The possible role of heat shock factor-1 in the negative regulation of heme oxygenase-1

Chou, Yenn Hwei; Ho, Feng Ming; Liu, Der Zen; Lin, Shyr Yi; Tsai, Li Hsueh; Chen, Chien Ho; Ho, Yuan Soon; Hung, Ling Fang; Liang, Yu Chih

doi:10.1016/j.biocel.2004.08.006

Cited by 22 publications

(13 citation statements)

References 45 publications

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“…In our study, thiopental was the only agent tested to induce the activation of HSF-1, which is responsible for mediating the expression of several but not all heat shock proteins. This observation, which is in accordance with our study, has become evident when overexpression of HSF-1 followed by heat shock experiments revealed that HSF-1 repressed heme oxygenase-1 (hsp32) gene expression by directly binding to the HSE of the heme oxygenase-1 gene promoter (Chou et al, 2005).…”

Section: Discussionsupporting

confidence: 92%

Thiopental Protects Human T Lymphocytes from Apoptosis in Vitro via the Expression of Heat Shock Protein 70

Roesslein¹,

Schibilsky²,

Muller³

et al. 2008

J Pharmacol Exp Ther

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Barbiturates, which are used for the treatment of intracranial hypertension after severe head injury, have been associated with anti-inflammatory side effects. Although all barbiturates inhibit T-cell function, only thiobarbiturates markedly reduce the activation of the transcription factor nuclear factor-B (NF-B). Various pharmacologic inhibitors of the NF-B pathway are concomitant nonthermal inducers of the heat shock response (HSR), a cellular defense system that is associated with protection of cells and organs. We hypothesize that thiopental mediates cytoprotection by inducing the HSR. Human CD3 ϩ T lymphocytes were incubated with thiopental, pentobarbital, etomidate, ketamine, midazolam, or propofol. Human Jurkat T cells were transfected with small interfering RNA (siRNA) targeting heat 70-kDa shock protein (hsp 70) before thiopental incubation. Apoptosis was induced by staurosporine. DNA binding activity of HSF-1 was analyzed by electrophoretic mobility shift assay; mRNA expression of hsp27, -32, -70, and -90 was analyzed by Northern blot, and protein expression of hsp70 was analyzed by Western blot and flow cytometry after fluorescein isothiocyanate (FITC)-hsp70-antibody staining. Apoptosis was assessed by flow cytometry after annexin V-FITC or annexin V-phycoerythrin staining. Activity of caspase-3 was measured by fluorogenic caspase activity assay. Thiopental induced hsp27, -70, and -90 but not hsp32 mRNA expression as well as hsp70 protein expression. Thiopental dose-dependently activated the DNA binding activity of HSF-1, whereas other substances investigated had no effect. In addition, pretreatment with thiopental significantly attenuated staurosporine-induced apoptosis and caspase-like activity. Transfection with hsp70-siRNA before thiopental treatment reduced this attenuation. Thiopental specifically and differentially induces a heat shock response, and it mediates cytoprotection via the expression of hsp70 in human T lymphocytes.

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Section: Discussionsupporting

confidence: 92%

Thiopental Protects Human T Lymphocytes from Apoptosis in Vitro via the Expression of Heat Shock Protein 70

Roesslein¹,

Schibilsky²,

Muller³

et al. 2008

J Pharmacol Exp Ther

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“…Cyclopentenone prostaglandins can activate HSF-1 (Koizumi et al, 1993), a transcription factor playing a key role as both a positive and negative regulator of several genes. In particular, HSF-1 was demonstrated to repress the expression of several proinflammatory genes, such as TNF-␣ and IL-1␤ (Cahill et al, 1996;Singh et al, 2002;Chou et al, 2005). As described previously (Cippitelli et al, 2003) and as confirmed in Fig.…”

Section: D-pgj 2 Inhibited Trail Expression and Promotermentioning

confidence: 52%

Inhibition ofTrailGene Expression by Cyclopentenonic Prostaglandin 15-Deoxy-Δ^12,14-Prostaglandin J₂in T Lymphocytes

