+ Site Statistics
References:
54,258,434
Abstracts:
29,560,870
PMIDs:
28,072,757
+ Search Articles
+ Subscribe to Site Feeds
Most Shared
PDF Full Text
+ PDF Full Text
Request PDF Full Text
+ Follow Us
Follow on Facebook
Follow on Twitter
Follow on LinkedIn
+ Translate
+ Recently Requested

Inhibitory role of reactive oxygen species in the differentiation of multipotent vascular stem cells into vascular smooth muscle cells in rats: a novel aspect of traditional culture of rat aortic smooth muscle cells



Inhibitory role of reactive oxygen species in the differentiation of multipotent vascular stem cells into vascular smooth muscle cells in rats: a novel aspect of traditional culture of rat aortic smooth muscle cells



Cell and Tissue Research 362(1): 97-113



Proliferative or synthetic vascular smooth muscle cells (VSMCs) are widely accepted to be mainly derived from the dedifferentiation or phenotypic modulation of mature contractile VSMCs, i.e., a phenotype switch from a normally quiescent and contractile type into a proliferative or synthetic form. However, this theory has been challenged by recent evidence that synthetic VSMCs predominantly originate instead from media-derived multipotent vascular stem cells (MVSCs). To test these hypotheses further, we re-examine whether the conventional rat aortic SMC (RASMC) culture involves the VSMC differentiation of MVSCs or the dedifferentiation of mature VSMCs and the potential mechanism for controlling the synthetic phenotype of RASMCs. We enzymatically isolated RASMCs and cultured the cells in both a regular growth medium (RGM) and a stem cell growth medium (SCGM). Regardless of culture conditions, only a small portion of freshly isolated RASMCs attaches, survives and grows slowly during the first 7 days of primary culture, while expressing both SMC- and MVSC-specific markers. RGM-cultured cells undergo a process of synthetic SMC differentiation, whereas SCGM-cultured cells can be differentiated into not only synthetic SMCs but also other somatic cells. Notably, compared with the RGM-cultured differentiated RASMCs, the SCGM-cultured undifferentiated cells exhibit the phenotype of MVSCs and generate greater amounts of reactive oxygen species (ROS) that act as a negative regulator of differentiation into synthetic VSMCs. Knockdown of phospholipase A2, group 7 (Pla2g7) suppresses ROS formation in the MVSCs while enhancing SMC differentiation of MVSCs. These results suggest that cultured synthetic VSMCs can be derived from the SMC differentiation of MVSCs with ROS as a negative regulator.

(PDF emailed within 0-6 h: $19.90)

Accession: 058121806

Download citation: RISBibTeXText

PMID: 26022334

DOI: 10.1007/s00441-015-2193-9


Related references

Adult vascular smooth muscle cells in culture express neural stem cell markers typical of resident multipotent vascular stem cells. Cell and Tissue Research 358(1): 203-216, 2015

Endothelial cells negatively modulate reactive oxygen species generation in vascular smooth muscle cells: role of thioredoxin. Hypertension 54(2): 427-433, 2009

Thrombin causes vascular endothelial growth factor expression in vascular smooth muscle cells: role of reactive oxygen species. Arteriosclerosis, Thrombosis, and Vascular Biology 21(9): 1550-1555, 2001

Thrombin upregulates the expression of vascular endothelial growth factor in vascular smooth muscle cells: Role of several protein kinases and reactive oxygen species. Atherosclerosis 151(1): 21-22, 2000

Ox-LDL-induced LOX-1 expression in vascular smooth muscle cells: role of reactive oxygen species. Fundamental and Clinical Pharmacology 25(5): 572-579, 2012

Oxidation Prevents HMGB1 Inhibition on PDGF-Induced Differentiation of Multipotent Vascular Stem Cells to Smooth Muscle Cells: A Possible Mechanism Linking Oxidative Stress to Atherosclerosis. Biomed Research International 2018: 4019814, 2018

The role of vascular smooth-muscle cells in atherogenesis: phenotypic modulation of the medial smooth-muscle cells in the aortic bifurcation. Japanese Circulation Journal 55(10): 1003-1009, 1991

Role of reactive oxygen species in bradykinin-induced proliferation of vascular smooth muscle cells. Biological Research 37(3): 419-430, 2004

Angiotensin II effect on vascular smooth muscle cells of prehypertensive rats Relationship with reactive oxygen species. Biocell 24(3): 295, 2000

Mitochondrial reactive oxygen species and c-Src play a critical role in hypoxic response in vascular smooth muscle cells. Cardiovascular Research 67(4): 714-722, 2005

Characterization of vascular smooth muscle progenitor cells in circulating human peripheral blood Potential origin of intimal smooth muscle cells in vascular lesions and involvement in vascular inflammation. Circulation 108(17 Supplement): IV-285, October 28, 2003

Reactive oxygen species mediate angiotensin II-induced vascular endothelial growth factor expression in rat vascular smooth muscle cells. European Heart Journal 19(ABST SUPPL ): 271, 1998

Inhibition of the p53 tumor suppressor gene results in growth of human aortic vascular smooth muscle cells. Potential role of p53 in regulation of vascular smooth muscle cell growth. Hypertension 34(2): 192-200, 1999

In vitro differentiation of porcine aortic vascular precursor cells to endothelial and vascular smooth muscle cells. American Journal of Physiology. Cell Physiology 309(5): C320-C331, 2015

Upregulation of antioxidants by endothelial cells negatively modulates production of reactive oxygen species in co-cultured human vascular smooth muscle cells. 2007