Mesenchymal stem cell dysfunction in diabetes

被引:46
作者
Fijany, Arman [1 ]
Sayadi, Lohrasb R. [1 ]
Khoshab, Nima [1 ]
Banyard, Derek A. [1 ]
Shaterian, Ashkaun [1 ]
Alexander, Michael [2 ]
Lakey, Johnathan R. T. [2 ]
Paydar, Keyianoosh Z. [1 ]
Evans, Gregory R. D. [1 ,2 ]
Widgerow, Alan D. [1 ,2 ,3 ]
机构
[1] UC Irvine, Dept Plast Surg, Ctr Tissue Engn, Orange, CA 92868 USA
[2] UC Irvine, Dept Surg & Biomed Engn, Orange, CA 92868 USA
[3] Univ Calif Irvine, Suite 108a Bldg 55,101 S City Dr, Orange, CA 92868 USA
关键词
Diabetes; Mesenchymal stem cell; MSC; Dysfunction; ENDOTHELIAL GROWTH-FACTOR; STROMAL-VASCULAR FRACTION; GLYCATION END-PRODUCTS; BONE-MARROW; HIGH GLUCOSE; INSULIN-RESISTANCE; ADIPOSE-TISSUE; EXTRACELLULAR VESICLES; OXIDATIVE STRESS; AQUEOUS-HUMOR;
D O I
10.1007/s11033-018-4516-x
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
070307 [化学生物学]; 071010 [生物化学与分子生物学];
摘要
Diabetes mellitus (DM) is a chronic disease that results in a variety of systemic complications. Recently, stem cell-based therapies have been proposed as potential modalities to manage DM related complications. Mesenchymal stem cell (MSC) based therapies are often considered as an ideal stem cell-based treatment for DM management due to their immunosuppressive characteristics, anti-inflammatory properties and differentiation potential. While MSCs show tremendous promise, the underlying functional deficits of MSCs in DM patients is not well understood. Using the MEDLINE database to define these functional deficits, our search yielded 1826 articles of which 33 met our inclusion criteria. This allowed us to review the topic and illuminate four major molecular categories by which MSCs are compromised in both Type 1 DM and Type II DM models which include: (1) changes in angiogenesis/vasculogenesis, (2) altered pro-inflammatory cytokine secretion, (3) increased oxidative stress markers and (4) impaired cellular differentiation and decreased proliferation. Knowledge of the deficits in MSC function will allow us to more clearly assess the efficacy of potential biologic therapies for reversing these dysfunctions when treating the complications of diabetic disease.
引用
收藏
页码:1459 / 1475
页数:17
相关论文
共 118 条
[1]
Receptor for Advanced Glycation End Products-Mediated Signaling Impairs the Maintenance of Bone Marrow Mesenchymal Stromal Cells in Diabetic Model Mice [J].
Aikawa, Eriko ;
Fujita, Ryo ;
Asai, Maiko ;
Kaneda, Yasufumi ;
Tamai, Katsuto .
STEM CELLS AND DEVELOPMENT, 2016, 25 (22) :1721-1732
[2]
Adiponectin serum levels correlate with insulin resistance in type 2 diabetic patients [J].
Aleidi, Shereen ;
Issa, Ala ;
Bustanji, Haidar ;
Khalil, Mohammad ;
Bustanji, Yasser .
SAUDI PHARMACEUTICAL JOURNAL, 2015, 23 (03) :250-256
[3]
Ali Fatima, 2017, Chronic Dis Transl Med, V3, P105, DOI 10.1016/j.cdtm.2017.02.006
[4]
[Anonymous], 2014, CELLR4
[5]
[Anonymous], 2017, National Diabetes Statistics Report, P20
[6]
[Anonymous], 2013, ISRN OPHTHALMOL
[7]
[Anonymous], SUN
[8]
[Anonymous], BROWN ML
[9]
[Anonymous], ENDOCR RES
[10]
In vitro angiogenesis: endothelial cell tube formation on gelled basement membrane extract [J].
Arnaoutova, Irina ;
Kleinman, Hynda K. .
NATURE PROTOCOLS, 2010, 5 (04) :628-635