- 作者: Bor-Show Tzang; Der-Yuan Chen; Chun-Chou Tsai; Szu-Yi Chiang; Tsung-Ming Lin; Tsai-Ching Hsu
- 作者服務機構: Institute of Biochemistry and Biotechnology, Chung Shan Medical University, Taichung, Taiwan, R.O.C.
- 中文摘要: --
- 英文摘要:
Background: Human parvovirus B19 (B19) is known to induce apoptosis that has
been associated with a variety of autoimmune disorders. Although we have previously
reported that B19 non-structural protein (NS1) induces mitochondrial-dependent
apoptosis in COS-7 cells, the precise mechanism of B19-NS1 in developing
autoimmunity is still obscure.
Methods: To further examine the effect of B19-NS1 in presence of autoantigens,
COS-7 cells were transfected with pEGFP, pEGFP-B19-NS1 and pEGFP-NS1K334E,
a mutant form of B19-NS1, and detected the expressions of autoantigens by various
autoantibodies against Sm, U1 small nuclear ribonucleoprotein (U1-snRNP), SSA/Ro,
SSB/La, Scl-70, Jo-1, Ku, and centromere protein (CENP) A/B by using
Immunoblotting.
Results: Significantly increased apoptosis was detected in COS-7 cells transfected
with pEGFP-B19-NS1 compared to those transfected with pEGFP. Meanwhile, the
apoptotic 70kDa U1-snRNP protein in COS-7 cells transfected with pEGFP-B19-NS1
is cleaved by caspase-3 and converted into a specific 40kDa product, which were
recognized by anti-U1-snRNP autoantibody. In contrast, significantly decreased
apoptosis and cleaved 40kDa product were observed in COS-7 cells transfected with
pEGFP-NS1K334E compared to those transfected with pEGFP-B19-NS1. - 中文關鍵字: --
- 英文關鍵字: --