Bcl-2 Knockdown Accelerates T Cell Receptor-Triggered Activation-Induced Cell Death in Jurkat T Cells.
10.4196/kjpp.2014.18.1.73
- Author:
Yun Jung LEE
1
;
Tae Joon WON
;
Kyeong Eun HYUNG
;
Mi Ji LEE
;
Young hye MOON
;
Ik Hee LEE
;
Byung Sung GO
;
Kwang Woo HWANG
Author Information
1. Laboratory of Host Defense Modulation, College of Pharmacy, Chung-Ang University, Seoul 156-756, Korea. khwang@cau.ac.kr
- Publication Type:Original Article
- Keywords:
AICD;
Apoptosis;
Bcl-2;
shRNA;
T cell
- MeSH:
Apoptosis;
Autoimmune Diseases;
Caspase 3;
Cell Death*;
Gene Expression;
Humans;
NF-kappa B;
Peptide Hydrolases;
Physiology;
Receptors, Death Domain;
RNA, Small Interfering;
Signal Transduction;
T-Lymphocytes*;
TNF Receptor-Associated Factor 4;
Tumor Necrosis Factor Receptor-Associated Peptides and Proteins
- From:The Korean Journal of Physiology and Pharmacology
2014;18(1):73-78
- CountryRepublic of Korea
- Language:English
-
Abstract:
Cell death and survival are tightly controlled through the highly coordinated activation/inhibition of diverse signal transduction pathways to insure normal development and physiology. Imbalance between cell death and survival often leads to autoimmune diseases and cancer. Death receptors sense extracellular signals to induce caspase-mediated apoptosis. Acting upstream of CED-3 family proteases, such as caspase-3, Bcl-2 prevents apoptosis. Using short hairpin RNAs (shRNAs), we suppressed Bcl-2 expression in Jurkat T cells, and this increased TCR-triggered AICD and enhanced TNFR gene expression. Also, knockdown of Bcl-2 in Jurkat T cells suppressed the gene expression of FLIP, TNF receptor-associated factors 3 (TRAF3) and TRAF4. Furthermore, suppressed Bcl-2 expression increased caspase-3 and diminished nuclear factor kappa B (NF-kappaB) translocation.
