Cu2+ and acute thermal stress induce protective events<i>via</i>the p38-MAPK signalling pathway in the perfused<i>Rana ridibunda</i>heart

Gaitanaki, Catherine; Pliatska, Maria; Σταθοπούλου, Κωνσταντίνα; Beis, Isidoros

doi:10.1242/jeb.02680

Cited by 12 publications

(5 citation statements)

References 47 publications

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“…Activation of ERK has been shown to promote or block H 2 O 2 -dependent apoptosis (69,73). In the present work, H 2 O 2 accelerated rVacA-induced cell death, especially in p38 inhibitor-pretreated AGS cells, suggesting that p38 MAP kinase plays a pivotal role in protection against H 2 O 2 -induced cell death (11,27) and, conversely, that ERK1/2 aggravates H 2 O 2 -induced cell death.…”

Section: Apoptosis Of Gastric Epithelial Cells Induced By H Pylorisupporting

confidence: 53%

Differential regulation of ERK1/2 and p38 MAP kinases in VacA-induced apoptosis of gastric epithelial cells

Lee²,

Goo³

et al. 2008

American Journal of Physiology-Gastrointestinal and Liver Physi

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Helicobacter pylori vacuolating cytotoxin A (VacA) has been considered as an apoptosis-inducing factor. Here, we investigated the mechanism of VacA-induced apoptosis in relation to the defense mechanism and MAP kinases pathway in gastric epithelial cells. AGS cells exposed to enriched VacA extracts affected the level of SOD-1 and villin. We further investigated the role of VacA in those inductions using a functional recombinant VacA (rVacA). Activation of p38 MAPK and Bax dimerization by rVacA were increased in a dose-dependent manner. rVacA-induced ERK1/2 MAPK activation was maximal at 30 min and 4 h and 1-4 microg/ml of rVacA. rVacA-induced SOD-1 expression was considerably diminished by inhibiting ERK1/2 MAPK and it was slightly increased by inhibiting p38 MAPK. rVacA increased or decreased villin expression depending on dose and exposure time and its expression was mainly appeared in the contractile actin ring of the dividing cells. Despite its cytoprotective effect, SB-203580, a p38 inhibitor, was unlikely to reduce VacA-induced Bax dimerization and rather inhibited villin and Bcl2 expression, indicating that p38 may also play a role in cell proliferation or differentiation for survival after VacA intoxication. Furthermore, p38 inhibitor accelerated rVacA-induced cell death after exposure of AGS cells to H(2)O(2) but ERK1/2 inhibitor protected cells from H(2)O(2) insult. These results suggest that SOD-1 and villin are expressed differentially upon VacA insult depending on dose and exposure time via ERK and p38 MAP kinases; decrease in SOD-1 and villin expression coupled with Bax dimerization leads to apoptosis of gastric epithelial cells.

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Section: Apoptosis Of Gastric Epithelial Cells Induced By H Pylorisupporting

confidence: 53%

Differential regulation of ERK1/2 and p38 MAP kinases in VacA-induced apoptosis of gastric epithelial cells

Lee²,

Goo³

et al. 2008

American Journal of Physiology-Gastrointestinal and Liver Physi

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“…Recently, studies have demonstrated that p38-MAPK and JNK play crucial roles in the adaptive responses to thermal, osmotic, oxidative and heavy metal stresses in mussels (Kefaloyianni et al, 2005;Gaitanaki et al, 2007;Evans and Somero, 2010;Gourgou et al, 2010). For example, hyperthermia (30°C), hypothermia (4°C) and heavy metals induced a significant activation of p38-MAPK in gill and mantle tissue of M. galloprovincialis (Kefaloyianni et al, 2005).…”

Section: Stress-signaling Proteinsmentioning

confidence: 99%

The impact of acute temperature stress on hemocytes of invasive and native mussels (Mytilus galloprovincialisandM. californianus): DNA damage, membrane integrity, apoptosis and signalling pathways

Yao

Somero

2012

Journal of Experimental Biology

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SUMMARYWe investigated the effects of acute heat stress and cold stress on cell viability, lysosome membrane stability, double-and singlestranded DNA breakage, and signaling mechanisms involved in cellular homeostasis and apoptosis in hemocytes of native and invasive mussels, Mytilus californianus and Mytilus galloprovincialis, respectively. Both heat stress (28, 32°C) and cold stress (2, 6°C) led to significant double-and single-stranded breaks in DNA. The type and extent of DNA damage were temperature and time dependent, as was caspase-3 activation, an indicator of apoptosis, which may occur in response to DNA damage. Hemocyte viability and lysosomal membrane stability decreased significantly under heat stress. Western blot analyses of hemocyte extracts with antibodies for proteins associated with cell signaling and stress responses [including members of the phospho-specific mitogen-activated protein kinase (MAPK) family c-JUN NH 2 -terminal kinase (JNK) and p38-MAPK, and apoptosis executor caspase-3] revealed that heat and cold stress induced a time-dependent activation of JNK, p38-MAPK and caspase-3 and that these signaling and stress responses differed between species. The thermal limits for activation of cell signaling processes linked to the repair of stress-induced damage may help determine cellular thermal tolerance limits. Our results show similarities in responses to cold and heat stress and suggest causal linkages between levels of DNA damage at both extremes of temperature and downstream regulatory responses, including induction of apoptosis. Compared with M. californianus, M. galloprovincialis might have a wider temperature tolerance due to a lower amount of single-and double-stranded DNA damage, faster signaling activation and transduction, and stronger repair ability against temperature stress.

