Neuronal cell apoptosis by a receptor-binding domain peptide of ApoE4, not through low-density lipoprotein receptor-related protein.

Neuronal cell apoptosis by a receptor-binding domain peptide of ApoE4, not through low-density lipoprotein receptor-related protein.
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神经元细胞凋亡是通过 ApoE4 的受体结合域肽进行的,而不是通过低密度脂蛋白受体相关蛋白进行的。

DOI:
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发表时间:
2000
期刊:
Biochemical and Biophysical Research Communications - BBRC
影响因子:
--
通讯作者:
K. Umezawa
K. Umezawa
中科院分区:
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文献类型:
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作者:
A. Hagiwara;Y. Hashimoto;T. Niikura;Y. Ito;K. Terashita;Y. Kita;I. Nishimoto;K. Umezawa

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由于由低密度脂蛋白(LDL)受体相关蛋白(LRP)结合结构域组成的载脂蛋白E4(ApoE 4)肽[ApoE 4(141-149)(2)或ApoE(141-155)(2)]在原代神经元和神经元细胞系中发挥神经毒性,因此这些作用是否由LRP介导一直存在争议。在此,我们研究了ApoE 4(141-149)(2)诱导的毒性是否由LRP介导,在神经元细胞系统中,ApoE 4毒性由LRP介导:血清剥夺的F11神经元细胞。在这些细胞中,ApoE 4通过凋亡以对半胱天冬酶抑制剂和百日咳毒素(PTX)敏感的方式发挥毒性,ApoE 4(141-149)(2)也通过凋亡引起细胞死亡,但以半胱天冬酶抑制剂抗性、PTX抗性方式。LRP的反义寡核苷酸不能抑制ApoE 4(141-149)(2)诱导的死亡。因此,我们得出结论,ApoE 4(141-149)(2)能够发挥神经毒性而不涉及LRP。
Since an apolipoprotein E4 (ApoE4) peptide composed of the low-density lipoprotein (LDL) receptor-related protein (LRP)-binding domain [ApoE4(141-149)(2) or ApoE(141-155)(2)] exerts neurotoxicity in primary neurons and neuronal cell lines, it has been controversial whether these effects are mediated by LRP. Here, we examined whether ApoE4(141-149)(2)-induced toxicity is mediated by LRP in a neuronal cell system where ApoE4 toxicity is mediated by LRP: serum-deprived F11 neuronal cells. In these cells, where ApoE4 exerted toxicity by apoptosis in a manner sensitive to both caspase inhibitors and pertussis toxin (PTX), ApoE4(141-149)(2) also caused cell death by apoptosis but in a caspase-inhibitor-resistant, PTX-resistant manner. ApoE4(141-149)(2)-induced death was not inhibited by antisense oligonucleotides to LRP. Therefore, we conclude that ApoE4(141-149)(2) is able to exert neurotoxicity without involving LRP.
DOI: --
发表时间: 1982-08
影响因子: 6.5
作者:
V. Zannis;J. Breslow
通讯作者: V. Zannis;J. Breslow
DOI: 10.1097/00001756-199611040-00025
发表时间: 1996-11-04
期刊: NEUROREPORT
影响因子: 1.7
作者:
Marques, MA;Tolar, M;Crutcher, KA
通讯作者: Crutcher, KA
DOI: 10.1126/science.8171342
发表时间: 1994-05-06
期刊: SCIENCE
影响因子: 56.9
作者:
NATHAN, BP;BELLOSTA, S;PITAS, RE
通讯作者: PITAS, RE