Heat shock protein hsp70 overexpression confers resistance against nitric oxide

Bellmann, Kerstin; Jäättelä, Marja; Wissing, Dorte; Burkart, Volker; Kolb, Hubert

doi:10.1016/0014-5793(96)00730-2

Cited by 162 publications

(108 citation statements)

References 25 publications

(23 reference statements)

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“…For example, activated RAW264.7 cells are more resistant to NO than inactivated cells (Okada et al, 1998), and LPS-activated BV-2 cells are resistant to NO toxicity while inactivated BV-2 cells are vulnerable (Sugaya et al, 1997). The susceptibility of activated macrophages to NO might be decreased because bacteria and LPS can stimulate expression of self-defenserelated genes in macrophages, such as Bcl-xL, metallothionein, and heat shock protein 70 (Kim et al, 1995;Bellmann et al, 1996;Okada et al, 1998). Based on those reports and our present data, it may be that the antiactivation cytokines IL-13 and IL-4 inhibit the expression of certain self-defense-related genes induced by microglial activators, which in turn leads to microglial cell death.…”

Section: Discussionmentioning

confidence: 99%

Interleukin‐13 and ‐4 induce death of activated microglia

Yang¹,

Park²,

Sohn³

et al. 2002

Glia

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When the brain suffers injury, microglia migrate to the damaged sites and become activated. These activated microglia are not detected several days later and the mechanisms underlying their disappearance are not well characterized. In this study, we demonstrate that interleukin (IL)-13, an anti-inflammatory cytokine, selectively induces cell death of activated microglia in vitro. Cell death was detected 4 days after the coaddition of IL-13 with any one of the microglial activators, lipopolysaccharide (LPS), ganglioside, or thrombin. This cell death occurred in a time-dependent manner. LPS, ganglioside, thrombin, or IL-13 alone did not induce cell death. Among antiinflammatory cytokines, IL-4 mimicked the effect of IL-13, while TGF-␤ did not. Cells treated with IL-13 plus LPS, or IL-13 plus ganglioside, showed the characteristics of apoptosis when analyzed by electron microscopy and terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling staining. Electron micrographs also showed microglia engulfing neighboring dead cells. We propose that IL-13 and IL-4 induce death of activated microglia, and that this process is important for prevention of chronic inflammation that can cause tissue damage. GLIA 38:273-280, 2002.

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Section: Discussionmentioning

confidence: 99%

Interleukin‐13 and ‐4 induce death of activated microglia

Yang¹,

Park²,

Sohn³

et al. 2002

Glia

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“…This was also investigated in the oyster (Shamseldin et al 1997;Clegg et al 1998;Hamdoun et al 2003). This thermoresistant status (or acquired thermotolerance as described by Kregel 2002) not only protects the cells against heat (Mosser and Martin 1992;Mosser et al 1997;Gabai et al 1997) but also against many kinds of stress such as chemotherapeutic agents (Samali and Cotter 1996;Jaattela 1999), nitric oxide (Bellmann et al 1996), UV (Simon et al 1995) and irradiation (Park et al 2000;Kang et al 2002). The protective effects of HSP against free oxygen radicals are thought to explain their effectiveness against these different sources of cellular stress conditions.…”

Section: Discussionmentioning

confidence: 99%

Transcriptional expression levels of cell stress marker genes in the Pacific oyster Crassostrea gigas exposed to acute thermal stress

Farcy

Voiseux

Lebel

et al. 2009

Cell Stress and Chaperones

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During the annual cycle, oysters are exposed to seasonal slow changes in temperature, but during emersion at low tide on sunny summer days, their internal temperature may rise rapidly, resulting in acute heat stress. We experimentally exposed oysters to a 1-h acute thermal stress and investigated the transcriptional expression level of some genes involved in cell stress defence mechanisms, including chaperone proteins (heat shock proteins Hsp70, Hsp72 and Hsp90 (HSP)), regulation of oxidative stress (Cu-Zn superoxide dismutase, metallothionein (MT)), cell detoxification (glutathione S-transferase sigma, cytochrome P450 and multidrug resistance (MDR1)) and regulation of the cell cycle (p53). Gene mRNA levels were quantified by reverse transcription-quantitative polymerase chain reaction and expressed as their ratio to actin mRNA, used as a reference. Of the nine genes studied, HSP, MT and MDR1 mRNA levels increased in response to thermal stress. We compared the responses of oysters exposed to acute heat shock in summer and winter and observed differences in terms of magnitude and kinetics. A larger increase was observed in September, with recovery within 48 h, whereas in March, the increase was smaller and lasted more than 2 days. The results were also compared with data obtained from the natural environment. Though the functional molecule is the protein and information at the mRNA level only has limitations, the potential use of mRNAs coding for cell stress defence proteins as early sensitive biomarkers is discussed.

