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淀粉样β肽在皮肤血栓形成过程中释放。

Amyloid Beta Peptide Is Released during Thrombosis in the Skin.

机构信息

Department of Biochemistry, School of Medicine, Universidad Central del Caribe, PO Box 60327, Bayamon, PR 00960-6032, USA.

Department of Biology, University of Puerto Rico Rio Piedras, San Juan, PR 00936-8377, USA.

出版信息

Int J Mol Sci. 2018 Jun 8;19(6):1705. doi: 10.3390/ijms19061705.

DOI:10.3390/ijms19061705
PMID:29890636
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6032379/
Abstract

While it is known that amyloid beta (Aβ) deposits are found in different tissues of both Alzheimer’s disease (AD) patients and healthy individuals, there remain questions about the physiological role of these deposits, the origin of the Aβ peptide, and the mechanisms of its localization to the tissues. Using immunostaining with specific antibodies, as well as enzyme-linked immunosorbent assay, this study demonstrated Aβ40 peptide accumulation in the skin during local experimental photothrombosis in mice. Specifically, Aβ peptide accumulation was concentrated near the dermal blood vessels in thrombotic skin. It was also studied whether the released peptide affects microorganisms. Application of Aβ40 (4 µM) to the external membrane of yeast cells significantly increased membrane conductance with no visible effect on mouse host cells. The results suggest that Aβ release in the skin is related to skin injury and thrombosis, and occurs along with clotting whenever skin is damaged. These results support the proposition that Aβ release during thrombosis serves as part of a natural defense against infection.

摘要

虽然已知淀粉样蛋白β(Aβ)沉积物存在于阿尔茨海默病(AD)患者和健康个体的不同组织中,但这些沉积物的生理作用、Aβ 肽的来源以及其在组织中定位的机制仍存在疑问。本研究通过使用特异性抗体的免疫染色和酶联免疫吸附试验,证明了在局部实验性光血栓形成的小鼠皮肤中 Aβ40 肽的积累。具体而言,Aβ 肽积累集中在血栓形成皮肤的真皮血管附近。还研究了释放的肽是否会影响微生物。将 Aβ40(4µM)应用于酵母细胞的外膜会显著增加膜电导,而对小鼠宿主细胞没有明显影响。结果表明,皮肤中 Aβ 的释放与皮肤损伤和血栓形成有关,并且只要皮肤受损就会与凝血同时发生。这些结果支持这样一种观点,即血栓形成过程中 Aβ 的释放是天然抗感染防御的一部分。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc00/6032379/7c07a76af1da/ijms-19-01705-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc00/6032379/b912e2058234/ijms-19-01705-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc00/6032379/95b216c47b94/ijms-19-01705-g002a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc00/6032379/9d898b8b2d90/ijms-19-01705-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc00/6032379/7c07a76af1da/ijms-19-01705-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc00/6032379/b912e2058234/ijms-19-01705-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc00/6032379/95b216c47b94/ijms-19-01705-g002a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc00/6032379/9d898b8b2d90/ijms-19-01705-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc00/6032379/7c07a76af1da/ijms-19-01705-g004.jpg

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A Peptide Originated from Platelets Promises New Strategy in Anti-Alzheimer's Drug Development.
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