PCSK9: A new participant in lipophagy in regulating atherosclerosis?

Proprotein convertase subtilisin kexin 9 (PCSK9) regulates lipid metabolism by degrading low-density lipoprotein receptor on the surface of hepatocytes. PCSK9-mediated lipid degradation is associated with lipophagy. Lipophagy is a process by which autophagosomes selectively sequester lipid-droplet-stored lipids and are delivered to lysosomes for degradation. Lipophagy was first discovered in hepatocytes, and its occurrence provides important fundamental insights into how lipid metabolism regulates cellular physiology and pathophysiology. Furthermore, PCSK9 may regulate lipid levels by affecting lipophagy. This review will discuss recent advances by which PCSK9 mediates lipid degradation via the lipophagy pathway and present lipophagy as a potential therapeutic target for atherosclerosis.

[Down-Regulation of MiR-125b Reverses Drug Resistance of Doxorubicin-Resistant Leukemia Cells].

OBJECTIVE: To investigate whether the down-regulation of miR-125b can reverse the drug-resistence of doxorubicine-resistant leukemia cell lines or not, so as to explore a new method for treatment of drug-resistant leukemia patients. METHODS: The expression levels of miR125b in doxorubicine drug-sensitive and doxorubicine drug-resistant leukemia cell lines.HL-60, K562 and HL-60/Dox, the K562/Dox were detected by using RT-qPCR; the up-regulation or inhibition of miR-1256 expression in HL-60/Dox were performed by electroporation transfection, then the viability of cells treated with doxorubicine of different concentration was detected by CCK-8 method, the proliferation inhibition curve of cells was drawed, and the IC50 was calculated. RESULTS: The miR-125b expression was obviously up-regulated in drug-resistant cell lines HL-60/DOX and K562/DOX, as compared with HL-60 and K562 cell lines. The miR-125b expression level in HL-60/DOX and K562/DOX cells was 15 times and 5 times higher than that in HL-60 and K562 cells, respectively. The up-regulating or inhibiting expression of miR-125b in HL-60/DOX cells found that the proliferation inhibition rate in cells transfected with miR-125b mimic significantly decreased, compared with control group (P<0.01), while the proliferation inhibition rate in cells transfected with miR-125b inhibitor significantly increased, compared with control group(P<0.01). CONCLUSION: The miR-125b expression in HL-60/Dox and K562/Dox cells has been up-regulated, down-regulation of miR-125b expression can reverse the drug resistance of leukemia cells to doxorubicine.

[Isolation and activity of bacteria for the biodegradation of microcystins].

The abilities of bacterial communities, which collected from the sediment and surface water of Dianchi Lake, for the biodegradation of microcystins (MCs) were firstly investigated. It was shown that the biodegradation rates of both MC-RR and LR by bacteria in sediment were apparently higher than those by bacteria on surface water. Five strains of bacteria, which have the abilities in the biodegradation of MCs, from the sediment were isolated using the liquid and solid medium containing MC-RR and LR as the carbon and nitrogen sources, which was extracted and purified from the cells of cyanobacterial bloom. Among the bacteria isolated, bacterium D was found to have a strong ability in the biodegradation of MCs. Initial MC-RR and LR of 60.1 mg x L(-1) and 38.7 mg x L(-1) were completely removed in 3 days and the average biodegradation rates per day for MC-RR and LR were 20.0 mg x L(-1) and 12.9 mg x L(-1), respectively.