Novel Modulator for Endothelial Adhesion Molecules Adipocyte-Derived Plasma Protein Adiponectin
Background —Among the many adipocyte-derived endocrine factors, we recently found an adipocyte-specific secretory protein, adiponectin, which was decreased in obesity. Although obesity is associated with increased cardiovascular mortality and morbidity, the molecular basis for the link between obesi...
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| Published in | Circulation (New York, N.Y.) Vol. 100; no. 25; pp. 2473 - 2476 |
|---|---|
| Main Authors | , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Hagerstown, MD
Lippincott Williams & Wilkins
21.12.1999
American Heart Association, Inc |
| Subjects | |
| Online Access | Get full text |
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| Abstract | Background
—Among the many adipocyte-derived endocrine factors, we recently found an adipocyte-specific secretory protein, adiponectin, which was decreased in obesity. Although obesity is associated with increased cardiovascular mortality and morbidity, the molecular basis for the link between obesity and vascular disease has not been fully clarified. The present study investigated whether adiponectin could modulate endothelial function and relate to coronary disease.
Methods and Results
—For the in vitro study, human aortic endothelial cells (HAECs) were preincubated for 18 hours with the indicated amount of adiponectin, then exposed to tumor necrosis factor-α (TNF-α) (10 U/mL) or vehicle for the times indicated. The adhesion of human monocytic cell line THP-1 cells to HAECs was determined by adhesion assay. The surface expression of vascular cell adhesion molecule-1 (VCAM-1), endothelial-leukocyte adhesion molecule-1 (E-selectin), and intracellular adhesion molecule-1 (ICAM-1) was measured by cell ELISA. Physiological concentrations of adiponectin dose-dependently inhibited TNF-α–induced THP-1 adhesion and expression of VCAM-1, E-selectin, and ICAM-1 on HAECs. For the in vivo study, the concentrations of adiponectin in human plasma were determined by a sandwich ELISA system that we recently developed. Plasma adiponectin concentrations were significantly lower in patients with coronary artery disease than those in age- and body mass index–adjusted control subjects.
Conclusions
—These observations suggest that adiponectin modulates endothelial inflammatory response and that the measurement of plasma adiponectin levels may be helpful in assessment of CAD risk. |
|---|---|
| AbstractList | Among the many adipocyte-derived endocrine factors, we recently found an adipocyte-specific secretory protein, adiponectin, which was decreased in obesity. Although obesity is associated with increased cardiovascular mortality and morbidity, the molecular basis for the link between obesity and vascular disease has not been fully clarified. The present study investigated whether adiponectin could modulate endothelial function and relate to coronary disease.BACKGROUNDAmong the many adipocyte-derived endocrine factors, we recently found an adipocyte-specific secretory protein, adiponectin, which was decreased in obesity. Although obesity is associated with increased cardiovascular mortality and morbidity, the molecular basis for the link between obesity and vascular disease has not been fully clarified. The present study investigated whether adiponectin could modulate endothelial function and relate to coronary disease.For the in vitro study, human aortic endothelial cells (HAECs) were preincubated for 18 hours with the indicated amount of adiponectin, then exposed to tumor necrosis factor-alpha (TNF-alpha) (10 U/mL) or vehicle for the times indicated. The adhesion of human monocytic cell line THP-1 cells to HAECs was determined by adhesion assay. The surface expression of vascular cell adhesion molecule-1 (VCAM-1), endothelial-leukocyte adhesion molecule-1 (E-selectin), and intracellular adhesion molecule-1 (ICAM-1) was measured by cell ELISA. Physiological concentrations of adiponectin dose-dependently inhibited TNF-alpha-induced THP-1 adhesion and expression of VCAM-1, E-selectin, and ICAM-1 on HAECs. For the in vivo study, the concentrations of adiponectin in human plasma were determined by a sandwich ELISA system that we recently developed. Plasma adiponectin concentrations were significantly lower in patients with coronary artery disease than those in age- and body mass index-adjusted control subjects.METHODS AND RESULTSFor the in vitro study, human aortic endothelial cells (HAECs) were preincubated for 18 hours with the indicated amount of adiponectin, then exposed to tumor necrosis factor-alpha (TNF-alpha) (10 U/mL) or vehicle for the times indicated. The adhesion of human monocytic cell line THP-1 cells to HAECs was determined by adhesion assay. The surface expression of vascular cell adhesion molecule-1 (VCAM-1), endothelial-leukocyte adhesion molecule-1 (E-selectin), and intracellular adhesion molecule-1 (ICAM-1) was measured by cell ELISA. Physiological concentrations of adiponectin dose-dependently inhibited TNF-alpha-induced THP-1 adhesion and expression of VCAM-1, E-selectin, and ICAM-1 on