RESUMEN
Apoptosis is a complex and highly self-regulating form of cell death, which is an important cause of the continuous decline in ventricular function and is widely involved in the occurrence and development of heart failure, myocardial infarction, and myocarditis. Endoplasmic reticulum stress plays a crucial role in apoptosis-inducing. Accumulation of misfolded or unfolded proteins causes cells to undergo a stress response called unfolded protein response (UPR). UPR initially has a cardioprotective effect. Nevertheless, prolonged and severe ER stress will lead up to apoptosis of stressed cells. Non-coding RNA is a type of RNA that does not code proteins. An ever-increasing number of studies have shown that non-coding RNAs are involved in regulating endoplasmic reticulum stress-induced cardiomyocyte injury and apoptosis. In this study, the effects of miRNA and LncRNA on endoplasmic reticulum stress in various heart diseases were mainly discussed to clarify their protective effects and potential therapeutic strategies for apoptosis.
RESUMEN
AIM: To express two fusion forms of hepatitis B virus surface antigen (HBsAg-s and s-HBsAg) in the Pichia pastoris expression system, and compare immunogenicity of the two fusion proteins. METHODS: Was fused GM-CSF to 5' or 3' terminal of HBsAg by inserting the gene fragment of connecting peptide (Gly(4)Ser)(3) to linker gene of GM-CSF and HBsAg. The two fusion proteins were expressed by secreting type expression plasmid pPIC9K in the Pichia pastoris, then the expressed products were detected by SDS-PAGE, Western blot and purified by DEAE-Sepharose Fast Flow ion exchange columns. Mice were inoculated with the two purified HBsAg/GM-CSF fusion proteins and HBsAg respectively in each, and the levels of anti-HBsAg in mice sera were tested by ELISA. RESULTS: Two HBsAg/GM-CSF fusion proteins were successfully expressed in the form of secretion in Pichia pastoris strain GS115, and exhibited specific reaction with both anti-HBsAg and anti-GM-CSF antibodies in Western blot. ELISA results showed after the inoculation the levels of anti-HBsAg induced by the two HBsAg/GM-CSF fusion proteins was higher than by HBsAg alone (P<0.05). Furthermore, the effect by fusing GM-CSF to C terminal of HBsAg was better than by fusing GM-CSF to N terminal of HBsAg. CONCLUSION: The immunogenicity of HBsAg could be enhanced by fusing GM-CSF.