Prévalence et facteurs associés au stress professionnel chez les enseignants du secondaire de Ouagadougou, Burkina Faso une étude observationnelle transversale / Prevalence and associated factors of occupational stress among secondary school teachers of Ouagadougou, Burkina Faso: a cross-sectional observational study

Contexte et objectif. Le stress au travail touche tous les secteurs d'activités dont celui de l'éducation. La présente avait pour objectif de déterminer la prévalence du stress chez les enseignants et d'identifier les facteurs associés au stress chez les enseignants du secondaire de Ouagadougou. Méthodes. Nous avons réalisé une étude transversale auprès des enseignants du secondaire de la ville de Ouagadougou. Le questionnaire teacher stress inventory de Fimian a été utilisé pour évaluer le niveau de stress chez les enseignants. Nous avons utilisé une analyse régression logistique multivariée pour identifier les facteurs associés au stress chez les enseignants. Résultats. Quatre cent trente-neuf enseignants ont été enrôlés. L'âge moyen des enseignants était de 43,5 ans. Ils avaient en moyenne un volume horaire hebdomadaire de 19,3 heures. Ils enseignaient en Moyenne depuis 15,6 ans. Les enseignants consommateurs de substances psychoactives représentaient 34,8 %, ceux qui avaient des pathologies en cours représentaient 37,1 %. La prévalence du stress professionnel chez les enseignants était de 16,4 %. Les pathologies en cours (OR ajusté =2,06, p=0,012), le volume horaire hebdomadaire supérieur à 22 heures (OR ajusté=1,92, p=0,024) augmentaient le risqué d'être stressé chez les enseignants. A l'inverse avoir des loisirs réduisait 3x ce risque (OR ajusté =0,31 ; p=0,020). Conclusion. La prévalence du stress chez les enseignants du secondaire est élevée. Les pathologies en cours chez les enseignants, un volume horaire hebdomadaire supérieur à 22 heures étaient des facteurs de risque tandis que les loisirs étaient un facteur protecteur.

Identification of heat stress transcription factors gene family in Setcreasea purpurea and analysis of its expression pattern under Cu2+ stress / 生物工程学报

Heat stress transcription factors (Hsf) family is one of the most important transcription factor families in plants, and plays an important role in the growth and development of plants when encountering abiotic stresses such as heat, drought, and heavy metals. In this study, 20 SpbHsf genes were identified from the full-length transcriptome database of Setcreasea purpurea, and the structure and function of the Hsf gene family were analyzed using bioinformatics tools and qRT-PCR. The results showed that all SpbHsf proteins were hydrophilic. There were 12 SpbHsf proteins located in the nucleus, and the content of α-helix and random coil in the secondary structure of all SpbHsf proteins was high. The SpbHsf genes are divided into three subfamilies, each of which contains unique conserved motifs. All SpbHsf proteins contain DBD and HR-A/B domains. Phylogenetic analysis showed that OsHsf in Oryza sativa protein had the highest homology with SpbHsf protein. All the 20 SpbHsf genes were expressed in the root tissues of S. purpurea. Among them, 8 were significantly up-regulated while 8 were significantly down-regulated under Cu2+ stress. This study may help better understand the function and expression pattern of the S. purpurea Hsf gene family.

Heat shock transcription factor family in plants: a review / 生物工程学报

With the constant change of global climate, plants are often affected by multiple abiotic stresses such as heat stress, drought stress, cold stress and saline-alkali stress. Heat shock transcription factors (HSFs) are a class of transcription factors widely existing in plants to respond to a variety of abiotic stresses. In this article, we review and summarize the structure, signal regulation mechanism of HSFs and some research in plants like Arabidopsis thaliana, tomato, rice and soybean, to provide reference for further elucidating the role of HSFs in the stress regulation network.

