共查询到20条相似文献,搜索用时 15 毫秒
1.
CD44v6 is a splice variant of CD44 (CD44v), probably promoting cancer cell adherence to vascular endothelium and base membranes and enhancing the invasion and metastasis of colonic carcinomas. Heat shock protein 72 (HSP72) as a molecular chaperone has been confirmed to be overexpressed in epithelial carcinoma cells. There may be a possible association between the expression of HSP72 and CD44v6 during the growth and progression of colonic carcinoma cells. The aim of the study was to investigate the interaction between heat shock protein 72 and CD44v6 in human colonic carcinomas. The localization of HSP72 and CD44v6 in human colonic carcinomas was determined by immunohistochemistry and confocal laser microscopy. The interaction between HSP72 and CD44v6 in colonic carcinoma cells was analyzed by immunoprecipitation and Western immunoblots. Our results revealed that colonic carcinoma synchronously co-expressed higher levels of HSP72 and CD44v6 than that in adjacent normal colonic tissues. HSP72 and CD44v6 were mainly immunolocalized in the cytoplasm, and also immunolabelled on the cell membrane. Based on immunoprecipitation and Western immunoblots, we found that HSP72 was associated with CD44v6 precursor fragments in human colonic carcinoma cells. The interaction between HSP72 and CD44v6 in human colonic carcinoma cells may contribute to study the pathogenesis and immunotherapy of colonic carcinoma. 相似文献
2.
P.A. Ruell M.W. Thompson K.M. Hoffman J.R. Brotherhood D.A.B. Richards 《Journal of thermal biology》2007,32(7-8):406-412
Heat shock protein 72 (HSP72) is the most inducible HSP, but is not always increased in lymphocytes following exercise. This field study examined whether lymphocyte HSP72 was increased in hyperthermic (Trec>39.0 °C) male athletes following a 14 km competitive race in cool conditions (ambient temperature 11.2 °C). A comparison was also made between control runners (n=7) and those treated for exertional heat illness (n=9). Lymphocyte HSP72 was not increased in control runners immediately post- compared with pre-race, and there was no difference between both groups of runners. A second study of the race (ambient temperature 14.6 °C) found that lymphocyte HSP72 in control (n=7) and treated (n=9) athletes was higher 2 days post- compared with immediately post-race (p<0.01) and these increases were correlated with post-exercise Trec (p<0.05). 相似文献
3.
4.
Expression of HSP72 after ELF-EMF exposure in three cell lines 总被引:1,自引:0,他引:1
5.
6.
Expression of HSP72 in the gastric mucosa is regulated by gastric acid in rats-correlation of HSP72 expression with mucosal protection 总被引:1,自引:0,他引:1
Wada I Otaka M Jin M Odashima M Komatsu K Konishi N Matsuhashi T Horikawa Y Ohba R Itoh H Watanabe S 《Biochemical and biophysical research communications》2006,349(2):611-618
BACKGROUND AND AIM: The real mechanism of adaptive cytoprotection in the gastric mucosa is not well established. In the present study, we investigated the effect of acid suppressing agents on a 72-kDa heat shock protein (HSP72) expression, which is known as endogenous cytoprotective factor, in the gastric mucosa. Also, the association of gastric mucosal protective function against HCl-challenge was compared between HSP72-induced and -reduced group. MATERIALS AND METHODS: Expression of HSP72 was measured by Western blotting in the gastric mucosa before and after administration of famotidine or omeprazole. The gastric mucosal protective function against 0.6 N HCl was compared between control group and HSP72-reduced group. Also, the effect of increased expression of gastric HSP72 by additional administration of zinc sulfate or zinc L-carnosine, which is known as HSP72-inducer, on mucosal protective function was studied. RESULTS: HSP72 expression in the gastric mucosa was reduced by acid suppressing agents. The lowest expression level of HSP72 was observed 12 h (famotidine, H2-receptor antagonist) or 48 h (omeprazole, proton pump inhibitor) after administration. The gastric mucosal protective ability against 0.6 N HCl was also reduced when HSP72 expression was decreased by famotidine or omeprazole. This phenomenon was reversed by HSP72 induction by additional administration of zinc derivatives. CONCLUSION: Our results might indicate that the expression of HSP72 in the gastric mucosa is physiologically regulated by gastric acid, and that HSP72 induction could be important in view of mucosal protection especially when HSP72 expression is reduced by administration of acid suppressing agents such as proton pump inhibitor or H2 receptor antagonist. 相似文献
7.
