Gender differences in the expression of heat shock proteins: the effect of estrogen

2003 ◽  
Vol 285 (2) ◽  
pp. H687-H692 ◽  
Author(s):  
M. R. Voss ◽  
J. N. Stallone ◽  
Min Li ◽  
R. N. M. Cornelussen ◽  
P. Knuefermann ◽  
...  
Keyword(s):  
Gender Differences ◽  
Heat Shock ◽  
Heat Shock Proteins ◽  
Cardiac Injury ◽  
Female Rats ◽  
Male Rats ◽  
Male Rat ◽  
Sprague Dawley ◽  
Shock Proteins ◽  
Hsp72 Expression

The heat shock proteins (HSPs) are an important family of endogenous, protective proteins that are found in all tissues. In the heart, HSP72, the inducible form of HSP70, has been the most intensely studied. It is well established that HSP72 is induced with ischemia and is cardioprotective. Overexpression of other HSPs also is protective against cardiac injury. Recently, we observed that 17β-estradiol increases levels of HSPs in male rat cardiac myocytes. We hypothesized that there were gender differences in HSP72 expression in the heart secondary to estrogen. To test this hypothesis, we examined cardiac levels of HSP72 by ELISA in male and female Sprague-Dawley rats. In addition, three other HSPs were assessed by Western blot (HSP27, HSP60, and HSP90). To determine whether estrogen status affected HSP72 expression in other muscles or tissues, two other muscle tissues, slow twitch muscle (soleus muscle) and fast twitch muscle (gastrocnemius muscle), were studied as well as two other organs, the kidney and liver. Because HSP72 is cardioprotective, and females are known to have less cardiovascular disease premenopause, the effects of ovariectomy were examined. We report that female Sprague-Dawley rat hearts have twice as much HSP72 as male hearts. Ovariectomy reduced the level of HSP72 in female hearts, and this could be prevented by estrogen replacement therapy. These data show that the expression of cardiac HSP72 is greater in female rats than in male rats, due to upregulation by estrogen.

scholarly journals Sex-, tissue-, and exposure duration-dependent effects of imidacloprid modulated by piperonyl butoxide and menadione in rats. Part I: oxidative and neurotoxic potentials

2014 ◽  
Vol 65 (4) ◽  
pp. 387-398 ◽  
Author(s):  
Mustafa Yardimci ◽  
Yusuf Sevgiler ◽  
Eyyup Rencuzogullari ◽  
Mehmet Arslan ◽  
Mehmet Buyukleyla ◽  
...  
Keyword(s):  
Cholinesterase Activity ◽  
Specific Effect ◽  
Piperonyl Butoxide ◽  
Female Rats ◽  
Male Rats ◽  
Male Rat ◽  
Total Protein Content ◽  
Sprague Dawley ◽  
Adverse Action ◽  
Liver And Kidney

Abstract Earlier research has evidenced the oxidative and neurotoxic potential of imidacloprid, a neonicotinoid insecticide, in different animal species. The primary aim of this study was to determine how metabolic modulators piperonyl butoxide and menadione affect imidacloprid’s adverse action in the liver and kidney of Sprague-Dawley rats of both sexes. The animals were exposed to imidacloprid alone (170 mg kg-1) or in combination with piperonyl butoxide (100 mg kg-1) or menadione (25 mg kg-1) for 12 and 24 h. Their liver and kidney homogenates were analysed spectrophotometrically for glutathione peroxidase, glutathione S-transferase, catalase, total cholinesterase specific activities, total glutathione, total protein content, and lipid peroxidation levels. Imidacloprid displayed its prooxidative and neurotoxic effects predominantly in the kidney of male rats after 24 h of exposure. Our findings suggest that the observed differences in prooxidative and neurotoxic potential of imidacloprid could be related to differences in its metabolism between the sexes. Co-exposure (90-min pre-treatment) with piperonyl butoxide or menadione revealed tissue-specific effect of imidacloprid on total cholinesterase activity. Increased cholinesterase activity in the kidney could be an adaptive response to imidacloprid-induced oxidative stress. In the male rat liver, co-exposure with piperonyl butoxide or menadione exacerbated imidacloprid toxicity. In female rats, imidacloprid+menadione co-exposure caused prooxidative effects, while no such effects were observed with imidacloprid alone or menadione alone. In conclusion, sex-, tissue-, and duration-specific effects of imidacloprid are remarkable points in its toxicity

scholarly journals Gender differences in skeletal muscle heat shock proteins induced by diathermy