Análise da forma fosforilada do fator de choque térmico 1 (pHSF 1) em carcinomas de células escamosas de língua oral / Analysis of the phosphorylated form of heat shock factor 1 (pHSF 1) in oral tongue squamous cell carcinomas

O carcinoma de células escamosas de língua oral (CCELO) apresenta altas taxas de morbimortalidade, apesar dos avanços recentes no tratamento das neoplasias. Assim, várias pesquisas vêm tentando detectar alterações morfológicas ou identificar biomarcadores que possam apresentar poder preditivo de recidiva e metástase e novas estratégias e/ou opções terapêuticas mais individualizadas com intuito de melhorar o prognóstico destes pacientes. O fator do choque térmico 1 (HSF1) atua de diferentes formas na progressão tumoral, favorecendo o surgimento, desenvolvimento e invasividade tumoral e sua superexpressão vem sendo pesquisada em neoplasias. Esta pesquisa objetivou analisar se a forma fosforilada do fator de choque térmico 1 (p-HSF1) exerce alguma influência na patogênese do CCELO. Foi realizado um estudo imunoistoquímico em 69 casos de CCELO, verificando-se a expressão do p-HSF1 e correlacionado esta imunoexpressão com alguns parâmetros clinicopatológicos e sobrevida dos pacientes. Foi avaliado e comparado o escore de imunopositividade do p-HSF1 entre CCELO e mucosa oral normal (MON) e esta expressão foi ainda correlacionada aos sistemas de gradação histológica propostos por Brandwein-Gensler et al. (2005) e pelo modelo BD (ALMANGUSH et al., 2014). As curvas de associação de análise de sobrevida aos outros parâmetros foram realizadas pelo método Kaplan Meier e as diferenças dessas curvas submetidas ao teste log-rank (p<0,05). Verificou-se maior escore de imunoexpressão (p<0,001) de p-HSF1 em CCELOs em relação a MON, sugerindo que esse fator pode influenciar a patogênese destes tumores. A imunoexpressão do p-HSF1 não foi associada aos parâmetros clinicopatológicos pesquisados nesta amostra. O tamanho do tumor (T) T3/T4 foi associado ao alto risco tanto pelo sistema de Brandwein-Gensler et al. (2005) quanto pelo modelo BD (ALMANGUSH et al., 2014), sugerindo que tumores maiores podem ser associados a piores parâmetros histopatológicos. Os resultados da análise por meio do método BD, mostraram relevância prognóstica, uma vez que pacientes classificados como de alto risco por este sistema, foram associados a uma menor sobrevida global e maior número de óbitos, sugerindo sua possível inclusão como uma ferramenta útil na determinação do prognóstico de pacientes com CCELO (AU).

The squamous cell carcinoma (SCC) of the oral tongue presents morbimortality high levels although recent achievements of malignancies treatment. This way, a lot of researches are trying to detect morphological alterations or identify biomarkers that may present recurrence prediction power and metastasis and new strategies and/or more individualized therapeutic options in order to improve the prognosis of these patients. The Heat shock factor 1 (HSF1) acts in different ways of tumoral progressing, facilitating the appearance, development and tumoral invasiveness and its overexpression has been researched in malignancies. This research had the aim to analize if the phosphorylated form of Heat shock factor 1 (p-HSF1) carries some influence in the SCC of the oral tongue pathogenesis. There was an immunohistochemical study in 69 cases of oral tongue squamous cell carcinoma observing the p-HSF1 expression and correlating this immunoexpression with some clinicopathological parameters and patients' survival. It was evaluated and compared the immunohistochemical score of the p-HSF1 between the squamous cell carcinoma (SCC) of the oral tongue and normal oral mucosa (MON) and this expression was correlated to the histological gradation systems proposed by Brandwein-Gensler et al. (2005) and by the model BD (ALMANGUSH et al., 2014). Survival analysis of association curves with the other parameters were carried out with the Kaplan Meier method and the differences of these curves submitted to the test logrank (p<0,05). It was found a bigger immunoexpression score (p<0,001) of p-HSF1 in squamous cell carcinoma (SCC) of the oral tongue in relation to the MON, suggesting this factor may influence the tumors pathogenesis.. The tumor size ( T ) T3/ T4 was associated to the high risk not only by system of Brandwein-Gensler et al. (2005) as by model BD (ALMANGUSH et al., 2014), suggesting bigger tumors may be associated to worse histopathological parameters. The analysis result through the BD method, showed prognostic implication, since as patients classified as high risk by this system were associated to a smaller global survival and bigger death number, suggesting its possible inclusion as a useful tool in the prognosis determination of patients with squamous cell carcinoma (SCC) of the oral tongue (AU).