HAECs. For the in vivo study, the concentrations of adiponectin in human plasma were determined by a sandwich ELISA system that we recently developed. Plasma adiponectin concentrations were significantly lower in patients with coronary artery disease than those in age- and body mass index-adjusted control subjects.These observations suggest that adiponectin modulates endothelial inflammatory response and that the measurement of plasma adiponectin levels may be helpful in assessment of CAD risk.CONCLUSIONSThese observations suggest that adiponectin modulates endothelial inflammatory response and that the measurement of plasma adiponectin levels may be helpful in assessment of CAD risk. Among the many adipocyte-derived endocrine factors, we recently found an adipocyte-specific secretory protein, adiponectin, which was decreased in obesity. Although obesity is associated with increased cardiovascular mortality and morbidity, the molecular basis for the link between obesity and vascular disease has not been fully clarified. The present study investigated whether adiponectin could modulate endothelial function and relate to coronary disease. For the in vitro study, human aortic endothelial cells (HAECs) were preincubated for 18 hours with the indicated amount of adiponectin, then exposed to tumor necrosis factor-alpha (TNF-alpha) (10 U/mL) or vehicle for the times indicated. The adhesion of human monocytic cell line THP-1 cells to HAECs was determined by adhesion assay. The surface expression of vascular cell adhesion molecule-1 (VCAM-1), endothelial-leukocyte adhesion molecule-1 (E-selectin), and intracellular adhesion molecule-1 (ICAM-1) was measured by cell ELISA. Physiological concentrations of adiponectin dose-dependently inhibited TNF-alpha-induced THP-1 adhesion and expression of VCAM-1, E-selectin, and ICAM-1 on HAECs. For the in vivo study, the concentrations of adiponectin in human plasma were determined by a sandwich ELISA system that we recently developed. Plasma adiponectin concentrations were significantly lower in patients with coronary artery disease than those in age- and body mass index-adjusted control subjects. These observations suggest that adiponectin modulates endothelial inflammatory response and that the measurement of plasma adiponectin levels may be helpful in assessment of CAD risk. Background —Among the many adipocyte-derived endocrine factors, we recently found an adipocyte-specific secretory protein, adiponectin, which was decreased in obesity. Although obesity is associated with increased cardiovascular mortality and morbidity, the molecular basis for the link between obesity and vascular disease has not been fully clarified. The present study investigated whether adiponectin could modulate endothelial function and relate to coronary disease. Methods and Results —For the in vitro study, human aortic endothelial cells (HAECs) were preincubated for 18 hours with the indicated amount of adiponectin, then exposed to tumor necrosis factor-α (TNF-α) (10 U/mL) or vehicle for the times indicated. The adhesion of human monocytic cell line THP-1 cells to HAECs was determined by adhesion assay. The surface expression of vascular cell adhesion molecule-1 (VCAM-1), endothelial-leukocyte adhesion molecule-1 (E-selectin), and intracellular adhesion molecule-1 (ICAM-1) was measured by cell ELISA. Physiological concentrations of adiponectin dose-dependently inhibited TNF-α–induced THP-1 adhesion and expression of VCAM-1, E-selectin, and ICAM-1 on HAECs. For the in vivo study, the concentrations of adiponectin in human plasma were determined by a sandwich ELISA system that we recently developed. Plasma adiponectin concentrations were significantly lower in patients with coronary artery disease than those in age- and body mass index–adjusted control subjects. Conclusions —These observations suggest that adiponectin modulates endothelial inflammatory response and that the measurement of plasma adiponectin levels may be helpful in assessment of CAD risk. BACKGROUND: Among the many adipocyte-derived endocrine factors, we recently found an adipocyte-specific secretory protein, adiponectin, which was decreased in obesity. Although obesity is associated with increased cardiovascular mortality and morbidity, the molecular basis for the link between obesity and vascular disease has not been fully clarified. The present study investigated whether adiponectin could modulate endothelial function and relate to coronary disease. METHODS AND RESULTS: For the in vitro study, human aortic endothelial cells (HAECs) were preincubated for 18 hours with the indicated amount of adiponectin, then exposed to tumor necrosis factor-alpha (TNF-alpha) (10 U/mL) or vehicle for the times indicated. The adhesion of human monocytic cell line THP-1 cells to HAECs was determined by adhesion assay. The surface expression of vascular cell adhesion molecule-1 (VCAM-1), endothelial-leukocyte adhesion molecule-1 (E-selectin), and intracellular adhesion molecule-1 (ICAM-1) was measured by cell ELISA. Physiological concentrations of adiponectin dose-dependently inhibited TNF-alpha-induced THP-1 adhesion and expression of VCAM-1, E-selectin, and ICAM-1 on HAECs. For the in vivo study, the concentrations of adiponectin in human plasma were determined by a sandwich ELISA system that we recently developed. Plasma adiponectin concentrations were significantly lower in patients with coronary artery disease than those in age- and body mass index-adjusted control subjects. CONCLUSIONS: These observations suggest that adiponectin modulates endothelial inflammatory response and that the measurement of plasma adiponectin levels may be helpful in assessment of CAD risk. |
