Diante do quadro atual de previsões de mudanças climáticas, estudos a respeito das possíveis respostas dos organismos a estas alterações são importantes. Com a finalidade de prever e verificar se estas serão de fato deletérias ou se os organismos são capazes de lidar com elas sem alterações na sua fisiologia, e consequentemente na estrutura do ambiente, E. brasiliensis foi utilizada como modelo para estudar possíveis impactos do aumento da temperatura e acidificação dos oceanos na sua fisiologia. Para isso, espécimes foram expostos a 9 possíveis combinações de temperatura (24ºC, 28ºC e 30ºC) e pH (8.0, 7.7 e 7.3) em diferentes intervalos de tempo (1, 3, 12, 24 e 48 h). Amostras de gônadas e fluido celomático foram coletadas para avaliar a expressão das proteínas de estresse HSP70, AIF-1 e p38-MAPK, e a variação no número e viabilidade dos celomócitos. Nossos resultados mostram que o modelo é sensibilizado pelas mudanças no ambiente, através da hiper-regulação das proteínas de estresse. O cenário considerado mais extremo (30°C + pH7.3) ocasionou a morte de 100% dos organismos após 24horas. E o segundo cenário mais severo (30°C + pH7.7) desencadeou o desenvolvimento de ulceração de pele. Os efeitos são mais pronunciados nos celomócitos e a acidificação da água parece ter efeitos antagônicos com a temperatura nos celomócitos e sinérgicos nas gônadas. Embora a resposta tenha sido sistêmica, o grau e a dinâmica foram distintos em relação às diferentes amostras e estresses. Podendo causar modificações na resposta imune dos organismos e consequentemente na sobrevivência da espécie a longo prazo. / Under the current Climate Change context, studies about the potential responses of the organisms to their changing environment are of extreme importance. Recent studies point out the synergy of temperature and ocean acidification altogether. In this study, we used the sea star E. brasiliensis to assess the physiological effects of rising temperature, seawater acidification and the interaction of both factors. Independent individuals (N=225) were exposed to 9 possible combinations of temperature (24ºC, 28ºC and 30ºC) and pH (8.0, 7.7 and 7.3), for 1, 3, 12, 24 and 48 h. We compared the stress produced by these treatments measuring the expression of heat shock proteins (HSP70), the production of the allograft inflammatory factor (AIF−1) and the activation of mitogen kinases (MAPKs) at both gonad and celomic fluid. Furthermore, we assessed the quantity and quality of coelomocytes. Our results demonstrated that E. brasiliensis is vulnerable to the interaction of temperature and acidification. All the stress proteins evaluated were upregulated. The extreme scenario (30°C + pH7.3) caused the death of 100% of organisms after 24 hours, while the second most severe scenario (30°C + pH7.7) triggered skin ulceration. Nevertheless, we found that water acidification produces antagonistic effects to the temperature in coelomocytes and synergistic effects in gonad cells. Furthermore, these effects were more pronounced in the coelomocytes than in the gonads. The systemic response found in this study suggest that the interactive effects of elevated temperatures in conjunction with ocean acidification may endanger the survival of this species, and it could compromise the ecosystem functioning at long term.

Diante do quadro atual de previsões de mudanças climáticas, estudos a respeito das possíveis respostas dos organismos a estas alterações são importantes. Com a finalidade de prever e verificar se estas serão de fato deletérias ou se os organismos são capazes de lidar com elas sem alterações na sua fisiologia, e consequentemente na estrutura do ambiente, E. brasiliensis foi utilizada como modelo para estudar possíveis impactos do aumento da temperatura e acidificação dos oceanos na sua fisiologia. Para isso, espécimes foram expostos a 9 possíveis combinações de temperatura (24ºC, 28ºC e 30ºC) e pH (8.0, 7.7 e 7.3) em diferentes intervalos de tempo (1, 3, 12, 24 e 48 h). Amostras de gônadas e fluido celomático foram coletadas para avaliar a expressão das proteínas de estresse HSP70, AIF-1 e p38-MAPK, e a variação no número e viabilidade dos celomócitos. Nossos resultados mostram que o modelo é sensibilizado pelas mudanças no ambiente, através da hiper-regulação das proteínas de estresse. O cenário considerado mais extremo (30°C + pH7.3) ocasionou a morte de 100% dos organismos após 24horas. E o segundo cenário mais severo (30°C + pH7.7) desencadeou o desenvolvimento de ulceração de pele. Os efeitos são mais pronunciados nos celomócitos e a acidificação da água parece ter efeitos antagônicos com a temperatura nos celomócitos e sinérgicos nas gônadas. Embora a resposta tenha sido sistêmica, o grau e a dinâmica foram distintos em relação às diferentes amostras e estresses. Podendo causar modificações na resposta imune dos organismos e consequentemente na sobrevivência da espécie a longo prazo. / Under the current Climate Change context, studies about the potential responses of the organisms to their changing environment are of extreme importance. Recent studies point out the synergy of temperature and ocean acidification altogether. In this study, we used the sea star E. brasiliensis to assess the physiological effects of rising temperature, seawater acidification and the interaction of both factors. Independent individuals (N=225) were exposed to 9 possible combinations of temperature (24ºC, 28ºC and 30ºC) and pH (8.0, 7.7 and 7.3), for 1, 3, 12, 24 and 48 h. We compared the stress produced by these treatments measuring the expression of heat shock proteins (HSP70), the production of the allograft inflammatory factor (AIF−1) and the activation of mitogen kinases (MAPKs) at both gonad and celomic fluid. Furthermore, we assessed the quantity and quality of coelomocytes. Our results demonstrated that E. brasiliensis is vulnerable to the interaction of temperature and acidification. All the stress proteins evaluated were upregulated. The extreme scenario (30°C + pH7.3) caused the death of 100% of organisms after 24 hours, while the second most severe scenario (30°C + pH7.7) triggered skin ulceration. Nevertheless, we found that water acidification produces antagonistic effects to the temperature in coelomocytes and synergistic effects in gonad cells. Furthermore, these effects were more pronounced in the coelomocytes than in the gonads. The systemic response found in this study suggest that the interactive effects of elevated temperatures in conjunction with ocean acidification may endanger the survival of this species, and it could compromise the ecosystem functioning at long term.

