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Hui Wang - One of the best experts on this subject based on the ideXlab platform.
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modulation of heat shock response is associated with di 2 ethylhexyl phthalate dehp induced cardiotoxicity in quail coturnix japonica
Chemosphere, 2019Co-Authors: Hui Wang, Wei LiuAbstract:Abstract Di(2-ethylhexyl) phthalate (DEHP) is an omnipresent environmental pollutant with endocrine disrupting properties. As a plasticizer, DEHP can be leach from the plastic to transfer the external environment and thus enters the animal food chain, causing serious damage to the animal organs. The heat-shock response (HSR) comprising heat-shock protein (HSPs) and heat-shock transcription factor (HSFs) plays a pivotal role in various toxic stress conditions. For the sake of investigating the effects of DEHP exposure on cardiac toxicity and the regulation of HSR, male quail were fed the diet with 0, 250, 500 and 750 mg/kg DEHP by gavage administration for 45 days. Histopathological changes including cardiomyocyte swelling and muscle fiber dilatation were observed in the hearts exposed to DEHP. During the DEHP treatment, the mRNA expression of HSP60 and HSP70 were universally reduced, while the expression of other HSPs (HSP10, HSP25, HSP27, HSP40, HSP47, HSP90, HSP110) had different degrees of growth. In addition, the levels of HSF1, HSF2, and HSF3 were significantly increased. Given the facts above, DEHP exposure induced the toxic effects of quail heart. DEHP exposure did great harm to HSR via affecting the synthesis of HSFs to mediate the transcription of the HSPs. Ultimately, this study provided new evidence that DEHP-induced cardiotoxicity in quail was related to activation of HSR and playing a protective role.
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di 2 ethyl hexyl phthalate dehp induced kidney injury in quail coturnix japonica via inhibiting hsf1 hsf3 dependent heat shock response
Chemosphere, 2018Co-Authors: Hui WangAbstract:Abstract Di (2-ethyl hexyl) phthalate (DEHP) as a plasticizer can leach away from the plastic and hence entrances into the animal food chain which caused serious hazard in organs of animals, but there are few studies on DEHP kidney toxicity. The heat-shock response (HSR) consisting of the HSPs and HSFs plays an important role in various toxicity stress conditions. To investigate the influence on kidney toxicity and the modulation of HSR during DEHP exposure, female quail were fed the diet with 0, 250, 500 and 750 mg/kg DEHP by gavage administration for 45 days. The shrinkages of glomeruli and dilation of kidney tubule epithelia cells were observed in the kidney of DEHP-exposed quail. DEHP treatment could significantly decrease the expressions of HSP25, HSP27, HSP47, HSP60, while the expressions of HSP10, HSP40, HSP70, HSP90, HSP110 were upregulated in the kidney. In addition, the expression levels of HSF1 and HSF3 were significantly increased under DEHP. This is the first study to demonstrate quail exposure to DEHP is in fact detrimental to bird kidney. Besides, DEHP could attack HSR by affecting the synthesis of HSFs to mediate the transcription of the HSPs resulting in kidney damage.
Wei Liu - One of the best experts on this subject based on the ideXlab platform.
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modulation of heat shock response is associated with di 2 ethylhexyl phthalate dehp induced cardiotoxicity in quail coturnix japonica
Chemosphere, 2019Co-Authors: Hui Wang, Wei LiuAbstract:Abstract Di(2-ethylhexyl) phthalate (DEHP) is an omnipresent environmental pollutant with endocrine disrupting properties. As a plasticizer, DEHP can be leach from the plastic to transfer the external environment and thus enters the animal food chain, causing serious damage to the animal organs. The heat-shock response (HSR) comprising heat-shock protein (HSPs) and heat-shock transcription factor (HSFs) plays a pivotal role in various toxic stress conditions. For the sake of investigating the effects of DEHP exposure on cardiac toxicity and the regulation of HSR, male quail were fed the diet with 0, 250, 500 and 750 mg/kg DEHP by gavage administration for 45 days. Histopathological changes including cardiomyocyte swelling and muscle fiber dilatation were observed in the hearts exposed to DEHP. During the DEHP treatment, the mRNA expression of HSP60 and HSP70 were universally reduced, while the expression of other HSPs (HSP10, HSP25, HSP27, HSP40, HSP47, HSP90, HSP110) had different degrees of growth. In addition, the levels of HSF1, HSF2, and HSF3 were significantly increased. Given the facts above, DEHP exposure induced the toxic effects of quail heart. DEHP exposure did great harm to HSR via affecting the synthesis of HSFs to mediate the transcription of the HSPs. Ultimately, this study provided new evidence that DEHP-induced cardiotoxicity in quail was related to activation of HSR and playing a protective role.
