scholarly journals Intramuscular Heating Through Fluidotherapy and Heat Shock Protein Response

2013 ◽  
Vol 48 (3) ◽  
pp. 353-361 ◽  
Author(s):  
John P. Vardiman ◽  
Laura Jefferies ◽  
Chad Touchberry ◽  
Phillip Gallagher
Keyword(s):  
Heat Treatment ◽  
Heat Shock ◽  
Heat Shock Protein ◽  
Lower Extremity ◽  
Skinfold Thickness ◽  
Inducible Expression ◽  
Peak Temperature ◽  
Hsp70 Expression ◽  
Estradiol Levels ◽  
Intramuscular Temperature

Context: Therapeutic modalities that can increase intramuscular temperature commonly are used to treat injuries in the clinical setting. Researchers recently have suggested that the physiologic changes occurring during an increase in temperature also could provide a cytoprotective effect for exercise-induced muscle damage. Objective(s): To determine if the Fluidotherapy treatment increases the inducible expression of heat shock protein (HSP), to identify the rate of heating that occurs in the lower extremity with Fluidotherapy treatment, and to evaluate the relationship between the inducible expression of HSP and temperature. Design: Controlled laboratory study. Setting: Laboratory. Patients or Other Participants: Six male (age = 21.67 ± 1.63 years, height = 180.09 ± 4.83 cm, mass = 87.60 ± 10.51 kg) and 6 female (age = 24.60 ± 4.59 years, height = 151.05 ± 35.76 cm, mass = 55.59 ± 14.58 kg) college-aged students. Intervention(s): One lower extremity was randomly selected to receive the heat treatment, and the other extremity received no treatment. Main Outcome Measure(s): We measured intramuscular temperature every 10 minutes, determining peak intramuscular temperature by 2 identical sequential measurements, and we analyzed the time to peak temperature. We analyzed the amount of HSP70 expression and HSP27P:T (ratio of HSP27 to the total HSP27 expression) in the gastrocnemius and soleus muscles and measured baseline skinfold thickness and estradiol levels. Results: Fluidotherapy increased intramuscular temperature by 5.66 ± 0.78°C (t11 = 25.67, P < .001) compared with baseline temperature, with a peak temperature of 39.08°C ± 0.39°C occurring at 84.17 ± 6.69 minutes. We did not find a heat treatment effect for HSP70 or HSP27P:T in the gastrocnemius or soleus muscles (P > .05). Peak temperature and the percentage change of HSP70 were positively correlated for the gastrocnemius and soleus muscles (P < .05). We found no other correlations for skinfold thickness, sex, or estradiol levels (P > .05). No effect of sex for skinfold thickness or estradiol levels at baseline was discovered (P > .05). Conclusions: This Fluidotherapy protocol increased the intramuscular temperature to a therapeutic level; however, it did not stimulate inducible HSP70 or HSP27P:T in the soleus and gastrocnemius muscles regardless of sex or skinfold thickness. These data confirmed that Fluidotherapy is an effective heating modality but suggested it is not an effective method for stimulating an HSP response in the lower limb.

scholarly journals Expression of heat shock protein 70 is insufficient to extend Drosophila melanogaster longevity

2019 ◽  
Author(s):  
Chengfeng Xiao ◽  
Danna Hull ◽  
Shuang Qiu ◽  
Joanna Yeung ◽  
Jie Zheng ◽  
...  
Keyword(s):  
Heat Treatment ◽  
Drosophila Melanogaster ◽  
Heat Shock ◽  
Heat Shock Protein ◽  
Stress Resistance ◽  
Heat Shock Protein 70 ◽  
Biological Effect ◽  
Hsp70 Expression ◽  
Gene Encoding ◽  
Shock Proteins

AbstractIt has been known for over 20 years that Drosophila melanogaster flies with twelve additional copies of the hsp70 gene encoding the 70 kDa heat shock protein lives longer after a non-lethal heat treatment. Since the heat treatment also induces the expression of additional heat shock proteins, the biological effect can be due either to HSP70 acting alone or in combination. This study used the UAS/GAL4 system to determine whether hsp70 is sufficient to affect the longevity and the resistance to thermal, oxidative or desiccation stresses of the whole organism. We observed that HSP70 expression in the nervous system or muscles has no effect on longevity or stress resistance but ubiquitous expression reduces the life span of males. We also observed that the down-regulation of Hsp70 using RNAi did not affect longevity.

scholarly journals Effects ofHelicobacter pyloriand Heat Shock Protein 70 on the Proliferation of Human Gastric Epithelial Cells

