| Autor: |
Kucheryavykh LY; Department of Biochemistry, School of Medicine, Universidad Central del Caribe, PO Box 60327, Bayamon, PR 00960-6032, USA. lilia.kucheryavykh@uccaribe.edu., Kucheryavykh YV; Department of Biochemistry, School of Medicine, Universidad Central del Caribe, PO Box 60327, Bayamon, PR 00960-6032, USA. yuriy.kucheryavykh@uccaribe.edu., Washington AV; Department of Biology, University of Puerto Rico Rio Piedras, San Juan, PR 00936-8377, USA. anthony.washington@upr.edu., Inyushin MY; Department of Physiology, School of Medicine, Universidad Central del Caribe, PO Box 60327, Bayamon, PR 00960-6032, USA. mikhail.inyushin@uccaribe.edu. |
| Abstrakt: |
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. |