Yuzhu Zuo - One of the best experts on this subject based on the ideXlab platform.
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di 2 ethylhexyl phthalate dehp induced hepatotoxicity in quail coturnix japonica via suppression of the heat shock response
Chemosphere, 2019Co-Authors: Yi Zhao, Jinghui Fan, Yu Luo, Milton Talukder, Yuzhu ZuoAbstract:Di-(2-ethylhexyl) phthalate (DEHP) is a widespread environmental toxicant that severely impacts agricultural production and animal and human health. Nevertheless, DEHP-induced hepatotoxicity at the molecular level in quail remains unexplored. The heat shock response (HSR), involving heat shock proteins (HSPs) and heat shock transcription factors (HSFs), is a highly conserved molecular response that is triggered by stressors, especially exposure to toxicants. To explore the DEHP-induced hepatotoxicity that occurs via regulation of HSR in birds, female quail were dosed with DEHP by oral gavage (0, 250, 500 and 1000 mg/kg) for 45 days. Based on histopathological analysis, the livers of the DEHP-treated groups exhibited structural alterations of hepatocytes, including mitochondrial swelling, derangement of hepatic plates, inflammatory cell infiltration and adipose degeneration. Ultrastructural evaluation of the livers of DEHP-treated quail revealed swollen mitochondria, partial disappearance of mitochondrial membranes and cristae, nuclear chromatin margination and nuclear condensation. The expression of HSF1 and HSF3 significantly decreased after DEHP exposure. The levels of HSPs (HSP10, HSP25, HSP27, HSP40, HSP47, HSP60, HSP70 and HSP90) were significantly downregulated in the livers of DEHP-treated quail. In this study, we concluded that DEHP exposure resulted in liver function damage and hepatotoxicity by reducing the expression of HSFs and HSPs in quail liver, which inhibited the protective effect of the HSR signaling pathway.
Aibin Zhan - One of the best experts on this subject based on the ideXlab platform.
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genome wide identification characterization and expression analyses of heat shock protein related genes in a highly invasive ascidian ciona savignyi
Frontiers in Physiology, 2018Co-Authors: Xuena Huang, Shiguo Li, Aibin ZhanAbstract:Biological response to rapid changing environments is an outstanding research question in ecology and evolution. Biological invasions provide excellent “natural” experiments to study such a complex response process, as invaders often encounter rapidly changing environments during biological invasions. The regulation of heat shock proteins (Hsp) is a common pathway responsible for various environmental stresses; however, the comprehensive study on Hsp system across the whole genome and potential roles in determining invasion success are still largely unexplored. Here we used a marine invasive model ascidian, Ciona savignyi, to investigate transcriptional response of heat shock protein-related genes to harsh environments. We identified 31 genes, including three Hsp20, six Hsp40, 10 HSP60, seven Hsp70, three Hsp90, one Hsp100 and one heat shock transcription factor (Hsf), acorss the whole genome of Ciona savignyi. We characterized gene structure and protein motifs, and identified potential heat shock elements (HSE) in promoters of Hsp genes. The expression analysis showed that most Hsp genes, but not all, were involved in transcriptional response to temperature and salinity changes in a time and stress-specific pattern, and the maximum amplitude of induction occurred in Hsp70-4 after 1-hour of high temperature treatment. However, the Hsf gene was scarcely induced and limited interactions were predicted between Hsp and Hsf genes. Our study provide the first systematic genome-wide analysis of Hsp and Hsf family in the marine invasive model ascidian, and Our results are expected to dissect heat shock protein-based molecular mechanisms responsible for extreme environmental adaptation using Ciona as a model system.
