Quantitative pathways for Northeast Atlantic fisheries based on climate, ecological–economic and governance modelling scenarios

Here we present quantitative projections of potential futures for ecosystems in the North Atlantic basin generated from coupling a climate change-driven biophysical model (representing ecosystem and fish populations under climate change) and a scenario-driven ecological–economic model (representing fleets and industries under economic globalization). Four contrasting scenarios (Baseline, Fortress, Global Commons, Free Trade) were defined from the perspective of alternative regional management and governance of the oceanic basin, providing pathways for the future of ecosystems in the Northeast Atlantic basin by 2040. Results indicate that in the time frame considered: (1) the effects of governance and trade decisions are more significant in determining outcomes than the effects of climate change alone, (2) climate change is likely to result in a poleward latitudinal shift of species ranges and thus resources, with implications for exploitation patterns, (3) the level of fisheries regulation is the most important factor in determining the long term evolution of the fisheries system, (4) coupling climate change and governance impacts demonstrates the complex interaction between different components of this social–ecological system, (5) an important driver of change for the future of the North Atlantic and the European fishing fleets appears to be the interplay between wild fisheries and aquaculture development, and finally (6) scenarios demonstrate that the viability and profit of fisheries industries is highly volatile. This study highlights the need to explore basin-scale policy that combines medium to long-term environmental and socio-economic considerations, and the importance of defining alternative sustainable pathways.

Glucose-potentiated chemotaxis in human vascular smooth muscle is dependent on cross-talk between the P13K and MAPK signalling pathways

Atheroma formation involves the movement of vascular smooth muscle cells (VSMC) into the subendothelial space. The aim of this study was to determine the involvement of PI3K and MAPK pathways and the importance of cross-talk between these pathways, in glucose-potentiated VSMC chemotaxis to serum factors. VSMC chemotaxis occurred in a serum gradient in 25 mmol/L glucose (but not in 5 mmol/L glucose) in association with increased phosphorylation (activation) of Akt and ERK1/2 in PI3K and MAPK pathways, respectively. Inhibitors of these pathways blocked chemotaxis, as did an mTOR inhibitor. VSMC expressed all class IA PI3K isoforms, but microinjection experiments demonstrated that only the p110beta isoform was involved in chemotaxis. ERK1/2 phosphorylation was reduced not only by MAPK pathway inhibitors but also by PI3K and mTOR inhibitors; when PI3K was inhibited, ERK phosphorylation could be induced by microinjected activated Akt, indicating important cross-talk between the PI3K and ERK1/2 pathways. Glucose-potentiated phosphorylation of molecules in the p38 and JNK MAPK pathways inhibited these pathways but did not affect chemotaxis. The statin, mevinolin, blocked chemotaxis through its effects on the MAPK pathway. Mevinolin-inhibited chemotaxis was restored by farnesylpyrophosphate but not by geranylgeranylpyrophosphate; in the absence of mevinolin, inhibition of farnesyltransferase reduced ERK phosphorylation and blocked chemotaxis, indicating a role for the Ras family of GTPases (MAPK pathway) under these conditions. In conclusion, glucose sensitizes VSMC to serum, inducing chemotaxis via pathways involving p110beta-PI3K, Akt, mTOR, and ERK1/2 MAPK. Cross-talk between the PI3K and MAPK pathways is necessary for VSMC chemotaxis under these conditions.