2007 ◽  
Vol 21 (6) ◽  
Author(s):  
Chad D. Touchberry ◽  
Tung Le ◽  
Scott Richmond ◽  
Mike Prewit ◽  
David Beck ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Gender Differences ◽  
Heat Shock ◽  
Heat Shock Proteins ◽  
Shock Proteins

Luminal bacterial flora determines physiological expression of intestinal epithelial cytoprotective heat shock proteins 25 and 72

2005 ◽  
Vol 288 (4) ◽  
pp. G696-G704 ◽  
Author(s):  
Donna L. Arvans ◽  
Stephan R. Vavricka ◽  
Hongyu Ren ◽  
Mark W. Musch ◽  
Lisa Kang ◽  
...  
Keyword(s):  
Small Intestine ◽  
Heat Shock ◽  
Small Bowel ◽  
Heat Shock Proteins ◽  
Ex Vivo ◽  
Short Circuit ◽  
Bacterial Flora ◽  
Short Chain Fatty Acids ◽  
Shock Proteins ◽  
Hsp72 Expression

Heat shock proteins (HSP) 25 and 72 are expressed normally by surface colonocytes but not by small intestinal enterocytes. We hypothesized that luminal commensal microflora maintain the observed colonocyte HSP expression. The ability of the small intestine to respond to bacteria and their products and modulate HSPs has not been determined. The effects of luminal bacterial flora in surgically created midjejunal self-filling (SFL) vs. self-emptying (SEL) small-bowel blind loops on epithelial HSP expression were studied. HSP25 and HSP72 expression were assessed by immunoblot and immunohistochemistry. SFL were chronically colonized, whereas SEL contained levels of bacteria normal for the proximal small intestine. SFL creation significantly increased HSP25 and HSP72 expression relative to corresponding sections from SEL. Metronidazole treatment, which primarily affects anaerobic bacteria as well as a diet lacking fermentable fiber, significantly decreased SFL HSP expression. Small bowel incubation with butyrate ex vivo induced a sustained and significant upregulation of HSP25 and altered HSP72 expression, confirming the role of short-chain fatty acids. To determine whether HSPs induction altered responses to an injury, effects of the oxidant, monochloramine, on epithelial resistance and short-circuit current ( Isc) responses to carbachol and glucose were compared. Increased SFL HSP expression was associated with protection against oxidant-induced decreases in transmural resistance and Iscresponses to glucose, but not secretory responses to carbachol. In conclusion, luminal microflora and their metabolic byproducts direct expression of HSPs in gut epithelial cells, an effect that contributes to preservation of epithelial cell viability under conditions of stress.

Trehalose protects against spinal cord injury through regulating heat shock proteins 27 and 70 and caspase-3 genes expression

2019 ◽  
Vol 31 (1) ◽  
Author(s):  
Roya Nasouti ◽  
Mohammad Khaksari ◽  
Moghaddameh Mirzaee ◽  
Mahdieh Nazari-Robati
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Heat Shock ◽  
Heat Shock Proteins ◽  
Caspase 3 ◽  
Male Rats ◽  
Vehicle Group ◽  
Genes Expression ◽  
Cord Injury ◽  
Shock Proteins

AbstractBackgroundHeat shock proteins (HSPs) are a class of highly conserved proteins responsible for various functions critical to cell survival. Pharmacological induction of HSPs has been implicated in the regulation of neuronal loss and functional deficits in peripheral and central nervous system injuries. Accordingly, the present study was conducted to investigate the effect of trehalose on spinal expression of HSP27, HSP70 and caspase-3 genes following traumatic spinal cord injury (SCI) in rats.MethodsMale rats weighing 250–300 g underwent laminectomy and were divided into four groups including sham, SCI (received SCI), vehicle (received SCI and phosphate buffer saline intrathecally) and trehalose (received 10 mM trehalose intrathecally following SCI). On days 1, 3 and 7 after injury, HSP27, HSP70 and caspase-3 genes transcripts were quantified in spinal cord tissues via a real-time PCR technique. In addition, locomotor function was assessed using the Basso, Beattie and Bresnahan (BBB) rating scale.ResultsSCI induced the expression of HSP27, HSP70 and caspase-3 genes and BBB score at all time points. Trehalose treatment upregulated HSP27, HSP70 genes expression at 1 day after SCI. Interestingly, a significant reduction in the expression of HSP27 and HSP70 genes was observed on days 3 and 7 following trauma compared with the vehicle group (p < 0.01). Caspase-3 gene showed a decrease in expression in the trehalose-treated group at all times. In addition, neurological function revealed an improvement after treatment with trehalose.ConclusionThis study suggests that the neuroprotective effect of trehalose is mediated via regulation of HSP27 and HSP70, which are involved in cytoprotection and functional recovery following SCI.

