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2型糖尿病期间循环血管前体细胞耗竭:对糖尿病缺血性并发症预防的转化性见解

Circulating Pro-Vascular Progenitor Cell Depletion During Type 2 Diabetes: Translational Insights Into the Prevention of Ischemic Complications in Diabetes.

作者信息

Terenzi Daniella C, Al-Omran Mohammed, Quan Adrian, Teoh Hwee, Verma Subodh, Hess David A

机构信息

Division of Cardiac Surgery, Keenan Research Centre for Biomedical Science and Li Ka Shing Knowledge Institute of St. Michael's Hospital, Toronto, Ontario, Canada.

Institute of Medical Science, University of Toronto, Toronto, Ontario, Canada.

出版信息

JACC Basic Transl Sci. 2018 Nov 5;4(1):98-112. doi: 10.1016/j.jacbts.2018.10.005. eCollection 2019 Feb.

Abstract

Detection of vascular regenerative cell exhaustion is required to combat ischemic complications during type 2 diabetes mellitus (T2D). We used high aldehyde dehydrogenase (ALDH) activity and surface marker co-expression to develop a high-throughput flow cytometry-based assay to quantify circulating proangiogenic and proinflammatory cell content in the peripheral blood of individuals with T2D. Circulating proangiogenic monocytes expressing anti-inflammatory M2 markers were decreased in patients with T2D. Individuals with longer duration of T2D exhibited reduced frequencies of circulating proangiogenic ALDHCD34+ progenitor cells with primitive (CD133) and migratory (CXCR4) phenotypes. This approach consistently detected increased inflammatory cell burden and decreased provascular progenitor content in individuals with T2D.

摘要

检测血管再生细胞耗竭对于对抗2型糖尿病(T2D)期间的缺血性并发症至关重要。我们利用高醛脱氢酶(ALDH)活性和表面标志物共表达,开发了一种基于高通量流式细胞术的检测方法,以量化T2D患者外周血中循环促血管生成和促炎细胞的含量。T2D患者中表达抗炎M2标志物的循环促血管生成单核细胞减少。T2D病程较长的个体,其循环中具有原始(CD133)和迁移(CXCR4)表型的促血管生成ALDHCD34+祖细胞频率降低。这种方法始终能检测到T2D患者炎症细胞负荷增加和血管前祖细胞含量减少。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0486/6390504/36dad2005923/fx1.jpg

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