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Genome-Wide Identification, Characterization and Expression Analyses of Heat Shock Protein-Related Genes in a Highly Invasive Ascidian Ciona savignyi
Frontiers Media S.A., 2018Co-Authors: Aibin Zhan, Xuena Huang, Yangchun GaoAbstract:Biological response to rapid changing environments is an outstanding research question in ecology and evolution. Biological invasions provide excellent “natural” experiments to study such a complex response process, as invaders often encounter rapidly changing environments during biological invasions. The regulation of heat shock proteins (Hsp) is a common pathway responsible for various environmental stresses; however, the comprehensive study on Hsp system across the whole genome and potential roles in determining invasion success are still largely unexplored. Here, we used a marine invasive model ascidian, Ciona savignyi, to investigate transcriptional response of Hsp-related genes to harsh environments. We identified 32 genes, including three Hsp20, six Hsp40, ten HSP60, eight Hsp70, three Hsp90, one Hsp100, and one heat shock transcription factor (Hsf), across the whole genome of C. savignyi. We further characterized gene structure and protein motifs, and identified potential heat shock elements (HSEs) in promoters of Hsp genes. The expression analysis showed that most Hsp genes, but not all, were involved in transcriptional response to temperature and salinity challenges in a duration- and stress-specific pattern, and the maximum amplitude of induction occurred in Hsp70-4 after 1-h of high temperature treatment. However, the Hsf gene was scarcely induced and limited interactions were predicted between Hsp and Hsf genes. Our study provide the first systematic genome-wide analysis of Hsp and Hsf family in the marine invasive model ascidian, and our results are expected to dissect Hsp-based molecular mechanisms responsible for extreme environmental adaptation using Ciona as a model system
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Data_Sheet_1_Genome-Wide Identification, Characterization and Expression Analyses of Heat Shock Protein-Related Genes in a Highly Invasive Ascidian Ciona savignyi.PDF
2018Co-Authors: Xuena Huang, Yangchun Gao, Aibin ZhanAbstract:Biological response to rapid changing environments is an outstanding research question in ecology and evolution. Biological invasions provide excellent “natural” experiments to study such a complex response process, as invaders often encounter rapidly changing environments during biological invasions. The regulation of heat shock proteins (Hsp) is a common pathway responsible for various environmental stresses; however, the comprehensive study on Hsp system across the whole genome and potential roles in determining invasion success are still largely unexplored. Here, we used a marine invasive model ascidian, Ciona savignyi, to investigate transcriptional response of Hsp-related genes to harsh environments. We identified 32 genes, including three Hsp20, six Hsp40, ten HSP60, eight Hsp70, three Hsp90, one Hsp100, and one heat shock transcription factor (Hsf), across the whole genome of C. savignyi. We further characterized gene structure and protein motifs, and identified potential heat shock elements (HSEs) in promoters of Hsp genes. The expression analysis showed that most Hsp genes, but not all, were involved in transcriptional response to temperature and salinity challenges in a duration- and stress-specific pattern, and the maximum amplitude of induction occurred in Hsp70-4 after 1-h of high temperature treatment. However, the Hsf gene was scarcely induced and limited interactions were predicted between Hsp and Hsf genes. Our study provide the first systematic genome-wide analysis of Hsp and Hsf family in the marine invasive model ascidian, and our results are expected to dissect Hsp-based molecular mechanisms responsible for extreme environmental adaptation using Ciona as a model system.
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Table_1_Genome-Wide Identification, Characterization and Expression Analyses of Heat Shock Protein-Related Genes in a Highly Invasive Ascidian Ciona savignyi.XLS
2018Co-Authors: Xuena Huang, Yangchun Gao, Aibin ZhanAbstract:Biological response to rapid changing environments is an outstanding research question in ecology and evolution. Biological invasions provide excellent “natural” experiments to study such a complex response process, as invaders often encounter rapidly changing environments during biological invasions. The regulation of heat shock proteins (Hsp) is a common pathway responsible for various environmental stresses; however, the comprehensive study on Hsp system across the whole genome and potential roles in determining invasion success are still largely unexplored. Here, we used a marine invasive model ascidian, Ciona savignyi, to investigate transcriptional response of Hsp-related genes to harsh environments. We identified 32 genes, including three Hsp20, six Hsp40, ten HSP60, eight Hsp70, three Hsp90, one Hsp100, and one heat shock transcription factor (Hsf), across the whole genome of C. savignyi. We further characterized gene structure and protein motifs, and identified potential heat shock elements (HSEs) in promoters of Hsp genes. The expression analysis showed that most Hsp genes, but not all, were involved in transcriptional response to temperature and salinity challenges in a duration- and stress-specific pattern, and the maximum amplitude of induction occurred in Hsp70-4 after 1-h of high temperature treatment. However, the Hsf gene was scarcely induced and limited interactions were predicted between Hsp and Hsf genes. Our study provide the first systematic genome-wide analysis of Hsp and Hsf family in the marine invasive model ascidian, and our results are expected to dissect Hsp-based molecular mechanisms responsible for extreme environmental adaptation using Ciona as a model system.
Francesco Cappello - One of the best experts on this subject based on the ideXlab platform.
