The Complete Mitochondrial Genome of Lepidotrigona flavibasis (Hymenoptera: Meliponini) and High Gene Rearrangement in Lepidotrigona Mitogenomes.

We reported the sequence and characteristics of the complete mitochondrial genome of an ecologically important stingless bee, Lepidotrigona flavibasis (Hymenoptera: Meliponini), that has suffered serious population declines in recent years. A phylogenetic analysis based on complete mitogenomes indicated that L. flavibasis was first clustered with another Lepidotrigona species (L. terminata) and then joined with the other two Melipona (Hymenoptera: Meliponini) stingless bees (M. scutellaris and M. bicolor), forming a single clade of stingless bees. The stingless bee clade has a closer relationship with bumblebees (Bombus) (Hymenoptera: Apidae) than with honeybees (Apis) (Hymenoptera: Apidae). Extremely high gene rearrangements involving tRNAs, rRNAs, D-loop regions, and protein-coding genes were observed in the Lepidotrigona mitogenomes, suggesting an overactive evolutionary status in Lepidotrigona species. These mitogenomic organization variations could provide a good system with which to understand the evolutionary history of Meliponini.

Inhibition of TRIM8 restrains ischaemia-reperfusion-mediated cerebral injury by regulation of NF-κB activation associated inflammation and apoptosis.

Stroke is a leading global cause of mortality and disability. However, the pathogenesis that contributes to stroke has not been fully understood. The tripartite motif (TRIM)-containing proteins usually exhibit essential regulatory roles during various biological processes. TRIM8 is a RING domain-containing E3 ubiquitin ligase, playing crucial roles in regulating inflammation and apoptosis. In the present study, we reported that TRIM8 expression was significantly induced in the peri-infarct cortex area of mice after stroke onset. TRIM8 siRNA in vivo transfection resulted in the attenuated cognitive impairments in mice with cerebral ischaemia-reperfusion (IR) injury. In addition, TRIM8 knockdown was neuroprotective, as evidenced by the reduced infarct area, decreased neurological deficit score and down-regulated number of TUNEL-positive cells in the peri-infarct area. Moreover, TRIM8 inhibition obviously repressed glial fibrillary acidic protein (GFAP) expression in peri-hematoma cortex and hippocampus. Furthermore, inflammation induced by cerebral IR injury was highly restrained by TRIM8 knockdown in serum, peri-infarct area and hippocampus, which were along with the remarkable decreases in the phosphorylated expression of IκB kinase alpha (IKKα), inhibitory κB α (IκBα) and nuclear factor kappa B (NF-κB). Moreover, TRIM8 knockdown significantly reduced apoptosis in hippocampus of mice with cerebral IR injury by reducing Caspase-3 cleavage. The in vitro experiment confirmed the neuroprotective role of TRIM8-knockdown in regulating cerebral IR injury. Intriguingly, we found that TRIM8 over-expression-promoted inflammatory response and apoptosis could be markedly attenuated by the inactivation of NF-κB signaling through pre-treatment of JSH-23 or QNZ in lipopolysaccharide (LPS)-incubated astrocytes (ASTs). Therefore, TRIM8 positively regulated cerebral IR injury by activating NF-κB pathway to enhance inflammation and apoptosis. Targeting TRIM8 could provide feasible therapeutic treatment for stroke.