RESUMO
Reef crests in the Caribbean have lost approximately 80% of the foundational habitat-forming coral Acropora palmata (Lamarck, 1816), with declines registered as early as the 1950s mainly from anthropogenic causes. We studied two reef crests in the northwestern region of Cuba over 17 years (2005 to 2021) to evaluate temporal changes in coral cover, dominated by A. palmata, and their potential drivers. The density of A. palmata generally showed a negative trend at both reefs, with the lowest density recorded in 2021 at 0.2 ± 0.05 col. m-2 at Playa Baracoa and 1.0 ± 0.1 col. m-2 at Rincon de Guanabo. The mean size of the colonies in the two reefs also decreased over time. In Playa Baracoa, the mean diameter of A. palmata colonies decreased from 2012 at 67 ± 5.9 cm to 2013 at 34 ± 2.2 cm, whereas in Rincon de Guanabo, a change in diameter was evident from 2015 at 44.3 ± 2.3 to 2021 at 21.6 ± 0.9 cm. Adult colonies (10 cm-50 cm diameter) predominated in most years on both reefs. The populations of A. palmata on both reefs were healthy, with an average of 70% colonies in good condition during the study period. However, A. palmata cover decreased by almost half by 2021, to 8.6% in Playa Baracoa and 16.8% in Rincon de Guanabo. By contrast, macroalgal cover increased two-fold to 87.1% in Playa Baracoa and four-fold to 77.2% in Rincon de Guanabo. The density of the sea urchin Diadema antillarum was higher in Playa Baracoa than in Rincon de Guanabo. The highest densities were 2.8 ± 0.2 ind. m-2 in Playa Baracoa in 2005 and 0.1 ± 0.03 ind. m-2 in Rincon de Guanabo in 2008. Although our results show an overall decline of A. palmata (density and percent cover) and an increase in macroalgae, these two reef crests are in better condition than most reefs in the Caribbean in terms of the density and health of A. palmata populations, and the density of D. antillarum at Playa Baracoa. Our results are important in establishing a management plan to ensure the condition of these reef crests does not degrade further.
Assuntos
Antozoários , Animais , Cuba , Ecossistema , Ouriços-do-Mar , Região do CaribeRESUMO
Recent studies have demonstrated that statins reduce cell viability and induce apoptosis in various types of cancer cells. The molecular mechanisms underlying these effects are poorly understood. The JAK/STAT pathway plays an important role in the regulation of proliferation and apoptosis in many tissues, and its deregulation is believed to be involved in tumorigenesis and cancer. The physiological activation of STAT proteins by GH is rapid but transient in nature and its inactivation is regulated mainly by the expression of SOCS proteins. UMR-106 osteosarcoma cells express a GH-responsive JAK2/STAT5 signaling pathway, providing an experimental model to study the influence of statins on this system. In this study we investigated the actions of simvastatin on cell proliferation, migration, and invasion on UMR-106 cells and examined whether alterations in GH-stimulated JAK/STAT/SOCS signaling may be observed. Results showed that treatment of osteosarcoma cells with simvastatin at 3 to 10 µM doses decreases cell proliferation, migration, and invasion in a time- and dose-dependent manner. At the molecular level, although the mechanisms used by simvastatin are not entirely clear, the effect of the statin on the reduction of JAK2 and STAT5 phosphorylation levels may partially explain the decrease in the GH-stimulated STAT5 transcriptional activity. This effect correlated with a time- and dose-dependent increase of SOCS-3 expression levels in cells treated with simvastatin, a regulatory role that has not been previously described. Furthermore, the finding that simvastatin is capable of inducing SOCS-3 and CIS genes expression shows the potential of the JAK/STAT pathway as a therapeutic target, reinforcing the efficacy of simvastatin as chemotherapeutic drug for the treatment of osteosarcoma.