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“…Among these genes are the putative protective agents heat shock protein (hsp) 70 (23)(24)(25), manganese superoxide dismutase (MnSOD) (26,27), and the pro-apoptotic gene Fas (28,29). It remains to be clarified whether induction of these genes is a direct effect of IL-1␤ or whether iNOS induction and NO production is a required intermediary step for mRNA expression.…”

Section: Cytokines Induce Apoptosis In ␤-Cellsmentioning

confidence: 99%

Cytokines induce apoptosis in beta-cells isolated from mice lacking the inducible isoform of nitric oxide synthase (iNOS-/-).

et al. 2000

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Prolonged exposure of rodent ␤-cells to combinations of cytokines induces the inducible form of nitric oxide synthase (iNOS) expression and Fas expression, nitric oxide (NO) production, and cell death. It also induces the expression of potential "defense" genes, such as manganese superoxide dismutase (MnSOD) and heat shock protein (hsp) 70. NO is a radical with multifaceted actions. Recent studies have shown that NO, in addition to having cytotoxic actions, may regulate gene transcription. It remains unclear whether NO mediates cytokine-induced gene expression and subsequent ␤-cell death. Previous studies using NO synthase blockers yielded conflicting results, which may be due to nonspecific effects of these agents. In this study, we examined the effects of cytokines on gene expression, determined by reverse transcriptase-polymerase chain reaction (RT-PCR), and viability, determined by nuclear dyes, of pancreatic islets or fluorescence-activated cell sorter (FACS)-purified ␤-cells isolated from iNOS knockout mice (iNOS -/ -, background C57BL/6x129SvEv) or their respective controls (C57BL/6x129SvEv). The combination of cytokines used was interleukin-1␤ (50 U/ml) plus ␥-interferon (1,000 U/ml) plus tumor necrosis factor-␣ (1,000 U/ml). The lack of cytokine-induced iNOS activity in the iNOS -/-islet cells was confirmed by RT-PCR and nitrite determination. Cytokines induced a >3-fold increase in Fas and MnSOD mRNA expression in wild-type (WT) and iNOS -/-islets. On the other hand, hsp 70 was induced in WT but not in iNOS -/-islets. Prolonged (6-9 days) exposure of WT islets to cytokines leads to an 80-90% decrease in islet cell viability, whereas viability decreased by only 10-30% in iNOS -/-islet cells. To determine the mode of cytokine-induced cell death, FACS-purified ␤-cells were exposed to the same cytokines. After 9 days, the apoptosis index was similarly increased in WT (39 ± 3%) and iNOS -/-(33 ± 4%) ␤-cells. On the other hand, cytokines increased necrosis in WT (20 ± 4%) but not in iNOS -/-(7 ± 3%) ␤-cells. From these data, we concluded that 1) NO is required for cytokine-induced hsp 70 mRNA expression but not for Fas and MnSOD expression, 2) cytokines induce both apoptosis and necrosis in mouse ␤-cells, and 3) cytokine-induced apoptosis is mostly NO-independent, whereas necrosis requires NO formation. Diabetes

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Heat shock protein hsp70 overexpression confers resistance against nitric oxide

Cited by 162 publications

References 25 publications

Interleukin‐13 and ‐4 induce death of activated microglia

Interleukin‐13 and ‐4 induce death of activated microglia

Transcriptional expression levels of cell stress marker genes in the Pacific oyster Crassostrea gigas exposed to acute thermal stress

Cytokines induce apoptosis in beta-cells isolated from mice lacking the inducible isoform of nitric oxide synthase (iNOS-/-).

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