The p38 mitogen-activated protein kinase [p38(MAPK)] mediates responses to extracellular stressors. An increase in the phosphorylated form of p38(MAPK) [p-p38(MAPK)] has been associated with early events in Alzheimer disease (AD). Although most often associated with processes including apoptosis, inflammation and oxidative stress, p-p38(MAPK) also mediates beneficial physiological functions, such as cell growth, survival and phagocytosis of cellular pathogens. Amyloid plaques [β-amyloid aggregates] are a hallmark of AD-related pathology. As p38(MAPK) has been detected in the vicinity of senile plaques, we combined immunohistochemistry and stereological sampling to quantify the distribution of plaques and p-p38(MAPK)-immunoreactive (IR) cells in the sensorimotor cortex of 3-, 6- and 10-month-old TgCRND8 mice. This animal model expresses an aggressive nature of the AD-related human amyloid-β protein precursor (APP). It was confirmed by the appearance of both dense-core (thioflavin-S-positive) and diffuse plaques, even in the youngest mice. p-p38(MAPK)-IR cells were associated with both dense-core and diffuse plaques, but the expected age-dependent increase in the density of plaque-associated p-p38(MAPK)-IR cells was restricted to dense-core plaques. Furthermore, the density of dense-core plaque-associated p-p38(MAPK)-IR cells was inversely correlated with the size of the core within the given plaque, which supports a role for these microglia in restricting core growth. p-p38(MAPK)-IR cells were also observed throughout wildtype and TgCRND8 mouse cortical parenchyma, but the density of these non-plaque-associated cells remained constant, regardless of age or genotype. We conclude that the constitutive presence of p-p38(MAPK)-IR microglia in aging mouse brain is indicative of a longitudinal role for this kinase in normal brain physiology. Additionally, the majority of p-p38(MAPK)-IR cells were predominantly co-immunoreactive for the Macrophage-1 (CD11b/CD18) microglial marker, regardless of whether they were associated with plaques or localized to the parenchyma. We suggest that the facts that a pool of p-p38(MAPK)-IR microglia appears to restrict b-amyloid plaque core development and the non-pathological role of p-p38(MAPK) in parenchyma, needs to be considered when anticipating targeted p38(MAPK) therapeutics in the context of clinical AD.

The p38 mitogen-activated protein kinase [p38(MAPK)] mediates responses to extracellular stressors. An increase in the phosphorylated form of p38(MAPK) [p-p38(MAPK)] has been associated with early events in Alzheimer disease (AD). Although most often associated with processes including apoptosis, inflammation and oxidative stress, p-p38(MAPK) also mediates beneficial physiological functions, such as cell growth, survival and phagocytosis of cellular pathogens. Amyloid plaques [β-amyloid aggregates] are a hallmark of AD-related pathology. As p38(MAPK) has been detected in the vicinity of senile plaques, we combined immunohistochemistry and stereological sampling to quantify the distribution of plaques and p-p38(MAPK)-immunoreactive (IR) cells in the sensorimotor cortex of 3-, 6- and 10-month-old TgCRND8 mice. This animal model expresses an aggressive nature of the AD-related human amyloid-β protein precursor (APP). It was confirmed by the appearance of both dense-core (thioflavin-S-positive) and diffuse plaques, even in the youngest mice. p-p38(MAPK)-IR cells were associated with both dense-core and diffuse plaques, but the expected age-dependent increase in the density of plaque-associated p-p38(MAPK)-IR cells was restricted to dense-core plaques. Furthermore, the density of dense-core plaque-associated p-p38(MAPK)-IR cells was inversely correlated with the size of the core within the given plaque, which supports a role for these microglia in restricting core growth. p-p38(MAPK)-IR cells were also observed throughout wildtype and TgCRND8 mouse cortical parenchyma, but the density of these non-plaque-associated cells remained constant, regardless of age or genotype. We conclude that the constitutive presence of p-p38(MAPK)-IR microglia in aging mouse brain is indicative of a longitudinal role for this kinase in normal brain physiology. Additionally, the majority of p-p38(MAPK)-IR cells were predominantly co-immunoreactive for the Macrophage-1 (CD11b/CD18) microglial marker, regardless of whether they were associated with plaques or localized to the parenchyma. We suggest that the facts that a pool of p-p38(MAPK)-IR microglia appears to restrict b-amyloid plaque core development and the non-pathological role of p-p38(MAPK) in parenchyma, needs to be considered when anticipating targeted p38(MAPK) therapeutics in the context of clinical AD.