et al. 2007

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15-Deoxy-⌬12,14 -prostaglandin J 2 (15d-PGJ 2 ) is a cyclopentenonic prostaglandin endowed with powerful anti-inflammatory activities, as shown in animal models of inflammatory/autoimmune diseases, where pharmacological administration of this prostanoid can ameliorate inflammation and local tissue damage via activation of the nuclear receptor peroxisome proliferator-activated receptor ␥ (PPAR␥) and/or covalent modifications of cellular proteins. Tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) is a member of the TNF superfamily expressed in most of the cells, including those of immune system such as T lymphocytes, in which it is upregulated upon antigen-specific stimulation. This cytokine plays an important role in regulating various physiological and immunopathological processes, such as immunosurveillance of tumors and tissue destruction associated with different inflammatory and autoimmune diseases. Here, we demonstrate that 15d-PGJ 2 inhibits trail mRNA and protein expression by down-regulating the activity of its promoter in human T lymphocytes. Our data indicate that both the chemically reactive cyclopentenone moiety of 15d-PGJ 2 and the activation of PPAR␥ may be involved in this repressive mechanism. We identified nuclear factor B (NF-B) as a direct target of the prostanoid. 15d-PGJ 2 significantly decreases the expression and/or DNA binding of c-rel, RelA, and p50 transcription factors to the NF-B1 site of trail promoter. Moreover, 15d-PGJ 2 -mediated activation of the transcription factor heat shock factor-1 may contribute to inhibit trail promoter activity in transfected Jurkat T cells. These results suggest that modulation of TRAIL gene expression by 15d-PGJ 2 in T cells may provide a novel pharmacological tool to modify the onset and the progression of specific autoimmune and inflammatory disorders.

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“…In fact, Bach1 is broadly expressed in mice and human tissues; in human cells, it is induced by the same stimuli that are able to repress HO-1 gene (5,325). Current hypothesis suggests that HO-1 repression is useful for the cell because it (a) decreases the energy costs necessary for heme degradation, (b) reduces the accumulation of CO and bilirubin, which can become toxic if produced in excess, and (c) increases the intracellular content of heme necessary for the preservation of vital functions such as respiration (5,126,232). Delineation of the diverse roles of HO-1 in brain senescence, aging-related human neurodegenerative disorders, and other CNS conditions has progressed substantially in these last years.…”

Section: Heme Oxygenasesmentioning

confidence: 99%

Cellular Stress Responses, The Hormesis Paradigm, and Vitagenes: Novel Targets for Therapeutic Intervention in Neurodegenerative Disorders

Calabrese

Cornelius

Dinkova‐Kostova

et al. 2010

Antioxidants & Redox Signaling

692

573

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Despite the capacity of chaperones and other homeostatic components to restore folding equilibrium, cells appear poorly adapted for chronic oxidative stress that increases in cancer and in metabolic and neurodegenerative diseases. Modulation of endogenous cellular defense mechanisms represents an innovative approach to therapeutic intervention in diseases causing chronic tissue damage, such as in neurodegeneration. This article introduces the concept of hormesis and its applications to the field of neuroprotection. It is argued that the hormetic dose response provides the central underpinning of neuroprotective responses, providing a framework for explaining the common quantitative features of their dose-response relationships, their mechanistic foundations, and their relationship to the concept of biological plasticity, as well as providing a key insight for improving the accuracy of the therapeutic dose of pharmaceutical agents within the highly heterogeneous human population. This article describes in mechanistic detail how hormetic dose responses are mediated for endogenous cellular defense pathways, including sirtuin and Nrf2 and related pathways that integrate adaptive stress responses in the prevention of neurodegenerative diseases. Particular attention is given to the emerging role of nitric oxide, carbon monoxide, and hydrogen sulfide gases in hormetic-based neuroprotection and their relationship to membrane radical dynamics and mitochondrial redox signaling.

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The possible role of heat shock factor-1 in the negative regulation of heme oxygenase-1

Cited by 22 publications

References 45 publications

Thiopental Protects Human T Lymphocytes from Apoptosis in Vitro via the Expression of Heat Shock Protein 70

Thiopental Protects Human T Lymphocytes from Apoptosis in Vitro via the Expression of Heat Shock Protein 70

Inhibition ofTrailGene Expression by Cyclopentenonic Prostaglandin 15-Deoxy-Δ^12,14-Prostaglandin J₂in T Lymphocytes

Cellular Stress Responses, The Hormesis Paradigm, and Vitagenes: Novel Targets for Therapeutic Intervention in Neurodegenerative Disorders

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The possible role of heat shock factor-1 in the negative regulation of heme oxygenase-1

Cited by 22 publications

References 45 publications

Thiopental Protects Human T Lymphocytes from Apoptosis in Vitro via the Expression of Heat Shock Protein 70

Thiopental Protects Human T Lymphocytes from Apoptosis in Vitro via the Expression of Heat Shock Protein 70

Inhibition ofTrailGene Expression by Cyclopentenonic Prostaglandin 15-Deoxy-Δ12,14-Prostaglandin J2in T Lymphocytes

Cellular Stress Responses, The Hormesis Paradigm, and Vitagenes: Novel Targets for Therapeutic Intervention in Neurodegenerative Disorders

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Product

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Inhibition ofTrailGene Expression by Cyclopentenonic Prostaglandin 15-Deoxy-Δ^12,14-Prostaglandin J₂in T Lymphocytes