Effect of heat shock factor 1 on airway hyperresponsiveness and airway inflammation in mice with allergic asthma / 中国当代儿科杂志

<p><b>OBJECTIVE</b>To investigate the effect of heat shock factor 1 (HSF1) on airway hyperresponsiveness and airway inflammation in mice with asthma and possible mechanisms.</p><p><b>METHODS</b>A total of 36 mice were randomly divided into four groups: control, asthma, HSF1 small interfering RNA negative control (siHSF1-NC), and siHSF1 intervention (n=9 each). Ovalbumin (OVA) sensitization and challenge were performed to induce asthma in the latter three groups. The mice in the siHSF1-NC and siHSF1 groups were treated with siHSF1-NC and siHSF1, respectively. A spirometer was used to measure airway responsiveness at 24 hours after the last challenge. The direct count method was used to calculate the number of eosinophils. ELISA was used to measure the serum level of OVA-specific IgE and levels of interleukin-4 (IL-4), interleukin-5 (IL-5), interleukin-13 (IL-13), and interferon-γ (IFN-γ) in lung tissues and bronchoalveolar lavage fluid (BALF). Quantitative real-time PCR was used to measure the mRNA expression of HSF1 in asthmatic mice. Western blot was used to measure the protein expression of HSF1, high-mobility group box 1 (HMGB1), and phosphorylated c-Jun N-terminal kinase (p-JNK).</p><p><b>RESULTS</b>The asthma group had significant increases in the mRNA and protein expression of HSF1 compared with the control group (P<0.05). The siHSF1 group had significantly reduced mRNA and protein expression of HSF1 compared with the siHSF1-NC group (P<0.05). The knockdown of HSF1 increased airway wall thickness, airway hyperresponsiveness, OVA-specific IgE content, and the number of eosinophils (P<0.05). Compared with the siHSF1-NC group, the siHSF1 group had significantly increased levels of IL-4, IL-5, and IL-13 and significantly reduced expression of IFN-γ in lung tissues and BALF (P<0.05), as well as significantly increased expression of HMGB1 and p-JNK (P<0.05).</p><p><b>CONCLUSIONS</b>Knockdown of HSF1 aggravates airway hyperresponsiveness and airway inflammation in asthmatic mice, and its possible mechanism may involve the negative regulation of HMGB1 and JNK.</p>

A novel HSF4 mutation in a Chinese family with autosomal dominant congenital cataract / 华中科技大学学报（医学）（英德文版）

This study was aimed to identify the mutation of the whole coding region of shock transcription factor 4 (HSF4) gene in a Chinese family with autosomal dominant congenital cataract (ADCC). All exons of HSF4 were amplified by PCR. Sequence analysis of PCR products was performed. Restriction fragment length polymorphism (RFLP) analysis was conducted to confirm the pathogenic mutation. The results showed that a C to T substitution occurred at nucleotide 331 in patients of this family, leading to the replacement of the amino acid arginine-111 with cysteine in exon 3. RFLP analysis showed that the amino acid change was co-segregated with all affected individuals. It was concluded that the new mutation of c.331C>T in HSF4 DNA may be responsible for the autosomal dominant congenital cataract in this family.