8.
Ogata T Oishi Y Roy RR Ohmori H 《Biochemical and biophysical research communications》2005,331(4):1317-1323
The content of both heat shock protein 72 (HSP72) and calcineurin (CaN) in skeletal muscle fibers have been reported to be associated with the slow phenotype. The purpose of the present study was to determine the adaptations/contributions of HSP72 and CaN to experimental conditions producing dramatic shifts in fiber phenotype. Two weeks of functional overload (FO) of the rat plantaris by cutting the tendons of its major synergists resulted in a shift towards a slower MHC profile. Two weeks of thyroid hormone (T3) administration (150 microg/kg/day, i.p.) resulted in a shift towards a faster MHC profile in control rats and an attenuation of the shift towards a slower profile in FO rats. HSP72 and CaN-A content were 63% and 47% higher, respectively, in the plantaris of FO than age-matched control rats. These increases were significantly attenuated by T3 treatment in FO rats. CaN-B levels were approximately 50% higher in FO and FO plus T3-treated than control rats. T3 treatment alone had no effect on the levels of HSP72, CaN-A or -B in control rats. Therefore, chronic overload of a muscle results in an increase in the percentage of slow fibers/MHC and enhances the levels of HSP72 and CaN. In turn, these FO-induced adaptations are attenuated by T3 treatment. Combined, these results indicate that muscle HSP72 and CaN protein levels are modulated by mechanical stress and that their levels appear to be related to changes in fiber type/MHC composition, at least in chronically overloaded muscles. 相似文献
9.
10.
Susanne Hedlund Hari Shanker Sharma Per-Ove Sjquist Jan Westman 《Journal of thermal biology》1999,24(5-6):409-414
Rats exposed to 4 h heat stress at 38°C exhibited upregulation of heat shock protein (HSP 72 kD) expression in several brain regions associated with brain edema and cell injury. Pretreatment with a new anti-oxidant compound H-290/51 (50 mg/kg, per os, 30 min before stress) significantly attenuated HSP expression, brain edema and cell injury. These results suggest that oxidative stress associated with brain edema plays important roles in HSP expression, not reported earlier. 相似文献
11.
Stress proteins have been proposed as markers of toxicity. This study investigated the sensitivity and specificity of stress proteins as markers of toxicity in primary hepatocyte cultures following exposure to two compounds, hydrazine and cadmium chloride (CdCl ). 2 Hepatocytes were exposed to increasing concentrations of hydrazine and CdCl for 2 h 2 and levels of the heat shock proteins HSP72/3, and HSP25 measured. In addition to this, ATP and GSH levels and LDH leakage were measured over the following 8 h. The results show that increasing concentrations of hydrazine caused dose-dependent decreases in ATP and GSH levels over 8 h. There was no change in the levels of HSP25 or HSP72/3 over that period. CdCl was found to significantly induce HSP72/3 at a concentration of 2 5 M when no other biochemical parameter was altered, levels were also elevated following administration of 10 M CdCl but ATP levels were found to be decreased at this 2 concentration. Levels of HSP25 were not increased following CdCl exposure at any 2 concentration. Higher concentrations of CdCl produced significant increases in LDH 2 leakage and depletion of intracellular levels of ATP and GSH. In addition to this levels of HSP25 and HSP72/3 were reduced to zero following administration of high concentrations of CdCl . In this study hydrazine does not induce either of the stress 2 proteins studied here whereas CdCl exposure causes the induction of HSP72/3 but not 2 HSP25. However it was determined that during the culture of primary hepatocytes basal levels of HSP25 and HSP72/3 were significantly increased when compared with levels determined in vivo . The results suggest that stress proteins may have the potential to be sensitive markers of toxicity in primary hepatocytes; however, the induction of individual stress proteins appears to be dependent upon the compound used. The apparent noninduction of the stress response by hydrazine and minor induction by CdCl might be 2 explained by the fact that whilst in culture the hepatocytes are under a continuous state of stress and therefore may not be able to elicit a full stress response following a chemical insult. 相似文献
12.
