Sphk1 mediates neuroinflammation and neuronal injury via TRAF2/NF-κB pathways in activated microglia in cerebral ischemia reperfusion.

Sphingosine kinase 1 (Sphk1), a key enzyme responsible for phosphorylating sphingosine into sphingosine1-phosphate (S1P), plays an important role in mediating post-stroke neuroinflammation. However, the pathway and mechanism of the Sphk1-mediated inflammatory response remains unknown. In this study, we found that suppression of Sphk1 decreased IL17 production and relieved neuronal damage induced by microglia in cerebral ischemia reperfusion (IR) or in an in vitro oxygen-glucose deprivation reperfusion (OGDR) system.

Molecular structure, expression pattern and functional characterisation of APRIL in an aquatic mammal.

The Yangtze finless porpoise (Neophocaena phocaenoides asiaorientalis) is listed on the First Order of Protected Animals in China and was identified as an endangered species by the International Union for Conservation of Nature and Natural Resources (IUCN) in 2011. A proliferation inducing ligand (APRIL), belonging to the tumour necrosis factor (TNF) family, is critical for immune regulation. In this study, we identified a finless porpoise APRIL cDNA (fAPRIL) by RACE (rapid amplification of cDNA ends) strategies, from the Yangtze finless porpoise (fAPRIL).

Positive selection at the ASPM gene coincides with brain size enlargements in cetaceans.

The enlargement of cetacean brain size represents an enigmatic event in mammalian evolution, yet its genetic basis remains poorly explored. One candidate gene associated with brain size evolution is the abnormal spindle-like microcephaly associated (ASPM), as mutations in this gene cause severe reductions in the cortical size of humans. Here, we investigated the ASPM gene in representative cetacean lineages and previously published sequences from other mammals to test whether the expansion of the cetacean brain matched adaptive ASPM evolution patterns.