Exercise preconditioning attenuates pressure overload-induced pathological cardiac hypertrophy: potential role of HSF1 and NF-κB p65 signaling / 中华心血管病杂志

<p><b>OBJECTIVE</b>To observe the effect of exercise preconditioning (EP) on pressure overload-induced pathological cardiac hypertrophy and explore related mechanisms.</p><p><b>METHODS</b>Ten-week-old male Sprague-Dawley rats (n = 80) were randomly divided into four groups via random number table method: sham, TAC, EP + sham and EP + TAC. Two EP groups were subjected to 4 weeks of treadmill training, and followed by sham and TAC operations. Eight weeks after the surgery, mean arterial pressure (MAP), cardiac morphology, mRNA expressions of the B-type natriuretic peptide (BNP) and heat shock protein (HSP) 70 and protein expression of the BNP, heat shock transcription factor 1 (HSF1), HSP70, nuclear factor κB (NF-κB) p65, and interleukin-2 (IL-2) were examined.</p><p><b>RESULTS</b>(1) Pathological cardiac hypertrophy index: eight weeks after TAC, MAP, heart size, HW/BW, cross-sectional area of the cardiomyocytes (CSA) and mRNA and protein expressions of BNP in the LV were all significantly higher in the TAC and EP + TAC groups than respective sham groups (all P < 0.05). HW/BW, CSA, and mRNA and protein expressions of BNP in the LV were significantly lower in EP + TAC group than in TAC group (all P < 0.05). (2) mRNA and protein expressions of HSF1 and HSP70 and nuclear HSF1 levels were significantly downregulated post TAC, however, EP treatment significantly increased the expression of HSF1 and nuclear HSF1 levels in TAC rats (all P < 0.05). (3) mRNA and protein expressions of NF-κB p65 and IL-2 were significantly increased in the TAC and EP + TAC groups compared with the respective sham groups (all P < 0.05), which were significantly downregulated in EP + TAC group compared to TAC group (all P < 0.05).</p><p><b>CONCLUSIONS</b>EP could effectively reduce the cardiac hypertrophic responses induced by TAC possibly through upregulating the expressions of HSF1 and HSP70 and inhibiting the expression of NF-κB p65 and its nuclear translocation.</p>

Advances in research of heat shock factor 1 and its relation with expression of heat shock protein / 中华烧伤杂志

This article reviews the advances in the research of the structural characteristics and the activating process of heat shock factor 1 (HSF-1), the factors that influence the expression of HSF-1, and the relationship between HSF-1 and the expression levels of NF-κB and heat shock protein (HSP). The expression of HSF-1 could be regulated in several stages in the course of interconversion between its active and inactive status. Unusual expression of HSF-1 mediated by NF-κB can lead to the quantitative and functional change of HSP. The quantitative and functional variation of HSP caused by regulation of HSF-1 could influence the normal synthesis and the pathological changes induced by excessive synthesis of protective proteins in cells under stress. We expect that further research would help elucidate novel pathways about the genesis and evolution mechanism of keloid, and it may finally help to find a novel strategy in the treatment of keloid.

Effects of human HSF1 on transcriptional regulation of prohibitin promoter / 中国应用生理学杂志

<p><b>AIM</b>To assay the transcriptional regulation effect of hHSF1 on prohibitin gene promoter.</p><p><b>METHODS</b>The total length of hHSF1 exon was amplified by PCR method and cloned into pcDNA3. 1(+) vector. pcDNA3. 1(+)-hHSF1 and pGI3 prohibitin were co-transfected into HEK293 cells. The luciferase activity was detected by Dual-Luciferase Reporter Assay System to evaluate the transcriptional regulation effect of hHSF1 on prohibitin gene promoter.</p><p><b>RESULTS</b>The pcDNA3.1(+)-hHSF1 vector was constructed successfully. The assay of luciferase activity showed that the transcription of pGL3-prohibitin was dramatically upregulated by hHSF1.</p><p><b>CONCLUSION</b>hHSF1 can transcriptionally regulate prohibitin expression.</p>

Expression of heat-shock transcription factor 1 and X-linked inhibitor of apoptosis protein-associated factor-1 in gastrointestinal cancer / 南方医科大学学报

