Amyloid beta-protein induces its own production in cultured degenerating cerebrovascular smooth muscle cells.
Amyloid beta-protein induces its own production in cultured degenerating cerebrovascular smooth muscle cells.
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β-淀粉样蛋白在培养的退化脑血管平滑肌细胞中诱导其自身产生。
DOI：
10.1046/j.1471-4159.1995.65020931.x
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发表时间：
1995
影响因子：
4.7
通讯作者：
VanNostrand,WE
中科院分区：
文献类型：
--
作者：
Davis-Salinas,J;Saporito-Irwin,SM;Cotman,CW;VanNostrand,WE
阿尔茨海默病及相关疾病的进展涉及淀粉样β蛋白（Aβ）沉积和实质及脑血管的病理改变。这些疾病的脑血管Aβ沉积与血管壁平滑肌细胞变性有关，平滑肌细胞表达Aβ前体（a - β pp）和Aβ。在这里，我们发现Aβ1 - 42， Aβ丰富的脑血管形式，导致培养的人脑血管平滑肌细胞的细胞变性。这种应激反应伴随着这些退化细胞中产生的细胞a β pp和可溶性a β肽水平的显著增加。这些数据提供了第一个实验证据，证明Aβ可能有助于脑血管病理的发生和进展。目前的研究结果表明，这一机制可能涉及一种具有新型产物-前体关系的分子级联反应，导致a β的不良产生和随后的积累。
The progression of Alzheimer's disease and related disorders involves amyloid β‐protein (Aβ) deposition and pathologic changes in the parenchyma as well as cerebral blood vessels. The cerebrovascular Aβ deposits in these disorders are associated with degenerating smooth muscle cells in the vessel wall, which have been shown to express the Aβ precursor (AβPP) and Aβ. Here, we show that Aβ1–42, an abundant cerebrovascular form of Aβ, causes cellular degeneration in cultured human cerebrovascular smooth muscle cells. This stress response is accompanied by a striking increase in the levels of cellular AβPP and soluble Aβ peptide produced in these degenerating cells. These data provide the first experimental evidence that Aβ can potentially contribute to the onset and progression of the cerebrovascular pathology. The present findings suggest that this mechanism may involve a molecular cascade with a novel product‐precursor relationship that results in the adverse production and subsequent accumulation of Aβ.