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expression of heat shock proteins in chronic obstructive pulmonary disease vernal keratoconjunctivitis and ulcerative colitis
European Respiratory Journal, 2013Co-Authors: Paola Brun, Andrea Leonardi, Elena Tarricone, Davide Vallese, Bruno Balbi, Francesco Cappello, Antonino Di StefanoAbstract:Background and Aim : Inflammatory response in different organs share many similarities, but site-specific signs. The aim of the study was to compare heat shock proteins (HSPs) levels and expression in chronic obstructive pulmonary disease (COPD) to other inflammatory states, such as vernal keratoconjunctivitis (VKC), a recurrent ocular inflammatory disease, and ulcerative colitis (UC), an inflammatory bowel disease in which autoimune aggression may have a pathogenetic role. Methods: We examined bronchial mucosal biopsies from COPD patients, conjunctival biopsies from VKC patients, and colon mucosa biopsies from patients with UC; age-matched controls were selected for each group. We evaluated levels (by immunohistochemistry) and expression (by RT-PCR) of Hsp10, Hsp27, Hsp40, HSP60, Hsp70, Hsp90, and the main heat shock transcription factor HSF-1 and pHSF-1. RESULTS: Hsp10 levels and expression increased in all pathological conditions, Hsp27 in VKC, Hsp40 in COPD and VKC, HSP60 in COPD and UC, Hsp70 in UC and Hsp90 in VKC and UC, compared to controls. pHSF-1+ cells were significantly increased in COPD compared to controls, while was unaltered in VKC. All pathological tissues showed increased levels of macrophages (CD68) in lamina propria; COPD tissues were also all positive for neutrophils and VKC for eosinophils markers. Finally, HSP60 co-localize with elastase positive cells in COPD and with CD68 positive cells in UC. CONCLUSION: These results indicate that Hsps levels and expression change during these different inflammatory states. Further studies will prove the HSPs active involvement in triggering and/or maintaining of this inflammatory status.
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heat shock proteins levels and expression in chronic obstructive pulmonary disease and vernal keratoconjunctivitis
Italian journal of anatomy and embryology, 2013Co-Authors: Paola Brun, Elena Tarricone, Davide Vallese, Bruno Balbi, Francesco Cappello, Antonino Di Stefano, Simona Corrao, Andrea LeonardiAbstract:Inflammatory response in different organs share many similarities, but site-specific signs. Symptoms can be related to mucosal structure changes. The aim of the study was to compare heat shock proteins (HSPs) levels and expression in chronic obstructive pulmonary disease (COPD) to other inflammatory status of mucosa, such as vernal keratoconjunctivitis (VKC), a recurrent ocular inflammatory disease in which autoimune aggression may have a pathogenetic role. We examined bronchial mucosal biopsies from COPD patients (moderate to severe stage) and conjunctival biopsies from VKC patients; age-matched controls were selected for each group. We evaluated levels (by immunohistochemistry) and expression (by RT-PCR) of a panel of HSPs, among which Hsp10, Hsp27, Hsp40, HSP60, Hsp70, Hsp90, and of the main heat shock transcription factor (both HSF-1 and pHSF-1). Hsp10 levels and expression increased in all pathological conditions, Hsp27 in VKC, Hsp40 in COPD and VKC, HSP60 in COPD, Hsp70 and Hsp90 in VKC, as compared to their appropriate controls. Transcription factor pHSF-1 positive cells were significantly increased in COPD compared to controls, while was unaltered in VKC. Moreover, all pathological tissues showed increased levels of macrophages (CD68 positive) in lamina propria, COPD showed increased levels of neutrophils (elastase positive) and VKC increased levels of eosinophils (EG2 positive). Finally, HSP60 colocalize with elastase positive cells in COPD. These results indicate that HSPs levels and expression change during development of different types of inflammation. Further studies will prove their active involvement and functions in triggering and/or maintaining the inflammatory status.
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convergent sets of data from in vivo and in vitro methods point to an active role of HSP60 in chronic obstructive pulmonary disease pathogenesis
PLOS ONE, 2011Co-Authors: Francesco Cappello, Gaetano Caramori, Claudia Campanella, Chiara Vicari, Isabella Gnemmi, Andrea Zanini, Antonio Spanevello, A Capelli, Giampiero La Rocca, Rita AnzaloneAbstract:Background It is increasingly clear that some heat shock proteins (Hsps) play a role in inflammation. Here, we report results showing participation of HSP60 in the pathogenesis of chronic obstructive pulmonary diseases (COPD), as indicated by data from both in vivo and in vitro analyses. Methods and Results Bronchial biopsies from patients with stable COPD, smoker controls with normal lung function, and non-smoker controls were studied. We quantified by immunohistochemistry levels of Hsp10, Hsp27, Hsp40, HSP60, Hsp70, Hsp90, and HSF-1, along with levels of inflammatory markers. Hsp10, Hsp40, and HSP60 were increased during progression of disease. We found also a positive correlation between the number of neutrophils and HSP60 levels. Double-immunostaining showed that HSP60-positive neutrophils were significantly increased in COPD patients. We then investigated in vitro the effect on HSP60 expression in bronchial epithelial cells (16HBE) caused by oxidative stress, a hallmark of COPD mucosa, which we induced with H2O2. This stressor determined increased levels of HSP60 through a gene up-regulation mechanism involving NFkB-p65. Release of HSP60 in the extracellular medium by the bronchial epithelial cells was also increased after H2O2 treatment in the absence of cell death. Conclusions This is the first report clearly pointing to participation of Hsps, particularly HSP60, in COPD pathogenesis. HSP60 induction by NFkB-p65 and its release by epithelial cells after oxidative stress can have a role in maintaining inflammation, e.g., by stimulating neutrophils activity. The data open new scenarios that might help in designing efficacious anti-inflammatory therapies centered on HSP60 and applicable to COPD.
