Role of HSF1 knock-out in protection of heat shock response against endotoxemia

Guang Wen Chen, Kang Kai Wang, Ying Liu, Dao Lin Tang, Xian Zhong Xiao

Research output: Contribution to journalArticle

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Abstract

Using LPS mediated-endotoxemia BalB/C mice, the role of heat shock factor 1 (HSF1) in heat shock response (HSR) was observed. HSR was performed with 42 °C for 15 min, and recovery for 24 h at room temperature. Endotoxemia model in mouse was achieved by intra-peritoneal injection of LPS at 14 or 15 mg/kg. Lung injury and expression of inflammatory mediators were evaluated with myeloperoxidase (MPO) and maleic dialdehyde (MDA) in heart and lung, RT-PCR, hemotoxylin-eosin (HE) staining and mortality. The data showed that the survival rate was higher in HSR+LPS (HSF1+/+) group (7/15) than that in LPS (HSF1+/+) group (0/15), LPS (HSF1-/-) group (0/14) or HSR+LPS (HSF1-/-) group (0/14) within 72 h after injection of LPS at 15 mg/kg. Similarly, the survival rate was also higher in LPS (HSF1+/+) group (5/15) than that in LPS (HSF1-/-) group (0/13) or HSR+LPS (HSF1-/-) group (0/13) within 72 h after injection of LPS at 14 mg/kg. HSR significantly suppressed production of MPO and MDA induced by LPS in lung and heart in HSF1+/+ mice, but had no such effects in HSF1-/-mice after 12 h treatment with 14 mg/kg LPS. The inflammatory mediators, including SOCS3, MCSF, GCSF, IL-1β, IL-6, CCL-2 and IL-15 were up-regulated both in HSF1+/+ and HSF1-/-mice after 12 h treatment with LPS at 14 mg/kg, and HSR repressed LPS-induced up-regulation of SOCS3, MCSF, GCSF, IL-15, IL-6 and of CCL-2 in HSF1+/+ mice, but not in HSF1-/-mice. HE staining indicated that LPS at 14 mg/kg could mediate significant morphological changes, including necrosis, intravascular coagulation and leukocytes aggregation, and adherence in lung, liver and kidney in HSF1+/+and HSF1-/-mice. The morphological changes in these organs were attenuated with HSR in HSF1+/+mice, but exacerbated in HSF1-/-mice. Those results suggested that HSF1 knock out could significantly block the protection of HSR against LPS mediated-endotoxemia in Ba1B/C mice.

Original languageEnglish (US)
Pages (from-to)424-430
Number of pages7
JournalProgress in Biochemistry and Biophysics
Volume35
Issue number4
StatePublished - Apr 1 2008
Externally publishedYes

Fingerprint

Heat-Shock Response
Endotoxemia
Shock
Hot Temperature
Interleukin-15
Hematoxylin
Eosine Yellowish-(YS)
Lung
Peroxidase
Injections
Interleukin-6
Survival Rate
Staining and Labeling
Mouse Hsf1 protein
Lung Injury
Interleukin-1
Leukocytes
Necrosis
Up-Regulation
Kidney

Keywords

  • Endotoxemia
  • Gene knock out
  • Heat shock factor 1 (HSF1)
  • Heat shock response (HSR)
  • Inflammatory mediators

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry

Cite this

Role of HSF1 knock-out in protection of heat shock response against endotoxemia. / Chen, Guang Wen; Wang, Kang Kai; Liu, Ying; Tang, Dao Lin; Xiao, Xian Zhong.

In: Progress in Biochemistry and Biophysics, Vol. 35, No. 4, 01.04.2008, p. 424-430.

