The effect of hyperbaric oxygen preconditioning on heat shock protein 72 expression following in vitro stress in human monocytes

Heat shock protein 72 (Hsp72) exhibits a protective role during times of increased risk of pathogenic challenge and/or tissue damage. The aim of the study was to ascertain Hsp72 protective effect differences between animal and human studies in sepsis using a hypothetical “comparative study” model. Forty-one in vivo (56.1%), in vitro (17.1%), or combined (26.8%) animal and 14 in vivo (2) or in vitro (12) human Hsp72 studies (P<0.0001) were enrolled in the analysis. Of the 14 human studies, 50% showed a protective Hsp72 effect compared to 95.8% protection shown in septic animal studies (P<0.0001). Only human studies reported Hsp72-associated mortality (21.4%) or infection (7.1%) or reported results (14.3%) to be nonprotective (P<0.001). In animal models, any Hsp72 induction method tried increased intracellular Hsp72 (100%), compared to 57.1% of human studies (P<0.02), reduced proinflammatory cytokines (28/29), and enhanced survival (18/18). Animal studies show a clear Hsp72 protective effect in sepsis. Human studies are inconclusive, showing either protection or a possible relation to mortality and infections. This might be due to the fact that using evermore purified target cell populations in animal models, a lot of clinical information regarding the net response that occurs in sepsis is missing.

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Heat Shock Protein 72 Protects Kidney Proximal Tubule Cells From Injury Induced by Triptolide by Means of Activation of the MEK/ERK Pathway

International Journal of Toxicology ◽

10.1177/1091581809337418 ◽

2009 ◽

Vol 28 (3) ◽

pp. 177-189 ◽

Cited By ~ 17

Author(s):

Zhipeng Wang ◽

Haifeng Jin ◽

Chen Li ◽

Ying Hou ◽

Qibing Mei ◽

...

Keyword(s):

Heat Shock ◽

Heat Shock Protein ◽

Proximal Tubule ◽

Kidney Injury ◽

Proximal Tubule Cell ◽

Erk Pathway ◽

Heat Shock Protein 72 ◽

Kidney Proximal Tubule

Triptolide, which has been used to treat inflammatory diseases, has also been reported to inhibit proliferation of cancer cells. However, it can cause severe nephrotoxicity, limiting its clinical use. Here, nephrotoxicity of triptolide was observed in vivo and in vitro. Heat shock protein 72 (HSP72) was upregulated during kidney injury in rats. HSP72 partially protected human kidney proximal tubule cell lines HK-2 and HKC from triptolide-induced injury. Phospho-Raf, phospho-MEK and phospho-ERK were elevated in HK-2 cells that overexpressed HSP72 after either heat shock or triptolide treatment, and downregulated when HSP72 was repressed by siRNA. The participation of the MEK/ERK1/2 pathway was confirmed by exposure of the cells to the MEK inhibitor U0126. Collectively, our results suggested that HSP72 plays a protective role by means of the MEK/ERK pathway, against triptolide-induced kidney injury.

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Hyperbaric oxygen preconditioning attenuated high‐altitude pulmonary edema via heat shock protein 70 overexpression

The FASEB Journal ◽

10.1096/fasebj.29.1_supplement.680.3 ◽

2015 ◽

Vol 29 (S1) ◽

Author(s):

Hung‐Jung Lin ◽

Ching‐Ping Chang ◽

Ming‐Che Tsai

Keyword(s):

Heat Shock ◽

Heat Shock Protein ◽

Pulmonary Edema ◽

High Altitude ◽

Hyperbaric Oxygen ◽

Heat Shock Protein 70 ◽

High Altitude Pulmonary Edema ◽

Hyperbaric Oxygen Preconditioning

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Accumulation of heat shock protein 72 (hsp 72) in postimplantation rat embryos after exposure to various periods of hyperthermia (40°-43°c) in vitro: Evidence that heat shock protein 72 is a biomarker of heat-induced embryotoxicity

Teratology ◽

10.1002/tera.1420460315 ◽

1992 ◽

Vol 46 (3) ◽

pp. 301-309 ◽

Cited By ~ 28

Author(s):

Philip E. Mirkes ◽

Barbara Doggett

Keyword(s):

Heat Shock ◽

Heat Shock Protein ◽

Heat Shock Protein 72 ◽

Rat Embryos

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Expression of Heat Shock Protein 72 in Peritoneal Leukocytes is Induced by Peritoneal Dialysis

Peritoneal Dialysis International ◽

10.1177/089686080702700314 ◽

2007 ◽

Vol 27 (3) ◽

pp. 288-295 ◽

Cited By ~ 6

Author(s):

Lukasz Marzec ◽

Tomasz Liberek ◽

Michal Chmielewski ◽

Ewa Bryl ◽

Jacek M. Witkowski ◽

...

Keyword(s):

Peritoneal Dialysis ◽

Heat Shock ◽

Heat Shock Protein ◽

Peripheral Blood ◽

Peritoneal Macrophages ◽

Mrna Levels ◽

Blood Monocytes ◽

Heat Shock Protein 72 ◽

Peritoneal Leukocytes

Background One of the main limitations of peritoneal dialysis (PD) is deterioration of functional and morphological characteristics of the peritoneum. This complication appears to be related to the low biocompatibility profile of PD fluids. Recently, induction of the heat shock protein (HSP) stress response was demonstrated in cultured human mesothelial cells exposed to PD fluid in vitro. We investigated whether expression of heat shock protein 72 (HSP-72) in peritoneal macrophages is induced upon exposure to PD fluid during continuous ambulatory PD. Methods Peritoneal leukocytes were isolated from 4-hour dwell dialysate; peripheral blood mononuclear cells (PBMC) and peripheral blood monocytes isolated from the same patients were used as a control. In separate experiments, PBMC from healthy individuals were exposed in vitro to different PD fluids or to culture media. Expression of HSP-72 was assessed by Western immunoblotting, flow cytometry, and reverse-transcription polymerase chain reaction analysis. Results Macrophages and leukocytes isolated from dialysis effluent expressed significantly increased HSP-72 and mRNA levels compared to blood monocytes and PBMC of the same patients. In vitro exposure of PBMC to fresh PD fluids resulted in significantly higher expression of HSP-72 compared to those incubated in culture medium. PBMC exposed in vitro to standard lactate-buffered dialysis fluids also expressed significantly more HSP-72 compared to cells exposed to bicarbonate/lactate-buffered fluids. Conclusion Our results indicate that exposure to PD fluids during dialysis triggers a shock response in peritoneal cells, which is manifested by significantly increased HSP-72 expression at both protein and mRNA levels. Analysis of this protein expression in peritoneal macrophages could be a new, convenient, and relevant way to assess the biocompatibility of PD fluids ex vivo.

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