<p><b>OBJECTIVE</b>To investigate the expressions of X-linked inhibitor of apoptosis protein (XIAP)-associated factor-1 (XAFI) and heat-shock transcription factor 1 (HSF1) and their relationship in human gastrointestinal cancers.</p><p><b>METHODS</b>Immunoblotting was used to analyze the expressions of HSF1 and XAF1 in gastric and colon cancer tissues and in gastrointestinal cancer cells. The gastrointestinal cancer cells were tranfected with a eukaryotic expression vector containing HSF1 gene fragment or subjected to RNA interference to induce up- or down-regulation of HSF1 expression, and the consequence changes in XAF1 expression in the cells was measured. XAF1 expression was also assayed in the cells after stress stimulation for HSF1 expression.</p><p><b>RESULTS</b>The expression of HSF1 was higher in gastrointestinal cancer tissues than in normal tissues. The expression of XAF1 and HSF1 was inversely correlated in the cancer cell lines, and stress stimuli of the cells up-regulated the expression of HSF1 but down-regulated XAF1 expression.</p><p><b>CONCLUSION</b>HSF1 expression is increased in gastrointestinal cancer tissues to result in suppressed expression of XAF1, which may be one of the reasons for the low expression of XAF1 in association with the defect of the apoptosis mechanisms in the cancer cells</p>

Influence of heat shock factor 1 gene transfection on the expression of inflammatory mediators in macrophages induced by burn serum / 中华烧伤杂志

<p><b>OBJECTIVE</b>To investigate the influence of heat shock factor1 (HSF1) on gene expression of inflammatory mediators in RAW264.7 murine macrophage cells induced by burn serum.</p><p><b>METHODS</b>Sera were separated from blood of normal rats and rats with severe burns, and the recombinant vector pcDNA3. 1/HSF1 was constructed. RAW264.7 macrophages were divided into non-transfection group, vacant vector group (with burn and normal sera stimulation, respectively after vacant vector transfection) and recombinant vector group (with burn and normal sera stimulation, respectively after recombinant vector transfection). Some recombinant vector transfected macrophages without serum stimulation were prepared for the determination of HSF 1 expression with Western blotting. The mRNA expressions of TNF-alpha, HMGB 1 and IL-10 were determined with RT-PCR.</p><p><b>RESULTS</b>The cell line attained after recombinant vector transfection was comparatively stable,with partial activation of HSF 1. Burn sera markedly upregulated TNF-alpha, HMGB1 mRNA expression (0.910 +/- 0.100, 0.860 +/- 0.020, respectively), but downregulated IL-10 expression (0.430 +/- 0.010, respectively) in normal macrophages, while these genes maintained in a very low level in normal macrophages with normal serum stimulation . macrophages with recombinant vector transfection and burn serum stimulation could obviously inhibit the expression of TNF-alpha and HMGB 1, but enhance the IL-10 gene expression (0.130 +/- 0.100, 0.450 +/- 0.020 , 0.450 +/- 0.020, respectively )when compared with that with vacant vector transfection and burn serum stimulation (0.800 +/- 0.050, 0.880 +/- 0.030, 0.420 +/- 0.010, respectively).</p><p><b>CONCLUSION</b>HSF1 can inhibit the expression of some pro-inflammatory mediators in macrophages after a severe burns, indicating that appropriate upregulation of anti-inflammatory mediators might exert protective effects on the organism.</p>

Expression of HSF1 and XAF1 in gastro-intestinal cancer / 南方医科大学学报

<p><b>OBJECTIVE</b>X-linked inhibitor of apoptosis protein (XIAP) To gastrointestinal (GI) investigate the expression of XAF1 and heat-shock transcription factors 1 èHSF1éand their relationship in human gastrointestinal cancers.</p><p><b>METHODS</b>Immunoblotting was used to analyze the expression of HSF1 and XAF1 in either gastric or colon cancer tissue and GI cancer cell line. Transient expression of the HSF1-containing vector in GI cell lines and RNA interference were used to up/down-regulae the expression of the HSF1, and the subsequent expression of XAF1 was measured.</p><p><b>RESULTS</b>The expression of HSF1 was higher in GI cancers than in normal tissues. The expression of XAF1 and HSF1 was negatively correlated in GI cancer cell lines. Stress stimuli up-regulated the expression of HSF1 while the alteration of XAF1 expression was negatively correlated with HSF1 expression.</p><p><b>CONCLUSION</b>The high expression of HSF1 in GI cancers is associated with suppressed expression of XAF1, which can be one of the mechanisms for low-expression of XAF1 and insufficient apoptosis in GI cancers.</p>