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the expression of HSP60 and hsp10 in large bowel carcinomas with lymph node metastase
BMC Cancer, 2005Co-Authors: Francesco Cappello, Sabrina David, Francesca Rappa, Felicia Farina, Fabio Bucchieri, L Marasa, Tommaso E Bartolotta, Giovanni ZummoAbstract:The involvement of Heat Shock Proteins (HSP) in cancer development and progression is a widely debated topic. The objective of the present study was to evaluate the presence and expression of HSP60 and HSP10 in a series of large bowel carcinomas and locoregional lymph nodes with and without metastases. 82 Astler and Coller's stage C2 colorectal cancers, of which 48 well-differentiated and 34 poorly-differentiated, were selected along with 661 lymph nodes, including 372 with metastases and 289 with reactive hyperplasia only, from the same tumours. Primitive tumours and both metastatic and reactive lymph nodes were studied; specifically, three different compartments of the lymph nodes, secondary follicle, paracortex and medullary sinus, were also analysed. An immunohistochemical research for HSP60 and HSP10 was performed and the semiquantitative results were analysed by statistical analysis to determine the correlation between HSPs expression and 1) tumour grading; 2) degree of inflammation; 3) number of lymph nodes involved; 4) lymph node compartment hyperplasia. Moreover, western blotting was performed on a smaller group of samples to confirm the immunohistochemical results. Our data show that the expression of HSP60, in both primary tumour and lymph node metastasis, is correlated with the tumoral grade, while the HSP10 expression is not. Nevertheless, the levels of HSP10 are commonly higher than the levels of HSP60. In addition, statistical analyses do not show any correlation between the degree of inflammation and the immunopositivity for both HSP60 and HSP10. Moreover, we find a significant correlation between the presence of lymph node metastases and the positivity for both HSP60 and HSP10. In particular, metastatic lymph nodes show a higher percentage of cells positive for both HSP60 and HSP10 in the secondary follicles, and for HSP10 in the medullary sinuses, when compared with hyperplastic lymph nodes. HSP60 and HSP10 may have diagnostic and prognostic significance in the management of this tumour and their overexpression in tumoral cells may be functionally related to tumoral progression. We hypothesise that their expression in follicular and medullary cells of lymph nodes may be induced by formation of metastases. Further studies based on these observations could lead to a better understanding of the HSPs involvement in colorectal cancer progression, as well as other neoplasms.
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immunohistochemical evaluation of pcna p53 HSP60 hsp10 and muc 2 presence and expression in prostate carcinogenesis
Anticancer Research, 2003Co-Authors: Francesco Cappello, Sabrina David, Francesca Rappa, Rita Anzalone, Giovanni ZummoAbstract:Background The study of the expression of different biological markers in non-neoplastic, pre-neoplastic and neoplastic lesions of prostate could help to better understand their role in carcinogenesis and to find new diagnostic and prognostic tools. Materials and methods In the present work we evaluated, by immunohistochemistry, the presence and the expression of PCNA, p53, HSP60, HSP10 and MUC-2 in a series of nodular hyperplasia, low- and high-grade prostatic intraepithelial lesions and adenocarcinomas. Results Our data confirmed that: 1) PCNA expression could be related to the grade of progression of cancer; and that 2) p53 mutation could be a late event in prostate carcinogenesis. Moreover, we reported that: 1) HPS60 and HPS10 were overexpressed early in prostate carcinogenesis; and that 2) MUC-2 is absent in both tumoral and non-tumoral prostatic tissue. Conclusion We suggest the further examination, by molecular and genetic studies, of the role of HSP60 and HSP10 during carcinogenesis of the prostate as well as of other organs.