Research output: Contribution to journalArticle

Chen, Guang Wen ; Wang, Kang Kai ; Liu, Ying ; Tang, Dao Lin ; Xiao, Xian Zhong. / Role of HSF1 knock-out in protection of heat shock response against endotoxemia. In: Progress in Biochemistry and Biophysics. 2008 ; Vol. 35, No. 4. pp. 424-430.
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abstract = "Using LPS mediated-endotoxemia BalB/C mice, the role of heat shock factor 1 (HSF1) in heat shock response (HSR) was observed. HSR was performed with 42 °C for 15 min, and recovery for 24 h at room temperature. Endotoxemia model in mouse was achieved by intra-peritoneal injection of LPS at 14 or 15 mg/kg. Lung injury and expression of inflammatory mediators were evaluated with myeloperoxidase (MPO) and maleic dialdehyde (MDA) in heart and lung, RT-PCR, hemotoxylin-eosin (HE) staining and mortality. The data showed that the survival rate was higher in HSR+LPS (HSF1+/+) group (7/15) than that in LPS (HSF1+/+) group (0/15), LPS (HSF1-/-) group (0/14) or HSR+LPS (HSF1-/-) group (0/14) within 72 h after injection of LPS at 15 mg/kg. Similarly, the survival rate was also higher in LPS (HSF1+/+) group (5/15) than that in LPS (HSF1-/-) group (0/13) or HSR+LPS (HSF1-/-) group (0/13) within 72 h after injection of LPS at 14 mg/kg. HSR significantly suppressed production of MPO and MDA induced by LPS in lung and heart in HSF1+/+ mice, but had no such effects in HSF1-/-mice after 12 h treatment with 14 mg/kg LPS. The inflammatory mediators, including SOCS3, MCSF, GCSF, IL-1β, IL-6, CCL-2 and IL-15 were up-regulated both in HSF1+/+ and HSF1-/-mice after 12 h treatment with LPS at 14 mg/kg, and HSR repressed LPS-induced up-regulation of SOCS3, MCSF, GCSF, IL-15, IL-6 and of CCL-2 in HSF1+/+ mice, but not in HSF1-/-mice. HE staining indicated that LPS at 14 mg/kg could mediate significant morphological changes, including necrosis, intravascular coagulation and leukocytes aggregation, and adherence in lung, liver and kidney in HSF1+/+and HSF1-/-mice. The morphological changes in these organs were attenuated with HSR in HSF1+/+mice, but exacerbated in HSF1-/-mice. Those results suggested that HSF1 knock out could significantly block the protection of HSR against LPS mediated-endotoxemia in Ba1B/C mice.",
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N2 - Using LPS mediated-endotoxemia BalB/C mice, the role of heat shock factor 1 (HSF1) in heat shock response (HSR) was observed. HSR was performed with 42 °C for 15 min, and recovery for 24 h at room temperature. Endotoxemia model in mouse was achieved by intra-peritoneal injection of LPS at 14 or 15 mg/kg. Lung injury and expression of inflammatory mediators were evaluated with myeloperoxidase (MPO) and maleic dialdehyde (MDA) in heart and lung, RT-PCR, hemotoxylin-eosin (HE) staining and mortality. The data showed that the survival rate was higher in HSR+LPS (HSF1+/+) group (7/15) than that in LPS (HSF1+/+) group (0/15), LPS (HSF1-/-) group (0/14) or HSR+LPS (HSF1-/-) group (0/14) within 72 h after injection of LPS at 15 mg/kg. Similarly, the survival rate was also higher in LPS (HSF1+/+) group (5/15) than that in LPS (HSF1-/-) group (0/13) or HSR+LPS (HSF1-/-) group (0/13) within 72 h after injection of LPS at 14 mg/kg. HSR significantly suppressed production of MPO and MDA induced by LPS in lung and heart in HSF1+/+ mice, but had no such effects in HSF1-/-mice after 12 h treatment with 14 mg/kg LPS. The inflammatory mediators, including SOCS3, MCSF, GCSF, IL-1β, IL-6, CCL-2 and IL-15 were up-regulated both in HSF1+/+ and HSF1-/-mice after 12 h treatment with LPS at 14 mg/kg, and HSR repressed LPS-induced up-regulation of SOCS3, MCSF, GCSF, IL-15, IL-6 and of CCL-2 in HSF1+/+ mice, but not in HSF1-/-mice. HE staining indicated that LPS at 14 mg/kg could mediate significant morphological changes, including necrosis, intravascular coagulation and leukocytes aggregation, and adherence in lung, liver and kidney in HSF1+/+and HSF1-/-mice. The morphological changes in these organs were attenuated with HSR in HSF1+/+mice, but exacerbated in HSF1-/-mice. Those results suggested that HSF1 knock out could significantly block the protection of HSR against LPS mediated-endotoxemia in Ba1B/C mice.

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