Major stress protein Hsp70 interacts with NF-kB regulatory complex in human T-lymphoma cells

Guzhova, Irina V.; Darieva, Zoulfia; Melo, Alessandra Rocha; Margulis, Boris A.

doi:10.1379/1466-1268(1997)002<0132:msphiw>2.3.co;2

Cited by 135 publications

(77 citation statements)

References 29 publications

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“…A second possibility is that p75NTR-dependent NF-B activation depends on culture conditions. Notably, NF-B responses can be altered under conditions of cellular stress (41), and in the first report of p75NTR-mediated NF-B activation (33), cells were subjected to two stressful conditions: a temperature shock and a period of serum starvation. 2 We therefore tested whether these conditions might increase the ability of PCNA cells to respond to NGF.…”

Section: Resultsmentioning

confidence: 99%

The p75 Neurotrophin Receptor (p75NTR) Alters Tumor Necrosis Factor-mediated NF-κB Activity under Physiological Conditions, but Direct p75NTR-mediated NF-κB Activation Requires Cell Stress

Bhakar¹,

Roux²,

Lachance³

et al. 1999

Journal of Biological Chemistry

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The p75 neurotrophin receptor (p75NTR) has been linked to activation of the NF-B transcriptional complex in oligodendrocytes, Schwann cells, and PCNA cells. In this report, tumor necrosis factor (TNF)-and neurotrophin-mediated NF (nuclear factor)-B activation were compared in several cell lines. All cell types showed TNF-mediated activation of NF-B, but direct neurotrophin-dependent activation of NF-B was never observed under normal growth conditions. In PCNA cells, a modest nerve growth factor (NGF)-dependent induction of NF-B was detected but only after cells were subjected to severe stress. Although NGF binding did not directly activate NF-B under normal conditions, NGF consistently altered TNF-dependent NF-B activation in each cell type examined, and extended exposure to NGF and TNF always increased NF-B activation over that achieved with TNF alone. The increase in NF-B activity mediated by NGF correlated with reduced levels of IB␣; NGF added alone had no effect on IB␣ levels, but when added with TNF, NGF treatment significantly reduced IB␣ levels. We propose that modulation of cytokine receptor signaling is a significant physiological function of the p75 neurotrophin receptor and that previous reports of direct NF-B activation through p75NTR reflect this modulatory activity.

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Section: Resultsmentioning

confidence: 99%

The p75 Neurotrophin Receptor (p75NTR) Alters Tumor Necrosis Factor-mediated NF-κB Activity under Physiological Conditions, but Direct p75NTR-mediated NF-κB Activation Requires Cell Stress

Bhakar¹,

Roux²,

Lachance³

et al. 1999

Journal of Biological Chemistry

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“…It is known that NF-B positively regulates the expression of pro-inflammatory cytokines, including TNF-␣, IL-1␤, and IL-6. Furthermore, it is also known that upregulation of HSP70 expression by heat shock inhibits the inflammatory stimuli-dependent activation of NF-B through various mechanisms (47)(48)(49)(50)(51)(52).…”

Section: Discussionmentioning

confidence: 99%

Genetic Evidence for a Protective Role for Heat Shock Factor 1 and Heat Shock Protein 70 against Colitis