scholarly journals RESEARCH OF REPARATIVE MECHANISMS IN THE OPTIC NERVE IN TOXIC NEUROPATHY CAUSED BY Cr (VI)

ScienceRise ◽  
2020 ◽  
pp. 31-39
Author(s):  
Olena Kuzenko ◽  
Yuri Demin ◽  
Yevhen Kuzenko
Keyword(s):  
Endothelial Cells ◽  
Optic Nerve ◽  
Heat Shock ◽  
Heat Shock Proteins ◽  
Optic Neuropathy ◽  
Nerve Fibers ◽  
Male Rats ◽  
Neurotoxic Effect ◽  
Toxic Optic Neuropathy ◽  
Shock Proteins

Intoxication lesions of the optic nerve (toxic optic neuropathy, TON) most often occur under the influence of exogenous factors, including heavy metals. Сell survival under stress have involves heat shock proteins (HSPs). The aim of the research. To assess the optic nerve’s immunoreactivity to heat shock proteins of the HSP70 and HSP90α families and reveal its relationship with the severity of morphological changes in toxic optic neuropathy caused by Cr (VI). Materials and methods. The study was conducted on 48 mature male rats. The experimental groups were given to drink water with Cr(VI) for 20, 40 and 60 days. This type of water is typical for the water basins in the northern districts of the Sumy region. Optic nerves сhanges under the influence of Cr(VI) have investigated by the morphometric method. Neuroglial cells and capillary endothelial cells were assessed by immunohistochemistry by HSP70α and HSP90 expression for intensity and spatial distribution. Results. The data analysis revealed that Cr (VI) has a neurotoxic effect on the optic nerve with the development of edema, which is manifested by the thickening of nerve fibers. The dynamics of HSP70 immunoexpression in the endothelium of the optic nerve capillaries of rats on 20 and 40 experimental days was characterized by stable values and was 1.5 times higher than the control. The maximum number of positively stained cells for the HSP70 marker was detected in endothelial cells of the microvasculature for 60 days – 82.44±12.42 %. HSP70 levels in neuroglia cells of optic nerve have decreased on day 40 (55.66±11.56% p=0.05) and lower than the control (70.44±4.81 %.) group. Optic nerve capillaries was highest immunoactivity on HSP90 in group II endothelial cells – 51.22±14.57% (p=0.05). The activity of HSP90α protein in optic neuroglia cells was characterized by a gradual increase in the duration of the experiment and was higher by 12, 4 % in experimental group III (81.77±21.67 %) compared with control (71.66±4.95 %). Conclusions. Our study provides an insight into the significant difference in the immunoreactivity of heat shock proteins of the HSP70 and HSP90α families in neuroglia and endothelial cells of the optic nerve capillaries under the influence of Cr(VI). The results obtained suggest that Cr (VI) has a neurotoxic effect on the optic nerve with the development of edema, which is manifested by the thickening of nerve fibers. A comparison of the dynamics of the development of the dystrophic process in the optic nerve with the results of the immunohistochemical analysis showed, that an increase in the thickness of nerve fibers is accompanied by an increase in immunoreactive neuroglial cells (HSP90α) and endothelial cells (HSP70).

scholarly journals Receptor-Mediated Suppression of Cardiac Heat-Shock Protein 72 Expression by Testosterone in Male Rat Heart

Endocrinology ◽  
2007 ◽  
Vol 148 (7) ◽  
pp. 3148-3155 ◽  
Author(s):  
Hiroaki Kohno ◽  
Naohiko Takahashi ◽  
Tetsuji Shinohara ◽  
Tatsuhiko Ooie ◽  
Kunio Yufu ◽  
...  
Keyword(s):  
Heat Shock ◽  
Heat Shock Protein ◽  
Ischemia Reperfusion ◽  
Male Rat ◽  
Sprague Dawley ◽  
Heat Shock Protein 72 ◽  
Heat Shock Element ◽  
Sprague Dawley Rats ◽  
The Impact ◽  
Hsp72 Expression