2014 ◽  
Vol 2014 ◽  
pp. 1-5 ◽  
Author(s):  
Liping Tao ◽  
Hai Zou ◽  
Zhimin Huang
Keyword(s):  
Helicobacter Pylori ◽  
Heat Shock ◽  
Epithelial Cells ◽  
Heat Shock Protein ◽  
Mtt Assay ◽  
Heat Shock Protein 70 ◽  
Hsp70 Expression ◽  
Gastric Epithelial Cells ◽  
Ags Cells ◽  
H Pylori

Infection ofHelicobacter pylori (H. pylori)changed the proliferation of gastric epithelial cells and decreased the expression of heat shock protein 70 (HSP70). However, the effects ofH. pylorion the proliferation of gastric epithelial cells and the roles of HSP70 during the progress need further investigation.Objective.To investigate the effects ofHelicobacter pylori (H. pylori)and heat shock protein 70 (HSP70) on the proliferation of human gastric epithelial cells.Methods. H. pyloriand a human gastric epithelial cell line (AGS) were cocultured. The proliferation of AGS cells was quantitated by an MTT assay, and the expression of HSP70 in AGS cells was detected by Western blotting. HSP70 expression in AGS cells was silenced by small interfering RNA (siRNA) to investigate the role of HSP70. ThesiRNA-treated AGS cells were cocultured withH. pyloriand cell proliferation was measured by an MTT assay.Results.The proliferation of AGS cells was accelerated by coculturing withH. pylorifor 4 and 8 h, but was suppressed at 24 and 48 h. HSP70 expression was decreased in AGS cells infected byH. pylorifor 48 h. The proliferation in HSP70-silenced AGS cells was inhibited after coculturing withH. pylorifor 24 and 48 h compared with the control group.Conclusions.Coculture ofH. pylorialtered the proliferation of gastric epithelial cells and decreased HSP70 expression. HSP70 knockdown supplemented the inhibitory effect ofH. pylorion proliferation of epithelial cells. These results indicate that the effects ofH. pylorion the proliferation of gastric epithelial cells at least partially depend on the decreased expression of HSP70 induced by the bacterium.

Effects of ferulic acid on oxidative stress, heat shock protein 70, connexin 43, and monoamines in the hippocampus of pentylenetetrazole-kindled rats

2017 ◽  
Vol 95 (6) ◽  
pp. 732-742 ◽  
Author(s):  
Abdelaziz M. Hussein ◽  
Khaled M. Abbas ◽  
Osama A. Abulseoud ◽  
El-Hussainy M.A. El-Hussainy
Keyword(s):  
Oxidative Stress ◽  
Heat Shock ◽  
Heat Shock Protein ◽  
Ferulic Acid ◽  
Group Treatment ◽  
Heat Shock Protein 70 ◽  
Connexin 43 ◽  
Hsp70 Expression ◽  
Neuroprotective Effects ◽  
Cx43 Expression

The present study investigated the effects of ferulic acid (FA) on pentylenetetrazole (PTZ)-induced seizures, oxidative stress markers (malondialdehyde (MDA), catalase, and reduced glutathione (GSH)), connexin (Cx) 43, heat shock protein 70 (Hsp 70), and monoamines (serotonin (5-HT) and norepinephrine (NE)) levels in a rat model of PTZ-induced kindling. Sixty Sprague Dawley rats were divided into 5 equal groups: (a) normal group; (b) FA group: normal rats received FA at a dose of 40 mg/kg daily; (c) PTZ group: normal rats received PTZ at a dose of 50 mg/kg i.p. on alternate days for 15 days; (d) FA-before group: treatment was the same as for the PTZ group, except rats received FA; and (e) FA-after group: rats received FA from sixth dose of PTZ. PTZ caused a significant increase in MDA, Cx43, and Hsp70 along with a significant decrease in GSH, 5-HT, and NE levels and CAT activity in the hippocampus (p < 0.05). Pre- and post-treatment with FA caused significant improvement in behavioral parameters, MDA, CAT, GSH, 5-HT, NE, Cx43 expression, and Hsp70 expression in the hippocampal region (p < 0.05). We conclude that FA has neuroprotective effects in PTZ-induced epilepsy, which might be due to attenuation of oxidative stress and Cx43 expression and upregulation of neuroprotective Hsp70 and neurotransmitters (5-HT and NE).

scholarly journals The effect of red-fleshed pitaya (Hylocereus polyrhizus) on heat shock protein 70 and cortisol expression in strenuous exercise induced rats

