Barley beta‐glucan promotes MnSOD expression and enhances angiogenesis under oxidative microenvironment. Issue 1 (11th November 2014)

• Record Type: Journal Article
• Authors: Agostini, Silvia; Chiavacci, Elena; Matteucci, Marco; Torelli, Michele; Pitto, Letizia; Lionetti, Vincenzo
• Is Part Of: Journal of cellular and molecular medicine. Volume 19:Issue 1(2015)
• Page Start: 227
• Page End: 238
• Publication Date: 2014-11-11
• Subjects: Cytology; Medicine; Molecular Biology; Cytologie -- Périodiques; Médecine -- Périodiques; Biologie moléculaire -- Périodiques; Cytology -- Periodicals; Medicine -- Periodicals; Molecular biology -- Periodicals; 611.01805
• DOI: 10.1111/jcmm.12442
• Languages: English
• ISSNs: 1582-1838

Abstract

<abstract abstract-type="main" id="jcmm12442-abs-0001"> <title>Abstract</title> <p>Manganese superoxide dismutase (MnSOD), a foremost antioxidant enzyme, plays a key role in angiogenesis. Barley‐derived (1.3) β‐<sc>d</sc>‐glucan (β‐<sc>d</sc>‐glucan) is a natural water‐soluble polysaccharide with antioxidant properties. To explore the effects of β‐<sc>d</sc>‐glucan on MnSOD‐related angiogenesis under oxidative stress, we tested epigenetic mechanisms underlying modulation of MnSOD level in human umbilical vein endothelial cells (HUVECs) and angiogenesis <italic>in vitro</italic> and <italic>in vivo</italic>. Long‐term treatment of HUVECs with 3% w/v β‐<sc>d</sc>‐glucan significantly increased the level of MnSOD by 200% ± 2% compared to control and by 50% ± 4% compared to untreated H<sub>2</sub>O<sub>2</sub>‐stressed cells. β‐<sc>d</sc>‐glucan‐treated HUVECs displayed greater angiogenic ability. <italic>In vivo</italic>, 24 hrs‐treatment with 3% w/v β‐<sc>d</sc>‐glucan rescued vasculogenesis in <italic>Tg</italic> (<italic>kdrl: EGFP) s843Tg</italic> zebrafish embryos exposed to oxidative microenvironment. HUVECs overexpressing MnSOD demonstrated an increased activity of endothelial nitric oxide synthase (eNOS), reduced load of superoxide anion (O<sub>2</sub><sup>−</sup>) and an increased survival under oxidative stress. In addition, β‐<sc>d</sc>‐glucan prevented the rise of hypoxia inducible factor (HIF)1‐α under oxidative stress. The level of histone H4 acetylation was significantly increased by β‐<sc>d</sc>‐glucan. Increasing histone acetylation by sodium butyrate, an inhibitor of class I histone deacetylases (HDACs I), did not activate MnSOD‐related angiogenesis and did not impair β‐<sc>d</sc>‐glucan effects. In conclusion, 3% w/v β‐<sc>d</sc>‐glucan activates endothelial expression of MnSOD independent of histone acetylation level, thereby leading to adequate removal of O<sub>2</sub><sup>−</sup>, cell survival and angiogenic response to oxidative stress. The identification of dietary β‐<sc>d</sc>‐glucan as activator of MnSOD‐related angiogenesis might lead to the development of nutritional approaches for the prevention of ischemic remodelling and heart failure.</p> </abstract>