cAMP-induced decrease in cell-surface laminin receptor and cellular prion protein attenuates amyloid-β uptake and amyloid-β-induced neuronal cell death.
cAMP-induced decrease in cell-surface laminin receptor and cellular prion protein attenuates amyloid-β uptake and amyloid-β-induced neuronal cell death.
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cAMP 诱导的细胞表面层粘连蛋白受体和细胞朊病毒蛋白的减少减弱了淀粉样蛋白 β 的摄取和淀粉样蛋白 β 诱导的神经元细胞死亡。
DOI:
10.1002/1873-3468.14467
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发表时间:
2022-11
期刊:
影响因子:
3.5
通讯作者:
Bhat, Narayan R.
中科院分区:
文献类型:
--
作者:
Gopalakrishna, Rayudu;Lin, Charlotte Y.;Oh, Andrew;Le, Calvin;Yang, Seolyn;Hicks, Alexandra;Kindy, Mark S.;Mack, William J.;Bhat, Narayan R.
Previous studies have shown that amyloid-β oligomers (AβO) bind with high affinity to cellular prion protein (PrPC). The AβO-PrPC complex binds to cell-surface co-receptors, including the laminin receptor (67LR). Our current studies revealed that in Neuroscreen-1 cells, 67LR is the major co-receptor involved in the cellular uptake of AβO and AβO-induced cell death. Both pharmacological (dibutyryl-cAMP, forskolin, rolipram) and physiological (pituitary adenylate cyclase-activating polypeptide) cAMP-elevating agents decreased cell-surface PrPC and 67LR, thereby attenuating the uptake of AβO and the resultant neuronal cell death. These cAMP protective effects are dependent on protein kinase A, but not dependent on the exchange protein directly activated by cAMP. Conceivably, cAMP protects neuronal cells from AβO-induced cytotoxicity by decreasing cell-surface associated PrPC and 67LR.
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影响因子:
4.7
作者:
Lee B;Cao R;Choi YS;Cho HY;Rhee AD;Hah CK;Hoyt KR;Obrietan K
通讯作者:
Obrietan K
影响因子:
4.1
作者:
BETHEA, CL
通讯作者:
BETHEA, CL
影响因子:
8.8
作者:
Gunther, Erik C.;Smith, Levi M.;Strittmatter, Stephen M.
通讯作者:
Strittmatter, Stephen M.
影响因子:
4.3
作者:
Kametani F;Hasegawa M
通讯作者:
Hasegawa M
DOI:
10.1038/s41572-021-00269-y
发表时间:
2021-05-13
期刊:
Nature reviews. Disease primers
影响因子:
--
作者:
Knopman DS;Amieva H;Petersen RC;Chételat G;Holtzman DM;Hyman BT;Nixon RA;Jones DT
通讯作者:
Jones DT