[Endoplasmic reticulum stress in INS-1-3 cell associated with the expression changes of MODY gene pathway].
Objective:To profile the gene expression changes associated with endoplasmic reticulum stress in INS-1-3 cells induced by thapsigargin (TG) and tunicamycin (TM).Methods:Normal cultured INS-1-3 cells were used as a control. TG and TM were used to induce endoplasmic reticulum stress in INS-1-3 cells. Digital gene expression profiling technique was used to detect differentially expressed gene. The changes of gene expression were detected by expression pattern clustering analysis, gene ontology (GO) function and pathway enrichment analysis. Real time polymerase chain reaction (RT-PCR) was used to verify the key changes of gene expression.Results:Compared with the control group, there were 57 (45 up-regulated, 12 down-regulated) and 135 (99 up-regulated, 36 down-regulated) differentially expressed genes in TG and TM group, respectively. GO function enrichment analyses indicated that the main enrichment was in the endoplasmic reticulum. In signaling pathway analysis, the identified pathways were related with endoplasmic reticulum stress, antigen processing and presentation, protein export, and most of all, the maturity onset diabetes of the young (MODY) pathway.Conclusion:Under the condition of endoplasmic reticulum stress, the related expression changes of transcriptional factors in MODY signaling pathway may be related with the impaired function in islet beta cells.
Laboratory of Endocrinology, China-Japan Friendship Hospital, Beijing 100029, China.
Y T
YT
Liu
S R
SR
Li
Z
Z
Wang
J Z
JZ
Xiao
D000818:Animals; D002460:Cell Line; D004721:Endoplasmic Reticulum; D059865:Endoplasmic Reticulum Stress; D051536:Hepatocyte Nuclear Factors / Q000235:genetics*; D015398:Signal Transduction; D019284:Thapsigargin; D014415:Tunicamycin; D015854:Up-Regulation
D051536:Hepatocyte Nuclear Factors; D014415:Tunicamycin; D019284:Thapsigargin