SiRNA-mediated PIAS1 silencing promotes inflammatory response and leads to injury of cerulein-stimulated pancreatic acinar cells via regulation of the P38MAPK signaling pathway

Corrigendum in: /10.3892/ijmm.2020.4803

  • Authors:
    • Ping Chen
    • Liya Huang
    • Yongping Zhang
    • Minmin Qiao
    • Yaozong Yuan
  • View Affiliations

  • Published online on: October 1, 2010     https://doi.org/10.3892/ijmm_00000507
  • Pages: 619-626
Metrics: Total Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )


Abstract

Our aim in this study was to investigate the changes of inflammatory response by protein inhibitor of activated signal transducer and activator of transcription 1 (PIAS1) gene silencing treatment in cerulein-stimulated AR42J cells, and relate them to changes in cell injury, thus providing evidence for developing clinical therapies. This study examined the effects of cerulein on the activity of P38 mitogen activated protein kinase (P38MAPK), c-jun NH2-terminal kinase/stress-activated protein kinase and the inflammatory mediators released by PIAS1 gene-silenced AR42J cells. Consequently, the markers including DNA ladder, cell apoptotic rat, cell cycles, levels of cell cycle and apoptotic related factors were used to determine the effects of PIAS1 gene silencing on the cerulein-induced cell injury. The results indicated that in the cerulein-stimulated PIASI silencing cells, the activity of P38MAPK was enhanced, while at the same time, the levels of inflammatory mediators such as the tumor necrosis factor-α, interleukin (IL)-1β, IL-6 and matrix metallopeptidase-9, were markedly higher than those of other cerulein-stimulated cells. Thus, the cerulein-stimulated PIASI gene-silenced cells obviously increased cell arrest in the G1/M phase by increasing P21 and P27 expression, and also induced apoptosis by regulating the P53 signaling pathway. This study suggests that the down-regulation of PIAS1 is efficacious at enhancing the expression of inflammatory mediators and inducing cell injury in acute pancreatitis (AP), thus deteriorating the severity of disease. It provides evidence that PIAS1 is a potential therapeutic target for AP.

Related Articles

Journal Cover

October 2010
Volume 26 Issue 4

Print ISSN: 1107-3756
Online ISSN:1791-244X

Sign up for eToc alerts

Recommend to Library

Copy and paste a formatted citation
x
Spandidos Publications style
Chen P, Huang L, Zhang Y, Qiao M and Yuan Y: SiRNA-mediated PIAS1 silencing promotes inflammatory response and leads to injury of cerulein-stimulated pancreatic acinar cells via regulation of the P38MAPK signaling pathway Corrigendum in /10.3892/ijmm.2020.4803 . Int J Mol Med 26: 619-626, 2010
APA
Chen, P., Huang, L., Zhang, Y., Qiao, M., & Yuan, Y. (2010). SiRNA-mediated PIAS1 silencing promotes inflammatory response and leads to injury of cerulein-stimulated pancreatic acinar cells via regulation of the P38MAPK signaling pathway Corrigendum in /10.3892/ijmm.2020.4803 . International Journal of Molecular Medicine, 26, 619-626. https://doi.org/10.3892/ijmm_00000507
MLA
Chen, P., Huang, L., Zhang, Y., Qiao, M., Yuan, Y."SiRNA-mediated PIAS1 silencing promotes inflammatory response and leads to injury of cerulein-stimulated pancreatic acinar cells via regulation of the P38MAPK signaling pathway Corrigendum in /10.3892/ijmm.2020.4803 ". International Journal of Molecular Medicine 26.4 (2010): 619-626.
Chicago
Chen, P., Huang, L., Zhang, Y., Qiao, M., Yuan, Y."SiRNA-mediated PIAS1 silencing promotes inflammatory response and leads to injury of cerulein-stimulated pancreatic acinar cells via regulation of the P38MAPK signaling pathway Corrigendum in /10.3892/ijmm.2020.4803 ". International Journal of Molecular Medicine 26, no. 4 (2010): 619-626. https://doi.org/10.3892/ijmm_00000507