F1000Research ◽  
2019 ◽  
Vol 8 ◽  
pp. 130
Author(s):  
Novita Sari Harahap ◽  
Aznan Lelo ◽  
Ambrosius Purba ◽  
Awaluddin Sibuea ◽  
Rina Amelia ◽  
...  
Keyword(s):  
Body Weight ◽  
Heat Shock ◽  
Heat Shock Protein ◽  
Heat Shock Protein 70 ◽  
The Body ◽  
Male Rats ◽  
Strenuous Exercise ◽  
Hsp70 Expression ◽  
Average Weight ◽  
Significant Difference

Background: Oxidative stress from exercise can contribute to damaging cells, increasing heat shock protein 70 (HSP70) and suppressing the immune system in the body. This research aimed to determine the antioxidant potential of red-fleshed pitaya extract on HSP70 and cortisol expression in rats which were subjected to strenuous exercise. Methods: The subjects of this research were 32 Sprague Dawley male rats, aged 3 months, with an average weight of 200 g. Red-fleshed pitaya extract was obtained from methanol extraction process; a maceration technique was performed and the extract was concentrated using an air-drying method. Rats were randomly divided into four groups. Group 1 were subjected to strenuous exercise and treated with distilled water only; while Groups 2, 3 and 4 were subjected to strenuous exercise and treated with 100 mg/kg body weight, 200 mg/kg body weight and 300 mg/kg body weight of red-fleshed pitaya extract, respectively. Strenuous exercises in rats was performed by intense swimming of 20 min/day, 3 days a week for 3 weeks. HSP70 expression and cortisol were measured with Enzyme-Linked Immune Sorbent Assay (ELISA) method. Results: There was a significant reduction of HSP70 (p=0.000) and cortisol expression (p=0.000) between the groups. Also, there was a significant difference in the average decreasing of HSP70 expression between group 4 and either groups 1 or 2 (p=0.000). However, a significant difference between groups 4 and 3 was not observed (p=0.813). Lastly, a significant difference was found in the average decrease of cortisol expression between groups 4 and 1 (p=0.000), 2 (p=0.000), and 3 (p=0.000) respectively. Conclusion: Red-fleshed pitaya is potential to be utilized as antioxidant to decrease the HSP70 and cortisol expression.

Thermally Induced Apoptosis, Necrosis, and Heat Shock Protein Expression in Three-Dimensional Culture

2014 ◽  
Vol 136 (7) ◽  
Author(s):  
Alfred S. Song ◽  
Amer M. Najjar ◽  
Kenneth R. Diller
Keyword(s):  
Prostate Cancer ◽  
Heat Shock ◽  
Heat Shock Protein ◽  
Fluorescent Protein ◽  
Three Dimensional ◽  
3D Culture ◽  
Hsp70 Expression ◽  
Three Dimensional Culture ◽  
Apoptosis And Necrosis ◽  
2D And 3D

This study was conducted to compare the heat shock responses of cells grown in 2D and 3D culture environments as indicated by the level of heat shock protein 70 expression and the incidence of apoptosis and necrosis of prostate cancer cell lines in response to graded hyperthermia. PC3 cells were stably transduced with a dual reporter system composed of two tandem expression cassettes—a conditional heat shock protein promoter driving the expression of green fluorescent protein (HSPp-GFP) and a cytomegalovirus (CMV) promoter controlling the constitutive expression of a “beacon” red fluorescent protein (CMVp-RFP). Two-dimensional and three-dimensional cultures of PC3 prostate cancer cells were grown in 96-well plates for evaluation of their time-dependent response to supraphysiological temperature. To induce controlled hyperthermia, culture plates were placed on a flat copper surface of a circulating water manifold that maintained the specimens within ±0.1 °C of a target temperature. Hyperthermia protocols included various combinations of temperature, ranging from 37 °C to 57 °C, and exposure times of up to 2 h. The majority of protocols were focused on temperature and time permutations, where the response gradient was greatest. Post-treatment analysis by flow cytometry analysis was used to measure the incidences of apoptosis (annexin V-FITC stain), necrosis (propidium iodide (PI) stain), and HSP70 transcription (GFP expression). Cells grown in 3D compared with 2D culture showed reduced incidence of apoptosis and necrosis and a higher level of HSP70 expression in response to heat shock at the temperatures tested. Cells responded differently to hyperthermia when grown in 2D and 3D cultures. Three-dimensional culture appears to enhance survival plausibly by activating protective processes related to enhanced-HSP70 expression. These differences highlight the importance of selecting physiologically relevant 3D models in assessing cellular responses to hyperthermia in experimental settings.

