αB-crystallin (R120G) in the heart can lead to cardiomyocyte death, dilation, and heart failure [50], suggesting that even molecular chaperones like Hsps need to be in a relatively stable state to play a protective role in vivo and in vitro.…”
Section: Discussionmentioning
confidence: 99%
“…However, after the addition of myogenic factor, Hsp27 and αB-crystallin expression increases significantly [29]. This is probably linked to the function of these Hsps in the protection of cells against stress or to a specific function in a particular tissue [6], [24]. Hsp27 and αB-crystallin may modulate interaction between cellular factors by forming small or large oligomers, undergoing phosphorylation, and inducing cell–cell contact [51].…”
Section: Discussionmentioning
confidence: 99%
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“…Biochemical and structural changes occur widely in the heart, liver, kidney and other organs of post-stressed animals [ 4 5 37 ]. Stress can induce specific pathological damage in the myocardium of heat-stressed broilers, as well as in transported pigs, and may even cause death [ 38 39 ]. Acute heart failure may be correlated with these stress phenomena.…”
Section: Introductionmentioning
confidence: 99%
“…Studies of chronic heat stress have demonstrated altered physiologic, metabolic, biochemical, and cellular responses in animal models and poultry (Hu et al, 2007;Lu et al, 2007). Studies have also confirmed that the sudden death of mammals can occur as a result of stress-induced damage to heart tissue and myocardial cells (Yu et al, 2008;Zhang et al, 2011). The mechanisms leading to cellular damage and the death of animals subjected to such stresses remain poorly understood, although several factors and physiologic reactions have been investigated (Kamarck and Jennings, 1991).…”
Section: Introductionmentioning
confidence: 99%