Induction of 72-kDa Inducible Heat Shock Protein (HSP72) in Cultured Rat Astrocytes After Energy Depletion 总被引:2,自引:1,他引:1
Naohiko Imuta Satoshi Ogawa ‡Yusuke Maeda †Keisuke Kuwabara †Osamu Hori Hirokazu Ueda Takehiko Yanagihara Masaya Tohyama 《Journal of neurochemistry》1998,70(2):550-557
Abstract: Protein synthesis is important in the readaptive processes for cultured astrocytes after hypoxia and subsequent reoxygenation. We have identified 72-kDa inducible heat shock protein (HSP72) as a major stress protein in reoxygenated astrocytes. To assess the mechanism for reoxygenation-mediated induction of HSP72, a reporter gene that consists of a human HSP promoter fused to the luciferase gene was transfected into cultured astrocytes. Analysis of cellular energy nucleotides showed an increase of the ADP/ATP ratio after reoxygenation, which synchronized with activation of the HSP promoter. Activation of the HSP promoter was also observed after an addition of iodoacetic acid to hypoxic astrocytes, which reached the maximum when the ADP/ATP ratio reached 50%, but further decline in the energy profile caused inactivation of this promoter. Inhibition of protein synthesis after reoxygenation resulted in temporary restoration of the energy profile and suppression of the DNA binding activity of the heat shock factor. Addition of quercetin greatly decreased the [3 H]leucine incorporation in the polysome fraction without any effect on the mature mRNA formation. These data suggest that the energy depletion in reoxygenation triggers induction of HSP72 after reoxygenation, which may act as a pivotal mediator in the stress response of reoxygenated astrocytes by facilitating protein synthesis. 相似文献
13.
Stress proteins have been proposed as markers of toxicity. This study investigated the sensitivity and specificity of stress proteins as markers of toxicity in primary hepatocyte cultures following exposure to two compounds, hydrazine and cadmium chloride (CdCl) . 2 Hepatocytes were exposed to increasing concentrations of hydrazine and CdCl for 2 h 2 and levels of the heat shock proteins HSP72/3, and HSP25 measured. In addition to this, ATP and GSH levels and LDH leakage were measured over the following 8 h. The results show that increasing concentrations of hydrazine caused dose-dependent decreases in ATP and GSH levels over 8 h. There was no change in the levels of HSP25 or HSP72/3 over that period. CdCl was found to significantly induce HSP72/3 at a concentration of 2 5 M when no other biochemical parameter was altered, levels were also elevated following administration of 10 M CdCl but ATP levels were found to be decreased at this 2 concentration. Levels of HSP25 were not increased following CdCl exposure at any 2 concentration. Higher concentrations of CdCl produced significant increases in LDH 2 leakage and depletion of intracellular levels of ATP and GSH. In addition to this levels of HSP25 and HSP72/3 were reduced to zero following administration of high concentrations of CdCl. In this study hydrazine does not induce either of the stress 2 proteins studied here whereas CdCl exposure causes the induction of HSP72/3 but not 2 HSP25. However it was determined that during the culture of primary hepatocytes basal levels of HSP25 and HSP72/3 were significantly increased when compared with levels determined in vivo. The results suggest that stress proteins may have the potential to be sensitive markers of toxicity in primary hepatocytes; however, the induction of individual stress proteins appears to be dependent upon the compound used. The apparent noninduction of the stress response by hydrazine and minor induction by CdCl might be 2 explained by the fact that whilst in culture the hepatocytes are under a continuous state of stress and therefore may not be able to elicit a full stress response following a chemical insult. 相似文献
14.
