Expression of HSP70 in cerebral ischemia and neuroprotetive action of hypothermia and ketoprofen

Tirapelli, Daniela Pretti da Cunha; Carlotti, Carlos Gilberto; Leite, João P.; Colli, Benedicto Oscar

doi:10.1590/s0004-282x2010000400021

Cited by 17 publications

(11 citation statements)

References 28 publications

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“…However, they showed that the number of Hsp70-positive cells in the ischemic areas was reduced by hypothermia. In our model, we observed the suppression of Hsp70 mRNA expression by hypothermia, in contrast to the protein level of Hsp70, as observed by Tirapelli et al (2010). Since we currently do not know the mechanism of induction or the neuroprotective roles of Hsp70 in hypothermia, it is worthy of further investigation.…”

Section: Chaperonessupporting

confidence: 53%

“…Recently, Hagiwara et al (2007) reported that mild hypothermia at 34°C increased the expression level of Hsp70 in LPS-stimulated RAW264.7 cells, although IL-1 , IL-6, and TNF-expression levels were reduced under the same conditions. In contrast, Tirapelli et al (2010) recently reported the increase of Hsp70 protein and gene expression in 1 h MCAO rat brains and the role of neuroprotection with hypothermia. However, they showed that the number of Hsp70-positive cells in the ischemic areas was reduced by hypothermia.…”

Section: Chaperonesmentioning

confidence: 90%

See 1 more Smart Citation

Molecular Mechanisms Underlying the Neuroprotective Effect of Hypothermia in Cerebral Ischemia

Shintani¹,

Terao²

2012

Advances in the Treatment of Ischemic Stroke

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Section: Chaperonessupporting

confidence: 53%

Section: Chaperonesmentioning

confidence: 90%

Molecular Mechanisms Underlying the Neuroprotective Effect of Hypothermia in Cerebral Ischemia

Shintani¹,

Terao²

2012

Advances in the Treatment of Ischemic Stroke

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“…Overexpression of HSP70 serves an important role in cell death and has neuroprotective effects via an anti-inflammatory underlying mechanism, and has been demonstrated to be positively associated with ICAS and ECAS (29,30). However, whether ICAS or ECAS is more closely associated with altered expression levels of HSP70 remains to be elucidated.…”

Section: Discussionmentioning

confidence: 99%

Proteomic analysis and comparison of intra- and extracranial cerebral atherosclerosis responses to hyperlipidemia in rabbits

Huang

et al. 2017

Molecular Medicine Reports

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The present study aimed to investigate protein expression levels of intra- and extracranial atherosclerosis in rabbits following administration of a high-fat diet. Rabbits were randomly divided into control (group A; n=9) and high-fat diet (group B; n=9) groups. At week 12, tissues were sectioned from the common carotid artery (CCA) and middle cerebral artery (MCA). Pathological analysis was performed. Differential protein expression levels were examined by 2-D gel electrophoresis (2-DE) and mass spectrometry (MS) analysis and validated by western blotting. Serum lipid levels, the intima-media thickness (IMT) and degree of atherosclerosis of the CCA and MCA were increased at week 12 in the high-fat diet group compared with rabbits that received a normal diet. 2-DE and MS analysis of the protein extracted from CCA and MCA detected >439 different proteins; the expression of 25 proteins was altered, and 8 proteins [albumin A chain, tropomyosin α-1 chain (TPM1), heat shock protein 70 (HSP70), α-smooth muscle actin, β-galactose binding agglutinin, TPM4 isoform 2, cell keratin 9, single octylic acid glyceride β-2) demonstrated significant alterations in expression levels. Due to limited antibody sources, only three differentially expressed proteins (TPM1, HSP70 and α-smooth muscle actin) were examined by western blotting. The results of our previous study demonstrated that hyperlipidemia affected the IMT of intracranial and extracranial cerebral arteries. In the present study, protein expression levels of TPM1 and α-smooth muscle actin from extracranial cerebral arteries were significantly increased compared with intracranial cerebral arteries; however, protein expression levels of HSP70 from intracranial cerebral arteries was increased compared with extracranial cerebral arteries. The differences may be closely associated with cell proliferation and metastasis, and oxidoreduction, in intra- and extracranial cerebral atherosclerosis. HSP70 may have protective properties against atherosclerosis via underlying anti-inflammatory mechanisms, furthermore, differential protein expression levels (TPM1, HSP70 and α-smooth muscle actin) between intra- and extracranial cerebral arteries may facilitate the identification of novel biological markers for the diagnosis and treatment of cerebral arteriosclerosis.

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“…In the present work, exposure to heat led to increase in the immunoexpression for HSP60. Similarly, increased intracellular HSP70 was observed in cultured astrocytes after heat stress [51] and in rat cerebral cortex due to ischemia after occlusion of the middle cerebral artery [52]. Similarly, Dangi and his colleagues observed increased immunocytochemical HSPs localization both in nucleus and cytoplasm of peripheral blood mononuclear cell with heat stress and suggesting a possible role of HSPs on heat stress amelioration [53].…”

Section: Hsp60 Immunoexpression After Heat Exposurementioning

confidence: 84%

Modulation of heat shock protein immunolocalization in cerebral cortex by melatonin therapy in heat stressed rats

Hashem¹,

Fikry²

2018

J Histol Histopathol

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Heat stress leads clinically to manifestations of central nervous system dysfunction. Heat shock proteins (HSPs) function as molecular chaperones protecting the cells from damage. Melatonin has therapeutic and prophylactic effects on heatstroke-induced multiple organ dysfunction. The present work aimed to investigate the protective effect of melatonin against heat stress-induced histological and HSP60 immunoexpression alterations of cerebral cortex in adult male albino rats. Forty adult male albino rats were used and divided into three groups; I (control) II (3 days heat stressed) and III (3 days heat stressed with melatonin treatment). Cerebral cortex specimens were processed to prepare sections for light microscope examination and blood samples were obtained for oxidative stress and antioxidant analysis. Hematoxylin and eosin stained sections showed degenerative changes in cerebral cortex of rats exposed to heat for 3 days in the form of apoptotic neurons and swelling of astrocytes processes. Neuropil edema, subarachnoid hemorrhage and congested blood vessels were also observed with accompanied increase in serum oxidative stress markers and decrease in antioxidant marker. Melatonin treatment with heat stress showed more preserved nervous tissue with accompanied increase in serum antioxidant marker. HSP60 immunoexpression was weak cytoplasmic in control group which significantly increased and became strong cytoplasmic after 3 days of heat exposure. With melatonin treatment with heat stress nuclear, HSP60 immunoexpression was moderate nuclear in some neurons and strong cyoplasmic in others. In conclusion, melatonin ameliorates heat exposure induced degenerative changes in cerebral cortex of adult male albino rats most probably through antioxidant effect with modulation in HSP60 immunoexpression pattern. Hence, more attention should be thrown to melatonin as a protective treatment to avoid heat stress degenerative effect on cerebral cortex.

show abstract

Expression of HSP70 in cerebral ischemia and neuroprotetive action of hypothermia and ketoprofen

Cited by 17 publications

References 28 publications

Molecular Mechanisms Underlying the Neuroprotective Effect of Hypothermia in Cerebral Ischemia

Molecular Mechanisms Underlying the Neuroprotective Effect of Hypothermia in Cerebral Ischemia

Proteomic analysis and comparison of intra- and extracranial cerebral atherosclerosis responses to hyperlipidemia in rabbits

Modulation of heat shock protein immunolocalization in cerebral cortex by melatonin therapy in heat stressed rats

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