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Serum Withdrawal‐Induced Apoptosis in ZrchI Prion Protein (PrP) Gene‐Deficient Neuronal Cell Line Is Suppressed by PrP, Independent of Doppel
Author(s) -
Nishimura Takuya,
Sakudo Akikazu,
Hashiyama Yoriko,
Yachi Akiko,
Saeki Keiichi,
Matsumoto Yoshitsugu,
Ogawa Masaharu,
Sakaguchi Suehiro,
Itohara Shigeyoshi,
Onodera Takashi
Publication year - 2007
Publication title -
microbiology and immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.664
H-Index - 70
eISSN - 1348-0421
pISSN - 0385-5600
DOI - 10.1111/j.1348-0421.2007.tb03920.x
Subject(s) - prnp , biology , apoptosis , programmed cell death , cell culture , immortalised cell line , microbiology and biotechnology , ectopic expression , oxidative stress , cell , sod1 , superoxide dismutase , gene , biochemistry , genetics , allele
Previous studies have shown that cellular prion protein (PrP C ) plays anti‐apoptotic and anti‐oxidative role against cell death induced by serum‐deprivation (SDP) in an immortalized prion protein gene‐deficient neuronal cell line derived from Rikn prion protein (PrP) gene‐deficient ( Prnp –/– ) mice, which ectopically produce excess Doppel (Dpl) (PrP‐like glycoprotein). To investigate whether PrP C inhibits apoptotic neuronal cell death without Dpl, an immortalized cell line was established from the brain of ZrchI Prnp –/– mice, which do not show ectopic expression of Dpl. The results using a ZrchI neuronal Prnp –/– cell line (NpL2) showed that PrP C potently inhibited SDP‐induced apoptotic cell death. Furthermore, PrP C expression enhanced the superoxide dismutase (SOD) activity in NpL2 cells. These results indicate that Dpl production did not affect anti‐apoptotic and anti‐oxidative functions of PrP, suggesting that PrP C may be directly correlated with protection against oxidative stress.