Chronic repeated exposure to hyperthermia in humans results in heat acclimation (HA), an adaptive process that is attained
in humans by repeated exposure to hyperthermia and is characterized by improved heat elimination and increased exercise capacity,
and acquired thermal tolerance (ATT), a cellular response characterized by increased baseline heat shock protein (HSP) expression
and blunting of the acute increase in HSP expression stimulated by re-exposure to thermal stress. Epidemiologic studies in
military personnel operating in hot environments and elite athletes suggest that repeated exposure to hyperthermia may also
exert long-term health effects. Animal models demonstrate that coincident exposure to mild hyperthermia or prior exposure
to severe hyperthermia can profoundly affect the course of experimental infection and injury, but these models do not represent
HA. In this study, we demonstrate that CD-1 mice continuously exposed to mild hyperthermia (ambient temperature ~37°C causing
~2°C increase in core temperature) for 5 days and then exposed to a thermal stress (42°C ambient temperature for 40 min) exhibited
some of the salient features of human HA, including (1) slower warming during thermal stress and more rapid cooling during
recovery and (2) increased activity during thermal stress, as well as some of the features of ATT, including (1) increased
baseline expression of HSP72 and HSP90 in lung, heart, spleen, liver, and brain; and (2) blunted incremental increase in HSP72
expression following acute thermal stress. This study suggests that continuous 5-day exposure of CD-1 mice to mild hyperthermia
induces a state that resembles the physiologic and cellular responses of human HA. This model may be useful for analyzing
the molecular mechanisms of HA and its consequences on host responsiveness to subsequent stresses. 相似文献
15.
16.
Nicole T. Brun V. Monica Bricelj Neil W. Ross 《Journal of experimental marine biology and ecology》2008,358(2):151-162
The effects of thermal stress on the induction of heat shock proteins (HSPs) were examined in northern bay scallops, Argopecten irradians irradians, a relatively heat tolerant estuarine species, and sea scallops, Placopecten magellanicus, a species residing in cooler, deeper water. Polyclonal antibodies used in this work for analysis of inducible HSP70 and HSP40 only recognized proteins of 72 and 40 kDa respectively from the mantles of both scallop species. Additionally, HSP quantification using the antibody to HSP70 was equally effective by either immunoprobing of western blots or ELISA, demonstrating that either approach could be successfully employed for analysis of thermal response in scallops. Sea scallop HSP70 and HSP40 did not change when animals were heat-shocked for 3 h by raising the temperature from 10 °C to 20 °C; however, a 24 h treatment of the same magnitude elicited a significant response. Conversely, bay scallops displayed rapid and prolonged HSP70 and HSP40 responses during the recovery period following a 3 h heat shock from 20 °C to 30 °C. Temperature reduction from 20 °C to 3 °C for 3 h also caused significant HSP70 and HSP40 increases in bay scallops; this represents the first time cold shock was shown to induce HSP synthesis in bivalve mollusks. The onset of the HSP40 response was more rapid than for HSP70, occurring at the end of the cold shock itself prior to transfer to a recovery temperature. Both proteins responded maximally during recovery at control temperature. HSP responses of sea and bay scallops to thermal stress may be related to their habitat in the natural environment and they suggest a differential capacity for adaptation to temperature change. This is an important consideration in assessing the response of these scallops to different culture conditions. 相似文献
17.
18.
Wheeler DS Dunsmore KE Wong HR 《Biochemical and biophysical research communications》2003,301(1):54-59
Heat shock protein 70 (HSP70) is an intracellular stress protein that confers cytoprotection to a variety of cellular stressors. Several lines of evidence have suggested that augmentation of the heat shock response by increasing the expression of HSP70 represents a potential therapeutic strategy for the treatment of critically ill patients. The Tat protein of human immunodeficiency virus 1 (HIV-1) has been used previously to deliver functional cargo proteins intracellularly when added exogenously to cultured cells. We generated a Tat-HSP70 fusion protein using recombinant methods and treated HSF -/- cells with either Tat-HSP70 or recombinant HSP70 prior to exposure to hyperoxia or lethal heat shock. We showed that biologically active, exogenous HSP70 can be delivered into cells using the HIV-1 Tat protein, and that the Tat-mediated delivery of HSP70 confers cytoprotection against thermal stress and hyperoxia and may represent a novel approach to augmenting intracellular HSP70 levels. 相似文献
19.