The impact of testosterone on cardiac expression of heat-shock protein 72 (HSP72) remains to be elucidated. Male Sprague Dawley rats 10 wk of age (adult) were castrated. Four weeks later, testosterone (10 mg/kg, ip) was administered as a single dose, followed by the application of hyperthermia (HT) (43 C) at 6 h after testosterone administration. Twenty-four hours later, each heart was isolated. Cardiomyocytes were prepared from 3- to 5-d-old Wistar rats and male Sprague Dawley rats 10 wk of age. Testosterone (0.1–10 μm) was added to the medium, followed by the application of HT (42 C). Twenty-four hours later, cells were collected. We observed the following: 1) Exogenous testosterone suppressed HT-induced HSP72 expression, but castration alone had no influence. 2) HT resulted in better reperfusion-induced cardiac performance in castrated rats comparable with sham-operated rats, which was inhibited by testosterone. The number of apoptotic cells after ischemia/reperfusion was also increased by testosterone. 3) HT-induced HSP72 expression in cultured cardiomyocytes was suppressed by testosterone. 4) HT resulted in less damage to cells, including apoptosis, in response to hypoxia/reoxygenation, which was inhibited by testosterone. 5) Flutamide, a testosterone receptor blocker, cancelled the suppressive effects of testosterone on HSP72 expression. 6) The HT-induced increase in heat-shock factor 1 activity to bind to heat-shock element DNA was suppressed by testosterone, and this was reversed by flutamide. Our results indicate that testosterone potentially has inhibitory effects on cardiac HSP72 expression by modulating transcription, through testosterone receptor-mediated genomic mechanisms.

Niacin-bound chromium enhances myocardial protection from ischemia-reperfusion injury

2006 ◽  
Vol 291 (2) ◽  
pp. H820-H826 ◽  
Author(s):  
Mahesh Thirunavukkarasu ◽  
Suresh Varma Penumathsa ◽  
Bela Juhasz ◽  
Lijun Zhan ◽  
Gerald Cordis ◽  
...  
Keyword(s):  
Heat Shock ◽  
Heat Shock Proteins ◽  
Infarct Size ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Female Rats ◽  
Male And Female ◽  
Male And Female Rats ◽  
Developed Pressure ◽  
Shock Proteins

A novel niacin-bound, chromium-based energy formula (EF; InterHealth Nutraceuticals, Benicia, CA) has been developed in conjunction with d-ribose, caffeine, ashwagandha extract (containing 5% withanolides), and selected amino acids. We have assessed the efficacy of oral administration of EF (40 mg·kg body wt−1·day−1) in male and female rats over a period of 90 consecutive days on the cardiovascular and pathophysiological functions in an isolated rat heart model. After 30, 60, and 90 days of treatment with EF, the hearts of male and female rats were subjected to 30 min of global ischemia followed by 2 h of reperfusion and were measured for myocardial ATP, creatine phosphate (CP), phosphorylated AMP kinase (p-AMPK), and heat shock proteins. Myocardial ATP and CP levels were increased in both male and female rats after EF treatment compared with the controls. Western blot analyses were performed to quantify the expression of stress-related proteins such as heat shock proteins (HSP-70, -32, and -25) and are found to be increased in both male and female rats after EF treatment. The p-AMPK level, which is a sensor for the energy state in various cell types, was also found to be increased after treatment with EF in both male and female rats. Aortic flow, maximum first derivative of developed pressure, left ventricular developed pressure, and infarct size were observed after ischemia-reperfusion and found to be significantly improved in EF-treated rats compared with control animals. Thus EF demonstrated long-term safety as well as exhibiting significant cardioprotective ability during ischemia and reperfusion injury by increased energy production, improved cardiac function, and reduced infarct size.

Heat shock proteins in willow (Salix viminalis)

1990 ◽  
Vol 80 (2) ◽  
pp. 301-306
Author(s):  
Tiina Vahala ◽  
Tage Eriksson ◽  
Peter Engstrom
Keyword(s):  
Heat Shock ◽  
Heat Shock Proteins ◽  
Salix Viminalis ◽  
Shock Proteins
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