Tanaka

Namba

Arai

et al. 2007

Journal of Biological Chemistry

130

126

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Inflammatory bowel disease (IBD) involves infiltration of leukocytes into intestinal tissue, resulting in intestinal damage induced by reactive oxygen species (ROS). Pro-inflammatory cytokines and cell adhesion molecules (CAMs) play important roles in this infiltration of leukocytes. The roles of heat shock factor 1 (HSF1) and heat shock proteins (HSPs) in the development of IBD are unclear. In this study, we examined the roles of HSF1 and HSPs in an animal model of IBD, dextran sulfate sodium (DSS)-induced colitis. The colitis worsened or was ameliorated in HSF1-null mice or transgenic mice expressing HSP70 (or HSF1), respectively. Administration of DSS up-regulated the expression of HSP70 in colonic tissues in an HSF1-dependent manner. Expression of pro-inflammatory cytokines and CAMs and the level of cell death observed in colonic tissues were increased or decreased in DSS-treated HSF1-null mice or transgenic mice expressing HSP70, respectively, relative to control wild-type mice. Relative to macrophages from control wildtype mice, macrophages prepared from HSF1-null mice or transgenic mice expressing HSP70 displayed enhanced or reduced activity, respectively, for the generation of pro-inflammatory cytokines in response to lipopolysaccharide stimulation. Suppression of HSF1 or HSP70 expression in vitro stimulated lipopolysaccharide-induced up-regulation of CAMs or ROS-induced cell death, respectively. This study provides the first genetic evidence that HSF1 and HSP70 play a role in protecting against DSS-induced colitis. Furthermore, this protective role seems to involve various mechanisms, such as suppression of expression of pro-inflammatory cytokines and CAMs and ROS-induced cell death. Inflammatory bowel disease (IBD),2 Crohn disease, and ulcerative colitis have become substantial health problems with an actual prevalence of 200 -500 cases/100,000 people in western countries, which almost double every 10 years (1). Although the etiology of IBD is not yet fully understood, recent studies suggest that IBD involves chronic inflammatory disorders in the intestine because of "a vicious cycle." Infiltration into intestinal tissues causes intestinal mucosal damage induced by reactive oxygen species (ROS) that are released from the activated leukocytes, and this intestinal mucosal damage further stimulates the infiltration of leukocytes (2). To understand the molecular mechanism underlying the pathogenesis of IBD and to develop new types of clinical drugs for IBD, identification of endogenous factors that positively or negatively affect the development of IBD is important. For this purpose, various experimental animal colitis models, in particular the dextran sulfate sodium (DSS)-and trinitrobenzenesulfonic acid-induced colitis models, have been used (3).Pro-inflammatory cytokines play an important role in the activation and infiltration of leukocytes that are associated with IBD. This conclusion is supported by a range of evidence. Increases in the levels of various pro-inflammatory cytokines (such as tumor necr...

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“…Other possible candidates of ETS components that contribute to NF-B inhibitory effects are hydroquinone, aldehydes (e.g., acrolein), and nicotine (44)(45)(46)(57)(58)(59). Furthermore, previous studies have shown tobacco smoke activates heat shock transcription factor (HSF) and expression of heat shock proteins (HSP), HSP 70 in particular, which could interact with NF-B as a partial substitute for IB and contribute to stress-induced NF-B suppression (60)(61)(62)(63)(64)(65)(66). In line with these observations, we also noted coordinate induction of HSP70 and inhibition of NF-B after ETS exposure.…”

Section: Discussionmentioning

confidence: 99%

Environmental Tobacco Smoke Suppresses Nuclear Factor-κB Signaling to Increase Apoptosis in Infant Monkey Lungs

Zhong

Zhou

Joad

et al. 2006

Am J Respir Crit Care Med

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Rationale: Exposure to environmental tobacco smoke in early life has adverse effects on lung development. Apoptosis plays an essential role in development; however, the molecular mechanisms of pulmonary apoptosis induced by environmental tobacco smoke is unknown. Objectives: To investigate the mechanistic role of nuclear factor (NF)-B, a critical cell survival pathway, in the developing lungs exposed to environmental tobacco smoke.

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Major stress protein Hsp70 interacts with NF-kB regulatory complex in human T-lymphoma cells

Cited by 135 publications

References 29 publications

The p75 Neurotrophin Receptor (p75NTR) Alters Tumor Necrosis Factor-mediated NF-κB Activity under Physiological Conditions, but Direct p75NTR-mediated NF-κB Activation Requires Cell Stress

The p75 Neurotrophin Receptor (p75NTR) Alters Tumor Necrosis Factor-mediated NF-κB Activity under Physiological Conditions, but Direct p75NTR-mediated NF-κB Activation Requires Cell Stress

Genetic Evidence for a Protective Role for Heat Shock Factor 1 and Heat Shock Protein 70 against Colitis

Environmental Tobacco Smoke Suppresses Nuclear Factor-κB Signaling to Increase Apoptosis in Infant Monkey Lungs

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