S. Vaithinathan B. Saradha P. P. Mathur 《Journal of biochemical and molecular toxicology》2009,23(1):29-35
Methoxychlor, an organochlorine pesticide, has been reported to induce abnormalities in male reproductive tract. However, the insight into the mechanisms of gonadal toxicity induced by methoxychlor is not well known. We investigated whether treatment with methoxychlor would alter the levels of stress proteins, heat shock proteins (HSP), and clusterin (CLU), and oxidative stress‐related parameters in the testis of adult male rats. Animals were exposed to a single dose of methoxychlor (50 mg/kg body weight) orally and were terminated at various time points (0, 3, 6, 12, 24, and 72 h) using anesthetic ether. The levels of HSP70, CLU, and the activities of superoxide dismutase (SOD), catalase, and lipid peroxidation levels were evaluated in a 10% testis homogenate. A sequential reduction in the activities of catalase and SOD with concomitant increase in the levels of thiobarbituric acid reactive substance (TBARS) was observed. These changes elicited by methoxychlor were very significant between 6–12 h of posttreatment. Immunoblot analysis of HSP revealed the expression of HSP72, an inducible form of HSP, at certain time points (3–24 h) following exposure to methoxychlor. Similarly, the levels of secretory CLU (sCLU) were also found to be elevated between 3–24 h of treatment. The present data demonstrate methoxychlor‐elicited increase in the levels of inducible HSP72 and sCLU, which could be a part of protective mechanism mounted to reduce cellular oxidative damage. © 2009 Wiley Periodicals, Inc. J Biochem Mol Toxicol 23:29–35, 2009; Published online in Wiley InterScience ( www.interscience.wiley.com ). DOI 10.1002/jbt.20262 相似文献
20.
The cell-surface expression patterns of major histocompatibility complex (MHC) class I, class II and heat-shock protein 72
(HSP72) molecules were measured on human lung (LX-1) and mammary (MX-1) carcinoma cells. No major differences were found in
the MHC cell-surface expression pattern of both cell lines. However, they differ significantly in their capacity to express
HSP72 on their cell surface. Under physiological conditions LX-1 cells express HSP72 molecules on more than 90% of the cells,
whereas MX-1 cells exhibit no significant HSP72 cell-surface expression (less than 5%). These expression patterns remained
stable in all further cell passages tested. The sensitivity to lysis mediated by an interleukin-2 (IL-2)-stimulated, adherent
natural killer (NK) cell population could be correlated with the amount of cell-surface-expressed HSP72 molecules. By antibody-blocking
studies, using HSP72-specific monoclonal antibody (mAb), a strong inhibition of lysis was only found with LX-1 cells but not
with MX-1 cells. In contrast to the cell-surface expression, the cytoplasmic amount of HSP72 in MX-1 cells was twice as high
compared to LX-1 cells under physiological conditions. After nonlethal heat-shock the rate of induction and the total cytoplasmic
amounts of HSP72 were comparable in both cell lines. The clonogenic cell viability of LX-1 cells after incubation at temperatures
ranging from 41°C to 44°C was significantly elevated compared to that of MX-1 cells. In conclusion we state the following:
(i) HSP72 cell-surface expression on human carcinoma cells is independent of the cytoplasmic amount of HSP72; (ii) the cell-surface
expression of HSP72 is associated with an increased sensitivity of tumour cells to lysis mediated by an IL-2-stimulated, adherent
NK cell population; (iii) thermoresistance is not related to the cytoplasmic HSP72 level but might be related to the amount
of HSP72 expressed on the cell surface.
Received: 20 June 1996 / Accepted: 25 September 1996 相似文献