Protective effect of transgenic expression of porcine heat shock protein 70 on hypothalamic ischemic and oxidative damage in a mouse model of heatstroke

Chen, Zhih Cherng; Wu, Wen Shian; Lin, Mao Tsun; Hsu, Chuan Chih

doi:10.1186/1471-2202-10-111

Cited by 43 publications

(34 citation statements)

References 37 publications

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“…Recent research has demonstrated that Hsp27 and Hsp70 have protective effects in cerebral I/R injury (29,30). In the present study, we also observed that Hsp27 and Hsp70 levels were significantly increased in the poly(I:C) group.…”

Section: Discussionsupporting

confidence: 77%

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Polyinosinic-Polycytidylic Acid Has Therapeutic Effects against Cerebral Ischemia/Reperfusion Injury through the Downregulation of TLR4 Signaling via TLR3

Wang

Huang

Chen

et al. 2014

The Journal of Immunology

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Recent reports have shown that preconditioning with the TLR3 ligand polyinosinic-polycytidylic acid (poly(I:C)) protects against cerebral ischemia/reperfusion (I/R) injury. However, it is unclear whether poly(I:C) treatment after cerebral I/R injury is also effective. We used mouse/rat middle cerebral artery occlusion and cell oxygen-glucose deprivation models to evaluate the therapeutic effects and mechanisms of poly(I:C) treatment. Poly(I:C) was i.p. injected 3 h after ischemia (treatment group). Cerebral infarct volumes and brain edemas were significantly reduced, and neurologic scores were significantly increased. TNF-α and IL-1β levels were markedly decreased, whereas IFN-β levels were greatly increased, in the ischemic brain tissues, cerebral spinal fluid, and serum. Injuries to hippocampal neurons and mitochondria were greatly reduced. The numbers of TUNEL-positive and Fluoro-Jade B+ cells also decreased significantly in the ischemic brain tissues. Poly(I:C) treatment increased the levels of Hsp27, Hsp70, and Bcl2 and decreased the level of Bax in the ischemic brain tissues. Moreover, poly(I:C) treatment attenuated the levels of TNF-α and IL-1β in serum and cerebral spinal fluid of mice stimulated by LPS. However, the protective effects of poly(I:C) against cerebral ischemia were abolished in TLR3−/− and TLR4−/−mice. Poly(I:C) downregulated TLR4 signaling via TLR3. Poly(I:C) treatment exhibited obvious protective effects 14 d after ischemia and was also effective in the rat permanent middle cerebral artery occlusion model. The results suggest that poly(I:C) exerts therapeutic effects against cerebral I/R injury through the downregulation of TLR4 signaling via TLR3. Poly(I:C) is a promising new drug candidate for the treatment of cerebral infarcts.

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Section: Discussionsupporting

confidence: 77%

“…1B). Recent studies have shown that Hsp27 and Hsp70 have protective effects against cerebral I/R injury (29,30). Our results also showed that poly(I:C) significantly increased the levels of Hsp27 ( Fig.…”

Section: Flow Cytometrysupporting

confidence: 77%

Polyinosinic-Polycytidylic Acid Has Therapeutic Effects against Cerebral Ischemia/Reperfusion Injury through the Downregulation of TLR4 Signaling via TLR3

Wang

Huang

Chen

et al. 2014

The Journal of Immunology

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“…Hyperthermia is a limiting factor in physical performance [21]; therefore, upregulation of genes encoding HSPs and interleukins could be essential for gaining thermotolerance [22]. There are not many reports in the literature on changes in gene expression upon one-off Finnish sauna bath that would include people who train regularly and those who do not exhibit regular physical activity.…”

Section: Discussionmentioning

confidence: 99%

Effects of sauna bathing on stress-related genes expression in athletes and non-athletes

Żychowska

Półrola

Chruściński

et al. 2017

Ann Agric Environ Med.

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Introduction and objective. Heat stress induces the expression of genes encoding heat-shock proteins and immune response mediators. The aim of this study was to determine the differences in the expression of genes encoding heat-shock proteins 70 kDa and27 kDa, interleukin 6, interleukin 10and C-reactive protein, between athletes and non-athletes after sauna bathing. Materials and method. Athletes (n=9) and non-athletes (n=9) were exposed to a Finnish sauna twice during one session at a temperature of 98.2 °C and humidity of 10% ± 2%, with a 5 min break for cooling down under a shower. The groups did not differ in terms of age, height or body mass. Blood samples were taken before and after sauna exposure in order to assess gene expression, using reverse transcription polymerase chain reaction. Results. Differences were observed in leukocyte mRNA levels of tested genes between athletes and non-athletes. In the non-athlete group, all the tested genes were expressed at higher levels as a response to the same heat challenge. Conclusion. It appears that expression of stress-related genes induced by heat stress is dependent on the level of physical activity.

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“…For example, the new mass spectroscopic technique MALDI MS revealed the changes of phospholipids, such as lysophosphatidylcholine, phosphatidylcholine, phosphatidylethanolamine, and sphingomyelin, in rat brains after focal cerebral ischemia (26). Studies have revealed that inducible Hsp70.1 has protective effects against ischemia and oxidative injury (27,28); however, whether its protection correlates with membrane lipids remains to be elucidated. A recent study has demonstrated that Hsp70 selectively interacts with the negatively charged phospholipids, such as cardiolipin (CL), phosphatidylserine (PS), and BMP.…”

Section: Journal Of Biological Chemistry 27439mentioning

confidence: 99%

Heat Shock Protein 70.1 (Hsp70.1) Affects Neuronal Cell Fate by Regulating Lysosomal Acid Sphingomyelinase

Zhu

Yoshimoto

Yamashima

2014

Journal of Biological Chemistry

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Background:The role of Hsp70.1 in neurodegeneration remains unknown. Results: We demonstrate differential profiles in activation of -calpain, bis(monoacylglycero)phosphate (BMP) levels, Hsp70.1-BMP interaction, and acid sphingomyelinase (ASM) activity between motor cortex and CA1 after ischemia/reperfusion. Conclusion: Hsp70.1-mediated ASM activity affects neuronal cell fate by regulating lysosomal membrane stability. Significance: This finding provides new insights into the mechanism of neuronal death.

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Protective effect of transgenic expression of porcine heat shock protein 70 on hypothalamic ischemic and oxidative damage in a mouse model of heatstroke

Cited by 43 publications

References 37 publications

Polyinosinic-Polycytidylic Acid Has Therapeutic Effects against Cerebral Ischemia/Reperfusion Injury through the Downregulation of TLR4 Signaling via TLR3

Polyinosinic-Polycytidylic Acid Has Therapeutic Effects against Cerebral Ischemia/Reperfusion Injury through the Downregulation of TLR4 Signaling via TLR3

Effects of sauna bathing on stress-related genes expression in athletes and non-athletes

Heat Shock Protein 70.1 (Hsp70.1) Affects Neuronal Cell Fate by Regulating Lysosomal Acid Sphingomyelinase

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