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“…in the case of direct exposure to H 2 O 2 both in our experimental model (Gaitanaki et al, 2003) and in rat neonatal cardiac myocytes (Clerk et al, 1998). The molecular mechanisms triggered during the amphibian heart response to cobalt perfusion have been evaluated to be specific to this metal, since our group has demonstrated that perfusion with copper, another metal that can induce rapid generation of ROS via a Haber-Weiss or Fentonlike reaction (Gutteridge, 1985;Shi and Dalal, 1992;Gaetke and Chow, 2003), does not stimulate p38-MAPK phosphorylation through O 2 -or H 2 O 2 (Gaitanaki et al, 2006b). The amphibian cardiac muscle is secreting an atrial natriuretic peptide (ANP) very similar to the mammalian one (Netchitailo et al, 1988) in order to prevent heart overloading under stressful conditions (Gisbert and Fischmeister, 1988;Netchitailo et al, 1988;Cerra et al, 2003).…”

Section: The Journal Of Experimental Biologymentioning

confidence: 99%

CoCl2 induces protective eventsviathe p38-MAPK signalling pathway and ANP in the perfused amphibian heart

Gaitanaki

Kalpachidou

Aggeli

et al. 2007

Journal of Experimental Biology

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RT-PCR). CoCl 2 treatment significantly increased ANP mRNA levels, whereas, in the presence of antioxidants, the transcript levels returned to basal values. All the above data indicate that CoCl 2 stimulates compensatory mechanisms involving the p38-MAPK signalling cascade along with ANP.Key words: CoCl 2 , hypoxia, frog heart, p38-MAPK, ANP, cardioprotection, oxidative stress, signalling. Summary 2268Nitric oxide (NO) is another member of the free radical family that diffuses rapidly and does not readily react with most biomolecules (Lancaster, 1994). However, NO reaction with O 2 -generates peroxynitrite (OONO -), which is highly cytotoxic (Beckman and Koppenol, 1996). Therefore, in the context of, for example, SOD competing with NO for binding to the superoxide anions, it becomes evident that SOD exerts its cardioprotective function by regulating formation of other ROS as well (peroxynitrite in this case). Given the interaction between these reactions one can deduce that, in this context, this is also the case for CAT.Oxidative stress (exemplified by perfusion with H 2 O 2 ) has also been found to transcriptionally upregulate atrial natriuretic peptide (ANP) levels in the amphibian heart (Vassilopoulos et al., 2005). There is also data implicating NO in the mechanism of this cardiac peptide hormone regulation (Sanchez-Ferrer et al., 1990; Carnio et al., 2004). Therefore, ANP appears to constitute another factor involved in the cardiac compensatory response to stimuli that could disturb extracellular fluid volume and electrolyte balance (Glass et al., 1996;Silberbach and Roberts, 2001), including redox perturbations.Oxidative stress may trigger activation of a plethora of signalling cascades (Kannan and Jain, 2000) including mitogen-activated protein kinase (MAPK) pathways (Feuerstein and Young, 2000). The three major subfamilies characterized in mammals are: the extracellular signalregulated kinases (ERKs), the c-jun N-terminal kinases (JNKs) and p38 reactivating kinase (p38-MAPK) (Kyriakis and Avruch, 2001;Pearson et al., 2001). The respective MAPKs have also been identified in the amphibian heart (Aggeli et al., 2001a). These kinases interact with their substrates in both the cytoplasm and the nucleus, transducing a variety of molecular signals (Bogoyevitch, 2000). Amphibian heart p38-MAPK, in particular, has been demonstrated to be activated by various forms of environmental stress, including mechanical and hyperosmotic as well as thermal (Aggeli et al., 2001b;Aggeli et al., 2002). Additionally, certain antioxidants (SOD and CAT) have been demonstrated to reverse H 2 O 2 -induced amphibian heart p38-MAPK activation (Gaitanaki et al., 2006a). H 2 O 2 -induced (oxidative stress) p38-MAPK interacts with MAPKactivated-protein-kinase 2 (MAPKAPK2), a kinase that subsequently phosphorylates the small heat shock protein Hsp27 (Gaitanaki et al., 2003). Phosphorylation of Hsp27 contributes to stabilization of the actin cytoskeleton, protecting cells against unfavourable stressful conditions (Paul et al., 2002; Con...

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Cu2+ and acute thermal stress induce protective eventsviathe p38-MAPK signalling pathway in the perfusedRana ridibundaheart

Cited by 12 publications

References 47 publications

Differential regulation of ERK1/2 and p38 MAP kinases in VacA-induced apoptosis of gastric epithelial cells

Differential regulation of ERK1/2 and p38 MAP kinases in VacA-induced apoptosis of gastric epithelial cells

The impact of acute temperature stress on hemocytes of invasive and native mussels (Mytilus galloprovincialisandM. californianus): DNA damage, membrane integrity, apoptosis and signalling pathways

CoCl2 induces protective eventsviathe p38-MAPK signalling pathway and ANP in the perfused amphibian heart

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