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Research Paper|Volume 15, Issue 10|pp 4334—4362

Plasma exosome proteomics reveals the pathogenesis mechanism of post-stroke cognitive impairment

Baoyun Qi1, Lingbo Kong1, Xinxing Lai3,4, Linshuang Wang2, Fei Liu5, Weiwei Ji6, Dongfeng Wei2
  • 1The Eastern Area, Dongzhimen Hospital, Beijing University of Chinese Medicine, Beijing 101121, China
  • 2Institute of Basic Research in Clinical Medicine, China Academy of Chinese Medical Sciences, Beijing 100700, China
  • 3Department of Neurology, Dongzhimen Hospital, Beijing University of Chinese Medicine, Beijing 100700, China
  • 4Institute for Brain Disorders, Beijing University of Chinese Medicine, Beijing 100013, China
  • 5Department of Neurology, Hohhot Mongolian Medicine of Traditional Chinese Medicine Hospital, Hohhot 010020, China
  • 6Institute of Information on Traditional Chinese Medicine, China Academy of Chinese Medical Sciences, Beijing 100700, China
Received: October 12, 2022Accepted: May 1, 2023Published: May 20, 2023
https://doi.org/10.18632/aging.204738

Copyright: © 2023 Qi et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

Exploration and utilization of exosome biomarkers and their related functions provide the possibility for the diagnosis and treatment of post-stroke cognitive impairment (PSCI). To identify the new diagnostic and prognostic biomarkers of plasma exosome were uzed label-free quantitative proteomics and biological information analysis in PSCI patients. Behavioral assessments were performed, including the Mini-Mental Status Examination (MMSE), the Montreal Cognitive Assessment (MoCA), the Barthel index, the Morse Fall Seale (MFS) between control group (n = 10) and PSCI group (n = 10). The blood samples were collected to analyse the biomarker and differentially expressed proteins of plasma exosome using label-free quantitative proteomics and biological information. The exosomes marker proteins were determined by Western blot. The exosome morphology was observed by transmission electron microscopy. The scores of MMSE and MoCA were significantly decreased in the PSCI group. The PT% and high-density lipoprotein decreased and the INR ratio increased in PSCI group. The mean size of exosome was approximately 71.6 nm and the concentration was approximately 6.8E+7 particles/mL. Exosome proteomics identified 259 differentially expressed proteins. The mechanisms of cognitive impairment are related to regulate the degradation of ubiquitinated proteins, calcium dependent protein binding, cell adhesive protein binding, formation of fibrin clot, lipid metabolism and ATP-dependent degradation of ubiquitinated proteins in plasma exosome of PSCI patients. Plasma levels of YWHAZ and BAIAP2 were significantly increased while that of IGHD, ABCB6 and HSPD1 were significantly decreased in PSCI patients. These proteins might be target-related proteins and provide global insights into pathogenesis mechanisms of PSCI at plasma exosome proteins level.