HSF1 inhibits heat stress-induced apoptosis in Raw264.7 macrophages / 中南大学学报(医学版)

OBJECTIVE@#To observe the effect of heat shock factor 1 (HSF1) on heat stress-induced apoptosis in Raw264.7 macrophages.@*METHODS@#Raw264.7 cells transfected with pcDNA3.1 and pcDNA3.1-HSF1 were exposed to heat stress (42.5 degrees C +/- 0.5 degrees C) for 1 h and recovered at 37 degrees C for 6, 9, 12, and 24 h respectively. Flow cytometry (FCM), Hoechst 33258 staining and DNA ladder assays were performed to assess the apoptosis.@*RESULTS@#After heat stress, FCM showed that apoptotic cells were increased significantly and reached the peak at 9 h in Raw 264.7 cells transfected with pcDNA3.1, and were characterized with classical morphologic changes including apoptotic body and nuclear condensation. Agarose gel electrophoresis showed that "DNA ladder" could be observed clearly at 6, 9, and 12 h after the heat stress. But the overexpression of HSF1 could reduce the number of apoptotic cells and inhibit DNA fragmentation.@*CONCLUSION@#HSF1 can inhibit heat stress-induced apoptosis in Raw264.7 macrophages.

Screen of inflammatory genes regulated by heat shock factor 1 and corroboration with SOCS3 gene / 中南大学学报(医学版)

OBJECTIVE@#To screen the inflammatory mediators genes regulated by HSF1, and explore the mechanism of downstream genes regulated by HSF1.@*METHODS@#HSF-/- and HSF1+/+ mice were injected with 15 mg/kg LPS intraperitoneally (ip), respectively, and were treated as previous after HSR. The total RNA of lung tissues were extracted and filtrated by SuperArray gene Microarry. The promoter of candidate genes were analyzed by transcription element search software to search for heat shock element (HSE). Select the suppressor of cytokine signaling 3 (SOCS3) with HSE. Macrophage cells were stimulated with 400 ng/mL LPS, and were treated as previous after HSR, then the total RNA was extracted respectively. RT-PCR and northern blot assay were performed to detect the expression levels of SOCS3 mRNA.@*RESULTS@#Fifteen genes were repressed by HSF1, including 9 genes with complete HSE. Eleven genes were accelerated by HSF1 possibly, including 8 genes with complete HSE. The promoter of SOCS3 gene contained one complete HSE. LPS stimulation obviously increased the levels of SOCS3 mRNA in macrophages of RAW264.7 mice, which was inhibited by HSR and over-expression of HSF1.@*CONCLUSION@#HSR or HSF1 inhibits LPS induced expression of SOCS3 mRNA; HSF1 might inhibit LPS-induced expression of SOCS3 mRNA by binding to HSE in the promoter of SOCS3 gene.

Immortalization of embryonic fibroblasts in heat shock transcription factor 1 knockout mouse / 中南大学学报(医学版)