Increased Heat Shock Protein 70 Expression following Toxicant-mediated Cytotoxicity: A Ubiquitous Marker of Toxicant Exposure?

2005 ◽  
Vol 33 (2) ◽  
pp. 105-110 ◽  
Author(s):  
Parivash Farzaneh ◽  
Abdolamir Allameh ◽  
Steven Pratt ◽  
Nicholas Moore ◽  
Lucy Travis ◽  
...  
Keyword(s):  
Heat Shock ◽  
Heat Shock Protein ◽  
Stress Component ◽  
Hepatoma Cell ◽  
The Other ◽  
Hsp70 Expression ◽  
Hepatoma Cell Line ◽  
Toxicant Exposure ◽  
Cellular Protection

The up-regulation of heat shock protein (HSP) expression has been proposed as a general biomarker of cellular protection against various environmental stresses and chemicals. The present study investigated the possibility of using HSP70 up-regulation as a biomarker of toxicant exposure in vitro. Cells of a rat hepatoma cell line (FGC4) were exposed to concentrations of 1,3-dichloroacetone, duroquinone, diquat dibromide, menadione, hydrogen peroxide, cadmium chloride (CdCl2) and sodium (meta)arsenite (NaAsO2) that elicited 20–50% cytotoxicity over a 24-hour period, and HSP70 levels were measured by ELISA. Up-regulation of HSP70 expression was demonstrated following treatment with menadione, CdCl2 and NaAsO2, but not with the other chemicals tested. A shorter exposure time (6 hours) and/or the use of non-toxic concentrations reduced the level of HSP70 up-regulation with menadione, CdCl2 and NaAsO2, but did not uncover any up-regulation with the other chemicals. Although the toxicity of the majority of the chemicals tested is believed to involve an oxidative stress component, the results of this study clearly demonstrate that up-regulation of HSP70 expression cannot be used as a general biomarker of toxicant exposure in vitro.

scholarly journals Decreased expression of heat shock protein 70 mRNA and protein after heat treatment in cells of aged rats.

1990 ◽  
Vol 87 (2) ◽  
pp. 846-850 ◽  
Author(s):  
J. Fargnoli ◽  
T. Kunisada ◽  
A. J. Fornace ◽  
E. L. Schneider ◽  
N. J. Holbrook
Keyword(s):  
Heat Treatment ◽  
Heat Shock ◽  
Heat Shock Protein ◽  
Heat Shock Protein 70 ◽  
Aged Rats ◽  
In Cells

scholarly journals miR-16-1 Promotes the Aberrantα-Synuclein Accumulation in Parkinson Disease via Targeting Heat Shock Protein 70

2014 ◽  
Vol 2014 ◽  
pp. 1-8 ◽  
Author(s):  
Zhelin Zhang ◽  
Yan Cheng
Keyword(s):  
Heat Shock ◽  
Heat Shock Protein ◽  
Parkinson Disease ◽  
Heat Shock Protein 70 ◽  
Neuroblastoma Cell ◽  
Neuroblastoma Cell Line ◽  
Hsp70 Expression ◽  
Human Neuroblastoma Cell ◽  
Human Neuroblastoma ◽  
Human Neuroblastoma Cell Line

There is striking evidence that heat shock protein 70 (Hsp70) negatively regulatesα-synuclein aggregation, which plays a significant role in the formation and progression of Parkinson disease (PD). However, how the Hsp70 in neurons fails to prevent or even reverseα-synuclein aggregation and toxicity in PD still remains to be determined. In the present study, we constructed anα-synuclein-overexpressed human neuroblastoma cell line, SH-SY5Y-Syn, in which the blockage of Hsp70 promotedα-synuclein aggregation. And we also found that miR-16-1 downregulated Hsp70 and promotedα-synuclein aggregation in the SH-SY5Y-Syn cells. This study revealed a novel regulatory mechanism of Hsp70 expression, which might contribute to the PD development.

Regulation of heat shock protein 27 expression of prostatic cells in response to heat treatment

The Prostate ◽  
1998 ◽  
Vol 37 (3) ◽  
pp. 174-181 ◽  
Author(s):  
Stephan Madersbacher ◽  
Marion Gröbl ◽  
Gero Kramer ◽  
Stephan Dirnhofer ◽  
Georg E. Steiner ◽  
...  
Keyword(s):  
Heat Treatment ◽  
Heat Shock ◽  
Heat Shock Protein ◽  
Heat Shock Protein 27
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