Abstract
BACKGROUND & OBJECTIVE: Mer is one member of Axl receptor tyrosine kinase family; its ligand Gas6 can bind Mer, then stimulate the tyrosine kinase activity and downstream cell signal pathway of Mer, and take part in cell inflammation, apoptosis and thrombosis. There are more and more reports on Mer function, while few on its association with malignant diseases. This study was to detect the expression of Mer on T-cell leukemia cell line--Jurkat, and investigate its anti-apoptosis function and the mechanism.
METHODS: Flow cytometry (FCM) was used to detect Mer expression on normal T cells and Jurkat cells. RNA interference (RNAi) was used to block the expression of Mer on Jurkat cells. The effect of Mer on the proliferation of Jurkat cells was assessed by MTT assay, and its effect on serum starvation-induced apoptosis was evaluated by FCM with Annexin V/PI double staining. The expression of apoptosis-associated genes Bcl-2 and Caspase-3 in Jurkat cells was detected by real-time polymerase chain reaction (PCR) after Mer blocking.
RUSELTS: Mer was not expressed in normal T cells both in peripheral blood and bone marrow, but highly expressed in Jurkat cells with a positive rate of 51.1%±5.2%. The inhibition rate of Mer expression in Jurkat cells by RNAi was 86.0%±10.3%. After 48-hour serum starvation, the apoptosis rate was 15.3%±4.3% in Mer-blocking Jurkat cells, and only 1.5%±1.0% in control Jurkat cells(P<0.01). There was no significant difference in Jurkat cell proliferation rate between these 2 groups. After Mer blocking, Bcl-2 expression was decreased by 42.7%±8.6% of control(P<0.01), Caspase-3 expression showed no significant change.
CONCLUSION: Mer is highly expressed in Jurkat cells, and could inhibit cell apoptosis via Bcl-2 signaling pathway.
Author notes
Disclosure: No relevant conflicts of interest to declare.
