Zinc deficiency decreased cell viability both in endothelial EA.hy926 cells and mouse aortic culture ex vivo and its implication for anti-atherosclerosis

Young-Eun Cho, Jee-Eun Choi, Md Jahangir Alam, Man-Hyo Lee, Ho-Yong Sohn, John Hamilton Beattie, In-Sook Kwun

    Research output: Contribution to journalArticle

    Abstract

    Zinc plays a protective role in anti-atherosclerosis but the clear mechanism has not been proposed yet. In the present study, we evaluated whether zinc modulates atherosclerotic markers, VACM-1 and ICAM-1 and cell viability both in endothelial cells in vitro and mouse aortic cell viability ex vivo. In study 1, as in vitro model, endothelial EA.hy926 cells were treated with TNFalpha for 5 hours for inducing oxidative stress, and then treated with Zn-adequacy (15 microM Zn) or Zn-deficiency (0 microM Zn) for 6 hours. Pro-atherosclerosis factors, VCAM-1 and ICAM-1 mRNA expression and cell viability was measured. In study 2, as ex vivo model, mouse aorta ring was used. Mourse aorta was removed and cut in ring then, cultured in a 96-well plate. Aortic ring was treated with various TNFalpha (0-30 mg/ml) and intracellular zinc chelator, N, N, N', N', -tetrakis (2-pyridylmethyl) ethylenediamine (TPEN, 0-30 microM) for cellular zinc depletion for 2 days and then cell viability was measured. The results showed that in in vitro study, Zn-adequate group induced more VCAM-1 & ICAM-1 mRNA expression than Zn-deficient group during 6-hour zinc treatment post-5 hour TNF-alpha treatment, unexpectedly. These results might be cautiously interpreted that zinc would biologically induce the early expression of anti-oxidative stress through the increased adhesion molecule expression for reducing atherosclerotic action, particularly under the present 6-hour zinc treatment. In ex vivo, mouse aortic ring cell viability was decreased as TNF-alpha and TPEN levels increased, which suggests that mouse aortic blood vessel cell viability was decreased, when oxidative stress increases and cellular zinc level decreases. Taken together, it can be suggested that zinc may have a protective role in anti-atherosclerosis by cell viability in endothelial cells and aorta tissue. Further study is needed to clarify how pro-atherosclerosis molecule expression is modulated by zinc.
    Original languageEnglish
    Pages (from-to)74-79
    Number of pages6
    JournalNutrition Research and Practice
    Volume2
    Issue number2
    Early online date30 Jun 2008
    DOIs
    Publication statusPublished - Jun 2008

    Fingerprint

    atherosclerosis
    cell viability
    Zinc
    Cell Survival
    Atherosclerosis
    zinc
    mice
    cells
    Intercellular Adhesion Molecule-1
    Tumor Necrosis Factor-alpha
    aorta
    Aorta
    Oxidative Stress
    oxidative stress
    Vascular Cell Adhesion Molecule-1
    endothelial cells
    tumor necrosis factor-alpha
    Endothelial Cells
    Messenger RNA
    Chelating Agents

    Keywords

    • Zn-deficiency
    • endothelial cells
    • EA.hy926 cell
    • mouse aorta
    • atherosclerosis

    Cite this

    Zinc deficiency decreased cell viability both in endothelial EA.hy926 cells and mouse aortic culture ex vivo and its implication for anti-atherosclerosis. / Cho, Young-Eun; Choi, Jee-Eun; Alam, Md Jahangir; Lee, Man-Hyo; Sohn, Ho-Yong; Beattie, John Hamilton; Kwun, In-Sook.

    In: Nutrition Research and Practice, Vol. 2, No. 2, 06.2008, p. 74-79.

    Research output: Contribution to journalArticle

    Cho, Young-Eun ; Choi, Jee-Eun ; Alam, Md Jahangir ; Lee, Man-Hyo ; Sohn, Ho-Yong ; Beattie, John Hamilton ; Kwun, In-Sook. / Zinc deficiency decreased cell viability both in endothelial EA.hy926 cells and mouse aortic culture ex vivo and its implication for anti-atherosclerosis. In: Nutrition Research and Practice. 2008 ; Vol. 2, No. 2. pp. 74-79.
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    AU - Choi, Jee-Eun

    AU - Alam, Md Jahangir

    AU - Lee, Man-Hyo

    AU - Sohn, Ho-Yong

    AU - Beattie, John Hamilton

    AU - Kwun, In-Sook

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    AB - Zinc plays a protective role in anti-atherosclerosis but the clear mechanism has not been proposed yet. In the present study, we evaluated whether zinc modulates atherosclerotic markers, VACM-1 and ICAM-1 and cell viability both in endothelial cells in vitro and mouse aortic cell viability ex vivo. In study 1, as in vitro model, endothelial EA.hy926 cells were treated with TNFalpha for 5 hours for inducing oxidative stress, and then treated with Zn-adequacy (15 microM Zn) or Zn-deficiency (0 microM Zn) for 6 hours. Pro-atherosclerosis factors, VCAM-1 and ICAM-1 mRNA expression and cell viability was measured. In study 2, as ex vivo model, mouse aorta ring was used. Mourse aorta was removed and cut in ring then, cultured in a 96-well plate. Aortic ring was treated with various TNFalpha (0-30 mg/ml) and intracellular zinc chelator, N, N, N', N', -tetrakis (2-pyridylmethyl) ethylenediamine (TPEN, 0-30 microM) for cellular zinc depletion for 2 days and then cell viability was measured. The results showed that in in vitro study, Zn-adequate group induced more VCAM-1 & ICAM-1 mRNA expression than Zn-deficient group during 6-hour zinc treatment post-5 hour TNF-alpha treatment, unexpectedly. These results might be cautiously interpreted that zinc would biologically induce the early expression of anti-oxidative stress through the increased adhesion molecule expression for reducing atherosclerotic action, particularly under the present 6-hour zinc treatment. In ex vivo, mouse aortic ring cell viability was decreased as TNF-alpha and TPEN levels increased, which suggests that mouse aortic blood vessel cell viability was decreased, when oxidative stress increases and cellular zinc level decreases. Taken together, it can be suggested that zinc may have a protective role in anti-atherosclerosis by cell viability in endothelial cells and aorta tissue. Further study is needed to clarify how pro-atherosclerosis molecule expression is modulated by zinc.

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