Antibodies to human heat shock protein 60, hypertension and dyslipidemia. A study of joint effects on coronary risk

Kervinen, Helena; Huittinen, Tiina; Vaarala, Outi; Leinonen, Maija; Saikku, Pekka; Manninen, Vesa; Mänttäri, Matti

doi:10.1016/s0021-9150(03)00229-6

Cited by 32 publications

(20 citation statements)

References 30 publications

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“…In addition, HSP60 and HSP10 exhibited a punctiform distribution in the mitochondria of heat-stressed cells. This was consistent with the results of a previous study, in which HSP60 was reported to be predominantly located in the cytoplasm and mitochondria of muscle fibers in humans (35). Furthermore, another study demonstrated that mammalian HSP60 was rapidly transported into the mitochondria following dehydration (36).…”

Section: Discussionsupporting

confidence: 92%

“…The protein expression levels of HSP60 were decreased following 100 min heat stress; however, the serum levels of HSP60 were high and histopathological analysis of the heat-stressed tissue revealed obvious lesions. In a previous study, HSP60 expression in the cytoplasm of myocardial cells was more prominent in intact areas than in degenerated areas (39). Concordantly, in the present study, HSP60 staining was markedly reduced in the cytoplasm of granular degenerated areas in myocardial cells.…”

Section: Discussionsupporting

confidence: 91%

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Expression and location of HSP60 and HSP10 in the heart tissue of heat-stressed rats

Cheng

Sun

Chen

et al. 2016

Experimental and Therapeutic Medicine

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Abstract.The present study aimed to analyze the expression levels and localizations of heat shock protein (HSP) 60 and HSP10 in the heart tissue of rats subjected to heat stress (42˚C) for 0, 20, 80 and 100 min. Histopathological injuries and increased serum activities of serum lactate dehydrogenase and creatine kinase isoenzyme MB were detected in the heated rat myocardial cells. These results suggested that heat stress-induced acute degeneration may be sufficient to cause sudden death in animals by disrupting the function and permeability of the myocardial cell membrane. In addition, the expression levels of HSP60 were significantly increased following 20 min heat stress, whereas the expression levels of its cofactor HSP10 were not. Furthermore, the location of HSP60, but not of HSP10, was significantly altered during periods of heat stress. These results suggested that HSP60 in myocardial tissue may be more susceptive to the effects of heat stress as compared with HSP10, and that HSP10 is constitutively expressed in the heart of rats. The expression levels and localizations of HSP60 and HSP10 at the different time points of heat stress were not similar, which suggested that HSP60 and HSP10 may not form a complex in the heart tissue of heat-stressed rats.

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Section: Discussionsupporting

confidence: 92%

Section: Discussionsupporting

confidence: 91%

Expression and location of HSP60 and HSP10 in the heart tissue of heat-stressed rats

Cheng

Sun

Chen

et al. 2016

Experimental and Therapeutic Medicine

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“…As revealed by immunocytochemistry, Hsp60 was primarily expressed in the cytoplasm of myocardial cells, consistent with previous findings of Hsp60 in muscle fibers in humans. Hsp60 expression in the cytoplasm of myocardial cells was more prominent in intact areas than in degenerated areas (Kervinen et al, 2003). In myocardial cells, Hsp60 staining was clearly lower in the cytoplasm of granular degenerated areas (Yu et al, 2008).…”

Section: Discussionmentioning

confidence: 91%

Temporal variations of Hsp60 and HSF-1 in primary rat myocardial cells in vitro under heat stress

Rehana

Lv²,

Islam³

et al. 2013

Genet. Mol. Res.

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ABSTRACT. The mechanisms involved in sudden animal death due to acute heart failure during heat stress are not well understood. We examined the relationship between heat stress-induced variations of protective Hsp60 and expression of its regulatory factor, HSF-1, in heat-stressed primary myocardial cells of neonatal rats in vitro through cardiac enzyme detection, immunoblotting, immunocytochemistry, and qPCR. Increases in cardiac damage-related enzyme levels demonstrated injury to myocardial cells after heat exposure at 42°C. Hsp60 expression levels fluctuated during heat stress; they decreased significantly after 20 min, then increased at 120 min and decreased again at 360 min after initiation of heat stress. The highest levels of Hsp60 were observed at 240 min, while the lowest were at 60 min. Damage to myocardial cells was characterized by increases in cardiac enzyme levels and low levels of Hsp60 due to functional disorder of myocardial cells at early stages of heat stress. However, the significant induction of hsp60 mRNA levels from the beginning up to 240 min of heat stress was not consistent with the classic regulatory mechanisms that link transcription and translation, suggesting that Hsp60 expression is delayed due to loss of Hsp60 during the early stages of heat stress. hsf-1 mRNA levels were significantly increased from 10 min of heat stress; however, HSF-1 protein levels did not simultaneously increase, indicating that HSF-1 is not the sole regulator of Hsp60 expression.

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“…[14][15][16][17] It has been reported that anti-Hsp-70 titres are not elevated in subjects with severe coronary atherosclerosis, whereas titres to Hsp-60 and -65 were significantly raised in these patients. 15,17 It has also been reported that patients with type 2 diabetes mellitus have significantly higher anti-Hsp titres compared with non-diabetic controls.…”

Section: Discussionmentioning

confidence: 96%

Association between indices of body mass and antibody titres to heat-shock protein-60, -65 and -70 in healthy Caucasians

et al. 2006

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We have previously shown that antibody titres to several heat-shock proteins (Hsps) are elevated in dyslipidaemic patients and subjects with established vascular disease. Obesity is known to be associated with raised serum inflammatory markers suggesting a state of heightened immune activation. Hence, we have investigated the association between indices of obesity and several Hsp antibody titres in healthy subjects. Subjects (n ¼ 170) were recruited from among employees at the University of Surrey and the Royal Surrey County Hospital, Guildford, UK. Of these subjects, 35 were obese with a body mass index (BMI)X30 kg/m 2 (19 male and 16 female subjects), 58 were overweight with 304BMIX25 kg/m 2 (36 male and 22 female subjects) and 77 were of a normal weight with BMIo25 kg/m 2 (31 male and 46 female subjects). Overall, obese subjects had significantly higher plasma anti-Hsp-60 (Po0.001), anti-Hsp-65 (Po0.05) and anti-Hsp-70 (Po0.05) compared with overweight and normal weight subjects.

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Antibodies to human heat shock protein 60, hypertension and dyslipidemia. A study of joint effects on coronary risk

Cited by 32 publications

References 30 publications

Expression and location of HSP60 and HSP10 in the heart tissue of heat-stressed rats

Expression and location of HSP60 and HSP10 in the heart tissue of heat-stressed rats

Temporal variations of Hsp60 and HSF-1 in primary rat myocardial cells in vitro under heat stress

Association between indices of body mass and antibody titres to heat-shock protein-60, -65 and -70 in healthy Caucasians

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