Ocean Acidification Accelerates Reef Bioerosion

In the recent discussion how biotic systems may react to ocean acidification caused by the rapid rise in carbon dioxide partial pressure (pCO₂) in the marine realm, substantial research is devoted to calcifiers such as stony corals. The antagonistic process – biologically induced carbonate dissolution via bioerosion – has largely been neglected. Unlike skeletal growth, we expect bioerosion by chemical means to be facilitated in a high-CO₂ world. This study focuses on one of the most detrimental bioeroders, the sponge Cliona orientalis, which attacks and kills live corals on Australia’s Great Barrier Reef. Experimental exposure to lowered and elevated levels of pCO₂ confirms a significant enforcement of the sponges’ bioerosion capacity with increasing pCO₂ under more acidic conditions. Considering the substantial contribution of sponges to carbonate bioerosion, this finding implies that tropical reef ecosystems are facing the combined effects of weakened coral calcification and accelerated bioerosion, resulting in critical pressure on the dynamic balance between biogenic carbonate build-up and degradation.     

ATP-Mediated Compositional Change in Peripheral Myelin Membranes: A Comparative Raman Spectroscopy and Time-Of-Flight Secondary Ion Mass Spectrometry Study

In the present paper we addressed a mechanism of the myelin reorganization initiated by extracellular ATP and adenosine in sciatic nerves of the frog Rana temporaria. In combination with Raman microspectroscopy, allowing noninvasive live-cell measurements, we employed time-of-flight secondary ion mass spectrometry (TOF-SIMS) to follow the underlying changes in chemical composition of myelin membranes triggered by the purinergic agents. The simultaneous increase in lipid ordering degree, decrease in membrane fluidity and the degree of fatty acid unsaturation were induced by both ATP and adenosine. Mass spectrometry measurements revealed that ATP administration also led to the marked elevation of membrane cholesterol and decrease of phosphotidylcholine amounts. Vesicular lipid transport pathways are considered as possible mechanisms of compositional and structural changes of myelin.     

Microparticle-Induced Activation of the Vascular Endothelium Requires Caveolin-1/Caveolae

Microparticles (MPs) are small membrane fragments shed from normal as well as activated, apoptotic or injured cells. Emerging evidence implicates MPs as a causal and/or contributing factor in altering normal vascular cell phenotype through initiation of proinflammatory signal transduction events and paracrine delivery of proteins, mRNA and miRNA. However, little is known regarding the mechanism by which MPs influence these events. Caveolae are important membrane microdomains that function as centers of signal transduction and endocytosis. Here, we tested the concept that the MP-induced pro-inflammatory phenotype shift in endothelial cells (ECs) depends on caveolae. Consistent with previous reports, MP challenge activated ECs as evidenced by upregulation of intracellular adhesion molecule-1 (ICAM-1) expression. ICAM-1 upregulation was mediated by activation of NF-κB, Poly [ADP-ribose] polymerase 1 (PARP-1) and the epidermal growth factor receptor (EGFR). This response was absent in ECs lacking caveolin-1/caveolae. To test whether caveolae-mediated endocytosis, a dynamin-2 dependent process, is a feature of the proinflammatory response, EC’s were pretreated with the dynamin-2 inhibitor dynasore. Similar to observations in cells lacking caveolin-1, inhibition of endocytosis significantly attenuated MPs effects including, EGFR phosphorylation, activation of NF-κB and upregulation of ICAM-1 expression. Thus, our results indicate that caveolae play a role in mediating the pro-inflammatory signaling pathways which lead to EC activation in response to MPs.