The nitric oxide precursor L-arginine reduces expression of hyaluronan synthase in experimental vein bypass grafts

Jeffery Dattilo, Mary Peace M. Dattilo, Joseph T. Crane, Dorne R. Yager, Raymond G. Makhoul

    Research output: Contribution to journalArticle

    5 Citations (Scopus)

    Abstract

    Background. The success of vascular bypass procedures is limited by the development of intimal hyperplasia (IH). The nitric oxide (NO) precursor, L- arginine (L-ARG) significantly reduces IH in both arteries and experimental vein grafts; however, the precise mechanism has yet to be elucidated. Hyaluronan synthase-1 (HAS-1) is one of the two enzymes believed to be responsible for making hyaluronan, a key component extracellular matrix composition. Purpose. To determine how L-ARG supplementation affects the gene expression of HAS-1 in experimental vein grafts. Methods. Thirty-four male New Zealand white rabbits were divided into three groups: control (no operation, regular chow and water, n = 4); L-ARG supplemented (n = 15); and no L-ARG (n = 15). The latter two groups underwent a right interposition carotid bypass using jugular vein. Vein grafts were harvested at 7, 14, and 21 days after surgery. Ribonuclease protection assays were performed using 32P-labeled riboprobes for HAS-1 and 18S rRNA as an internal control and expressed as a ratio (HAS-1/rRNA). Results. There was a significant rise in HAS-1 expression in the vein grafts 7 (1.57 ± 0.5), 14 (0.7 ± 0.2), and 21 days (2.82 ± 0.7) after grafting compared to control (0.14 ± 0.08) (P < 0.05). L-ARG-supplemented animals had a significant decrease in HAS-1 expression at 21 days (0.65 ± 0.1) compared to nonsupplemented vein grafts (2.82 ± 0.7) (P < 0.02). Conclusions. These results demonstrate for the first time a significant rise in HAS expression in the early experimental vein grafts. Furthermore, L-ARG supplementation significantly diminishes the expression of HAS at 21 days. These results may represent a potential mechanism by which augmentation of the L-ARG/NO pathway inhibits IH in experimental vein grafts and may ultimately provide for improved therapeutic interventions in alleviating IH.

    Original languageEnglish (US)
    Pages (from-to)39-42
    Number of pages4
    JournalJournal of Surgical Research
    Volume74
    Issue number1
    DOIs
    StatePublished - Jan 1 1998

    Fingerprint

    Arginine
    Veins
    Nitric Oxide
    Tunica Intima
    Transplants
    Hyperplasia
    Jugular Veins
    Hyaluronic Acid
    Ribonucleases
    hyaluronan synthase
    Ambulatory Surgical Procedures
    Extracellular Matrix
    Blood Vessels
    Arteries
    Rabbits
    Gene Expression
    Control Groups
    Water
    Enzymes

    All Science Journal Classification (ASJC) codes

    • Surgery

    Cite this

    The nitric oxide precursor L-arginine reduces expression of hyaluronan synthase in experimental vein bypass grafts. / Dattilo, Jeffery; Dattilo, Mary Peace M.; Crane, Joseph T.; Yager, Dorne R.; Makhoul, Raymond G.

    In: Journal of Surgical Research, Vol. 74, No. 1, 01.01.1998, p. 39-42.

    Research output: Contribution to journalArticle

    Dattilo, Jeffery ; Dattilo, Mary Peace M. ; Crane, Joseph T. ; Yager, Dorne R. ; Makhoul, Raymond G. / The nitric oxide precursor L-arginine reduces expression of hyaluronan synthase in experimental vein bypass grafts. In: Journal of Surgical Research. 1998 ; Vol. 74, No. 1. pp. 39-42.
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    abstract = "Background. The success of vascular bypass procedures is limited by the development of intimal hyperplasia (IH). The nitric oxide (NO) precursor, L- arginine (L-ARG) significantly reduces IH in both arteries and experimental vein grafts; however, the precise mechanism has yet to be elucidated. Hyaluronan synthase-1 (HAS-1) is one of the two enzymes believed to be responsible for making hyaluronan, a key component extracellular matrix composition. Purpose. To determine how L-ARG supplementation affects the gene expression of HAS-1 in experimental vein grafts. Methods. Thirty-four male New Zealand white rabbits were divided into three groups: control (no operation, regular chow and water, n = 4); L-ARG supplemented (n = 15); and no L-ARG (n = 15). The latter two groups underwent a right interposition carotid bypass using jugular vein. Vein grafts were harvested at 7, 14, and 21 days after surgery. Ribonuclease protection assays were performed using 32P-labeled riboprobes for HAS-1 and 18S rRNA as an internal control and expressed as a ratio (HAS-1/rRNA). Results. There was a significant rise in HAS-1 expression in the vein grafts 7 (1.57 ± 0.5), 14 (0.7 ± 0.2), and 21 days (2.82 ± 0.7) after grafting compared to control (0.14 ± 0.08) (P < 0.05). L-ARG-supplemented animals had a significant decrease in HAS-1 expression at 21 days (0.65 ± 0.1) compared to nonsupplemented vein grafts (2.82 ± 0.7) (P < 0.02). Conclusions. These results demonstrate for the first time a significant rise in HAS expression in the early experimental vein grafts. Furthermore, L-ARG supplementation significantly diminishes the expression of HAS at 21 days. These results may represent a potential mechanism by which augmentation of the L-ARG/NO pathway inhibits IH in experimental vein grafts and may ultimately provide for improved therapeutic interventions in alleviating IH.",
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    AU - Dattilo, Jeffery

    AU - Dattilo, Mary Peace M.

    AU - Crane, Joseph T.

    AU - Yager, Dorne R.

    AU - Makhoul, Raymond G.

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    AB - Background. The success of vascular bypass procedures is limited by the development of intimal hyperplasia (IH). The nitric oxide (NO) precursor, L- arginine (L-ARG) significantly reduces IH in both arteries and experimental vein grafts; however, the precise mechanism has yet to be elucidated. Hyaluronan synthase-1 (HAS-1) is one of the two enzymes believed to be responsible for making hyaluronan, a key component extracellular matrix composition. Purpose. To determine how L-ARG supplementation affects the gene expression of HAS-1 in experimental vein grafts. Methods. Thirty-four male New Zealand white rabbits were divided into three groups: control (no operation, regular chow and water, n = 4); L-ARG supplemented (n = 15); and no L-ARG (n = 15). The latter two groups underwent a right interposition carotid bypass using jugular vein. Vein grafts were harvested at 7, 14, and 21 days after surgery. Ribonuclease protection assays were performed using 32P-labeled riboprobes for HAS-1 and 18S rRNA as an internal control and expressed as a ratio (HAS-1/rRNA). Results. There was a significant rise in HAS-1 expression in the vein grafts 7 (1.57 ± 0.5), 14 (0.7 ± 0.2), and 21 days (2.82 ± 0.7) after grafting compared to control (0.14 ± 0.08) (P < 0.05). L-ARG-supplemented animals had a significant decrease in HAS-1 expression at 21 days (0.65 ± 0.1) compared to nonsupplemented vein grafts (2.82 ± 0.7) (P < 0.02). Conclusions. These results demonstrate for the first time a significant rise in HAS expression in the early experimental vein grafts. Furthermore, L-ARG supplementation significantly diminishes the expression of HAS at 21 days. These results may represent a potential mechanism by which augmentation of the L-ARG/NO pathway inhibits IH in experimental vein grafts and may ultimately provide for improved therapeutic interventions in alleviating IH.

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