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Conversion of xanthine dehydrogenase to xanthine oxidase in bovine carotid artery endothelial cells induced by activated neutrophils: involvement of adhesion molecules.
Biochim Biophys Acta. 1995 Mar 16; 1265(2-3):103-9.BB

Abstract

We have demonstrated that the endothelial cell-derived superoxide anion is deeply involved in the endothelial cell injury induced by activated neutrophils (Fujita, H., Morita, I. and Murota, S. (1994) Arch. Biochem. Biophys. 309, 62-69). To clarify the mechanism underlying the increase in the endothelial cell-derived superoxide anion induced by activated neutrophils, the conversion of xanthine dehydrogenase (XD) to xanthine oxidase (XO) in cultured endothelial cells isolated from bovine carotid arteries was investigated. Although the endothelial cells expressed both XD and XO activity, the XO activity of unstimulated cells comprised about 12% of the total (XD + XO) activity. When endothelial cells were exposed to neutrophils activated with phorbol 12-myristate 13-acetate (PMA), XO activity rapidly increased about 3-fold over the control. Whereas treatment of endothelial cells with PMA alone or unstimulated neutrophils alone did not increase the XO activity at all. The increase in XO activity in endothelial cells was also observed on the treatment of the cells with neutrophils activated with leukotriene B4 or thrombin. To determine whether or not proteases released from activated neutrophils are involved in the increased conversion of XD to XO in endothelial cells, the effects of the elastase specific inhibitor, ONO-5046, and protease inhibitors, such as aprotinin, gabexate mesylate and urinastatin, were examined. However, these protease inhibitors did not suppress the conversion of XD to XO induced by PMA-activated neutrophils. Moreover, the treatment of endothelial cells with purified human neutrophil elastase and H2O2 also did not affect the conversion at all. In contrast, monoclonal antibodies against CD11a and CD18 significantly inhibited the increased conversion of XD to XO induced by PMA-activated neutrophils. Moreover, tyrosine kinase inhibitors such as staurosporin and herbimysine also inhibited the increased conversion of XD to XO induced by PMA-activated neutrophils. These results indicate that the adhesion of activated neutrophils to endothelial cells via CD11a/CD18-ICAM-1 is involved in the conversion of XD to XO in endothelial cells induced by activated neutrophils.

Authors+Show Affiliations

Department of Applied Chemistry, Faculty of Science and Technology, Keio University, Yokohama, Japan.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

7696338

Citation

Wakabayashi, Y, et al. "Conversion of Xanthine Dehydrogenase to Xanthine Oxidase in Bovine Carotid Artery Endothelial Cells Induced By Activated Neutrophils: Involvement of Adhesion Molecules." Biochimica Et Biophysica Acta, vol. 1265, no. 2-3, 1995, pp. 103-9.
Wakabayashi Y, Fujita H, Morita I, et al. Conversion of xanthine dehydrogenase to xanthine oxidase in bovine carotid artery endothelial cells induced by activated neutrophils: involvement of adhesion molecules. Biochim Biophys Acta. 1995;1265(2-3):103-9.
Wakabayashi, Y., Fujita, H., Morita, I., Kawaguchi, H., & Murota, S. (1995). Conversion of xanthine dehydrogenase to xanthine oxidase in bovine carotid artery endothelial cells induced by activated neutrophils: involvement of adhesion molecules. Biochimica Et Biophysica Acta, 1265(2-3), 103-9.
Wakabayashi Y, et al. Conversion of Xanthine Dehydrogenase to Xanthine Oxidase in Bovine Carotid Artery Endothelial Cells Induced By Activated Neutrophils: Involvement of Adhesion Molecules. Biochim Biophys Acta. 1995 Mar 16;1265(2-3):103-9. PubMed PMID: 7696338.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Conversion of xanthine dehydrogenase to xanthine oxidase in bovine carotid artery endothelial cells induced by activated neutrophils: involvement of adhesion molecules. AU - Wakabayashi,Y, AU - Fujita,H, AU - Morita,I, AU - Kawaguchi,H, AU - Murota,S, PY - 1995/3/16/pubmed PY - 1995/3/16/medline PY - 1995/3/16/entrez SP - 103 EP - 9 JF - Biochimica et biophysica acta JO - Biochim Biophys Acta VL - 1265 IS - 2-3 N2 - We have demonstrated that the endothelial cell-derived superoxide anion is deeply involved in the endothelial cell injury induced by activated neutrophils (Fujita, H., Morita, I. and Murota, S. (1994) Arch. Biochem. Biophys. 309, 62-69). To clarify the mechanism underlying the increase in the endothelial cell-derived superoxide anion induced by activated neutrophils, the conversion of xanthine dehydrogenase (XD) to xanthine oxidase (XO) in cultured endothelial cells isolated from bovine carotid arteries was investigated. Although the endothelial cells expressed both XD and XO activity, the XO activity of unstimulated cells comprised about 12% of the total (XD + XO) activity. When endothelial cells were exposed to neutrophils activated with phorbol 12-myristate 13-acetate (PMA), XO activity rapidly increased about 3-fold over the control. Whereas treatment of endothelial cells with PMA alone or unstimulated neutrophils alone did not increase the XO activity at all. The increase in XO activity in endothelial cells was also observed on the treatment of the cells with neutrophils activated with leukotriene B4 or thrombin. To determine whether or not proteases released from activated neutrophils are involved in the increased conversion of XD to XO in endothelial cells, the effects of the elastase specific inhibitor, ONO-5046, and protease inhibitors, such as aprotinin, gabexate mesylate and urinastatin, were examined. However, these protease inhibitors did not suppress the conversion of XD to XO induced by PMA-activated neutrophils. Moreover, the treatment of endothelial cells with purified human neutrophil elastase and H2O2 also did not affect the conversion at all. In contrast, monoclonal antibodies against CD11a and CD18 significantly inhibited the increased conversion of XD to XO induced by PMA-activated neutrophils. Moreover, tyrosine kinase inhibitors such as staurosporin and herbimysine also inhibited the increased conversion of XD to XO induced by PMA-activated neutrophils. These results indicate that the adhesion of activated neutrophils to endothelial cells via CD11a/CD18-ICAM-1 is involved in the conversion of XD to XO in endothelial cells induced by activated neutrophils. SN - 0006-3002 UR - https://www.unboundmedicine.com/medline/citation/7696338/Conversion_of_xanthine_dehydrogenase_to_xanthine_oxidase_in_bovine_carotid_artery_endothelial_cells_induced_by_activated_neutrophils:_involvement_of_adhesion_molecules_ L2 - https://linkinghub.elsevier.com/retrieve/pii/0167-4889(94)00202-P DB - PRIME DP - Unbound Medicine ER -