OBJECTIVE@#To establish immortalized embryonic fibroblast lines in heat shock transcription factor 1 (HSF1) HSF1-/- and HSF1+/+ mice and to provide experimental models to study the function of HSF1.@*METHODS@#A mammalian expression vector (pSV3neo) containing the SV40 large T antigen was used to transfect the HSF1-/- and HSF1+/+ mouse embryonic fibroblast using Lipofectamine 2000. Colonies were screened by G418 and expanded to immortalized cell lines. PCR was used to detect the integration of the large T antigen with genome in the mouse embryonic fibroblast. Expression of SV40 large T antigen gene in expanded cells was identified by RT-PCR. HSP70 expression was examined by Western blot in the embryonic fibroblast lines.@*RESULTS@#The stable growth and serial propagation were observed in the HSF1-/- and HSF1+/+ cell lines for six months. The mRNA of SV40 T antigen gene expressed in the two cell lines. HSP70 expression could not be induced in the heat-treated HSF1-/- mouse embryo fibroblasts.@*CONCLUSION@#The immortalized cells of HSF1+/+ and HSF1-/- mouse embryo fibroblasts are successfully established.

The relationship between the polymerization of HSF1 and the expression of IL-1beta, TNF-alpha mRNA of monocytes in fever rabbits / 中国应用生理学杂志

<p><b>AIM</b>For further investigating of heat shock transcription factor 1 (HSF1) action in thermoregulation and its physiological mechanism.</p><p><b>METHODS</b>The relationship among the expression of HSF1 and interleukin 1beta (IL-1beta) mRNA and tumor necrosis factor alpha (TNF-alpha) mRNA in monocytes was studied during the different fever stages in rabbit fever model induced by LPS. The expressions of IL-1beta and TNF-alpha mRNA were measured by RT-PCR assay; HSF1 expression was measured by Western blot.</p><p><b>RESULTS</b>(1) Intravenous injection of LPS produced a double-peak temperature arisen at 60 min and 180 min. (2) The expression of IL-1beta mRNA in monocytes had a peak at 160 min, while the peak of TNF-alpha mRNA expression occurred at 80 min after intravenous injection of LPS. (3) The content of the HSF1 trimer increased gradually after 160 min intravenous injection of LPS. The results indicated that the content of the HSF1 trimer was negative correlation with the expressions of IL-1beta mRNA and TNF-alpha mRNA, and the change in body temperature was a positive correlation with IL-1beta mRNA.</p><p><b>CONCLUSION</b>It is possible that HSF1 limits the rise in body temperature by repressing the gene expressions of the endogenous pyrogen, IL-1beta and TNF-alpha.</p>

Expression of novel environmental responsive protein JWA involved in the oxidative stress responsiveness in MCF-7 cells / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To study the expression and the possible role of JWA protein in oxidative stress-induced damage of MCF-7 cells, especially the relationship between JWA and heat shock proteins (HSPs).</p><p><b>METHODS</b>MCF-7 cells were exposed to different concentration of H(2)O(2) (0.01,0.10, 1.00 mmol/L) for different time (10, 30, 60 and 180 min) respectively. DNA damage was detected by using DNA gel electrophoresis. The MTT assay was used to analyze the effect of H(2)O(2) on the cytotoxicity and relative cell proliferation ratio of the cells. The expressions of JWA, HSP70, HSP27 and HSF1 were determined by Western-blot.</p><p><b>RESULTS</b>The inhibitory effect on MCF-7 cells viability induced by H(2)O(2) was shown a dose-and time-dependent manner and MCF-7 cells proliferation, and was almost completely inhibited by the exposure of H(2)O(2) at 1.00 mmol/L for 180 min. Hydrogen peroxide treatment of MCF-7 cells caused oxidative stress which up-regulated the expressions of JWA, HSP70 and heat shock factor 1 (HSF1) in a dose-dependent manner, and the expression pattern of JWA was very similar to those of HSP70 and HSF1 but not to HSP27.</p><p><b>CONCLUSION</b>JWA might enhance intracellular defenses against H(2)O(2)-induced oxidative damage in human breast carcinoma cells. JWA is determined functioning as an effective environmental responsive protein and as a parallel molecule of HSP70 actively participates in the signal pathways of oxidative damage which might be regulated by HSF1.</p>

Effects of hsf1 genotype on the constitutive expression of alphaB-crystallin in mice myocardium / 中国应用生理学杂志

