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Human Umbilical Cord Mesenchymal Stem Cells Attenuate Abdominal Aortic Aneurysm Progression in Sprague-Dawley Rats: Implication of Vascular Smooth Muscle Cell Phenotypic Modulation
Author(s) -
Hao Wen,
Mingjing Wang,
Shiqiang Gong,
Xintong Li,
Jinze Meng,
Jie Wen,
Yifei Wang,
Shuqing Zhang,
Shijie Xin
Publication year - 2020
Publication title -
stem cells and development
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.99
H-Index - 114
eISSN - 1557-8534
pISSN - 1547-3287
DOI - 10.1089/scd.2020.0058
Subject(s) - mesenchymal stem cell , biology , vascular smooth muscle , elastin , cancer research , extracellular matrix , phenotype , abdominal aortic aneurysm , umbilical cord , aortic aneurysm , immunology , microbiology and biotechnology , medicine , aneurysm , endocrinology , surgery , aorta , smooth muscle , gene , biochemistry , genetics
Abdominal aortic aneurysm (AAA) is life-threatening, for which efficient nonsurgical treatment strategy has not been available so far. Several previous studies investigating the therapeutic effect of mesenchymal stem cells (MSCs) in AAA indicated that MSCs could inhibit aneurysmal inflammatory responses and extracellular matrix destruction, and suppress aneurysm occurrence and expansion. Vascular smooth muscle cell (VSMC) phenotypic plasticity is reported to be predisposed in AAA initiation and progression. However, little is known about the effect of MSCs on VSMC phenotypic modulation in AAA. In this study, we investigate the therapeutic efficacy of umbilical cord mesenchymal stem cells (UC-MSCs) in elastase-induced AAA model and evaluate the effect of UC-MSC on VSMC phenotypic regulation. We demonstrate that the intravenous injection of UC-MSC attenuates elastase-induced aneurysmal expansion, reduces elastin degradation and fragmentation, inhibits MMPs and TNF-α expression, and preserves and/or restores VSMC contractile phenotype in AAA. Taken together, these results highlight the therapeutic and VSMC phenotypic modulation effects of UC-MSC in AAA progression, which further indicates the potential of applying UC-MSC as an alternative treatment candidate for AAA.

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