<p><b>AIM</b>Try to clarify the effects of HSF1 gene on the constitutively expressed alphaBC.</p><p><b>METHODS</b>To investigate the levels of constitutively expressed alphaB-Crystallin (alphaBC) in hsf1 knockout (hsf1 -/-) and hsf1 wild type (hsf1 +/+) mice myocardium by Western blot and immunohistochemistry.</p><p><b>RESULTS</b>The alphaBC levels in hsf1 -/- and hsf1 +/+ were 68.42% +/- 4.16%, 100% +/- 7.58%, respectively (P < 0.05, cytosolic fraction), and 20.53% +/- 1.01%, 37.55% +/- 1.91%, respectively (P < 0.05, pellet fraction). The alphaBC signals decreased significantly in hsf1 -/- myocardium compared with hsf1 +/+ myocardium stained with fluorescence immunohistochemistry.</p><p><b>CONCLUSION</b>hsf1 is the important, but not the only factor, which mediates the constitutively expressed alphaBC.</p>

Induction of HSF1 expression and sporadic colorectal cancer / 浙江大学学报·医学版

<p><b>OBJECTIVE</b>To explore the activation of the signal transduction pathways related with the carcinogenesis of sporadic colon cancers.</p><p><b>METHODS</b>A gene microarray monitoring activation of 8 signal transduction pathways (PathwayFinder GEArray) was used to screen the differentially expressed genes between colorectal cancer and normal colon tissue. The differentially expressed genes were further analyzed by RT-PCR, using RNA extracted from cancer tissue and matched normal colon mucosa of 35 patients with colorectal cancer.</p><p><b>RESULTS</b>The expression of hsf1, hsf27 and inos was increased in colon cancer compared with normal colon mucosa using PathwayFinder GEArray. The RT-PCR results showed that the expression of hsf1 was detected in 86% of patients(30/35)and the expression of inos detected in 63% patients(22/35).</p><p><b>CONCLUSION</b>Hsf1 induces heat shock stress signaling pathway, which might play a role in the carcinogenesis of sporadic colorectal cancer.</p>

Expressions of JWA protein and heat stress protein 70 induced by cell differentiation inducers combined with heat stress in K562 cells / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To study how the combined effects of various differentiation inducers and heat stress on the expression of JWA protein in K562 cell, the relationship between JWA and Hsp70 expression, and the signal regulation mechanism possibly involved.</p><p><b>METHODS</b>The experimental model was established in K562 cells. Various directional differentiation inducers (TPA, Ara-C, hemin, adriamycin, ATRA and As(2)O(3)) were used alone or combined with heat shock treatment (42 degrees C, 2 h). Western blot was used for detecting expressions of JWA, Hsp70, heat stress factor 1 (HSF1) and HSF2.</p><p><b>RESULTS</b>(1) The expressions of both JWA protein and Hsp70 were significantly up-regulated after K562 cells treated by TPA (100, 200 ng/ml) or adriamycin (4 x 10(-8) mol/L) 48 h, and followed by heat shock (42 degrees C, 2 h). However, the opposite effects were observed when the cells treated by hemin (3 x 10(-5) mol/L, 48 h), Ara-C (80 ng/ml, 48 h) and As(2)O(3) (1 x 10(-6) mol/L, 48 h) followed by 2 h heat shock. No obvious changes were found when the cells treated by ATRA (1 x 10(-6) mol/L, 48 h) alone or followed by heat shock. (2) Both the heat shock transcriptional factors HSF1 and HSF2 did not show any significant changes when K562 cells were treated with various differentiation inducers and followed by heat stress.</p><p><b>CONCLUSION</b>JWA not only takes part in the regulation of K562 cellular differentiation, but also of heat stress, it might be the co-target gene of several differentiation inducers and heat stress. The expression of Hsp70 seems not mediated by both HSF1 and HSF2 in K562 cells undergoing directional differentiation or heat stress treatment. JWA is likely to be a new signal molecule similar to Hsp70 signal pathways. The results show that JWA takes part in the mechanism of K562 cell response to heat stress.</p>