| Author | Nakamura, Tadashi Kihara, Shinji Arita, Yukio Takahashi, Masahiko Matsuzawa, Yuji Nishida, Makoto Funahashi, Tohru Yamashita, Shizuya Ouchi, Noriyuki Maeda, Kazuhisa Kuriyama, Hiroshi Okamoto, Yoshihisa Hotta, Kikuko |
| Author_xml | – sequence: 1 givenname: Noriyuki surname: Ouchi fullname: Ouchi, Noriyuki organization: From the Department of Internal Medicine and Molecular Science, Graduate School of Medicine, Osaka University, Osaka, Japan. Drs Ouchi and Kihara contributed equally to the work – sequence: 2 givenname: Shinji surname: Kihara fullname: Kihara, Shinji organization: From the Department of Internal Medicine and Molecular Science, Graduate School of Medicine, Osaka University, Osaka, Japan. Drs Ouchi and Kihara contributed equally to the work – sequence: 3 givenname: Yukio surname: Arita fullname: Arita, Yukio organization: From the Department of Internal Medicine and Molecular Science, Graduate School of Medicine, Osaka University, Osaka, Japan. Drs Ouchi and Kihara contributed equally to the work – sequence: 4 givenname: Kazuhisa surname: Maeda fullname: Maeda, Kazuhisa organization: From the Department of Internal Medicine and Molecular Science, Graduate School of Medicine, Osaka University, Osaka, Japan. Drs Ouchi and Kihara contributed equally to the work – sequence: 5 givenname: Hiroshi surname: Kuriyama fullname: Kuriyama, Hiroshi organization: From the Department of Internal Medicine and Molecular Science, Graduate School of Medicine, Osaka University, Osaka, Japan. Drs Ouchi and Kihara contributed equally to the work – sequence: 6 givenname: Yoshihisa surname: Okamoto fullname: Okamoto, Yoshihisa organization: From the Department of Internal Medicine and Molecular Science, Graduate School of Medicine, Osaka University, Osaka, Japan. Drs Ouchi and Kihara contributed equally to the work – sequence: 7 givenname: Kikuko surname: Hotta fullname: Hotta, Kikuko organization: From the Department of Internal Medicine and Molecular Science, Graduate School of Medicine, Osaka University, Osaka, Japan. Drs Ouchi and Kihara contributed equally to the work – sequence: 8 givenname: Makoto surname: Nishida fullname: Nishida, Makoto organization: From the Department of Internal Medicine and Molecular Science, Graduate School of Medicine, Osaka University, Osaka, Japan. Drs Ouchi and Kihara contributed equally to the work – sequence: 9 givenname: Masahiko surname: Takahashi fullname: Takahashi, Masahiko organization: From the Department of Internal Medicine and Molecular Science, Graduate School of Medicine, Osaka University, Osaka, Japan. Drs Ouchi and Kihara contributed equally to the work – sequence: 10 givenname: Tadashi surname: Nakamura fullname: Nakamura, Tadashi organization: From the Department of Internal Medicine and Molecular Science, Graduate School of Medicine, Osaka University, Osaka, Japan. Drs Ouchi and Kihara contributed equally to the work – sequence: 11 givenname: Shizuya surname: Yamashita fullname: Yamashita, Shizuya organization: From the Department of Internal Medicine and Molecular Science, Graduate School of Medicine, Osaka University, Osaka, Japan. Drs Ouchi and Kihara contributed equally to the work – sequence: 12 givenname: Tohru surname: Funahashi fullname: Funahashi, Tohru organization: From the Department of Internal Medicine and Molecular Science, Graduate School of Medicine, Osaka University, Osaka, Japan. Drs Ouchi and Kihara contributed equally to the work – sequence: 13 givenname: Yuji surname: Matsuzawa fullname: Matsuzawa, Yuji organization: From the Department of Internal Medicine and Molecular Science, Graduate School of Medicine, Osaka University, Osaka, Japan. Drs Ouchi and Kihara contributed equally to the work |
| BackLink | http://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1217835$$DView record in Pascal Francis https://www.ncbi.nlm.nih.gov/pubmed/10604883$$D View this record in MEDLINE/PubMed |
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| Cites_doi | 10.1006/bbrc.1999.0255 10.1126/science.7678183 10.1038/nm0796-800 10.1006/bbrc.1996.0587 10.1002/j.1550-8528.1995.tb00481.x 10.1002/path.1711710311 10.1097/00041433-199708000-00002 10.1016/0021-9150(94)90025-6 10.1016/S0021-9258(18)53107-0 10.1038/372425a0 10.1126/science.1990440 10.1016/0092-8674(94)90337-9 10.1016/S0378-1119(96)00730-5 10.1038/362801a0 10.1161/res.80.6.810 |
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| SubjectTerms | Adipocytes - chemistry Adipocytes - metabolism Adiponectin Adult Aged Aorta Biological and medical sciences Blotting, Northern Body Mass Index Cardiology. Vascular system Cardiovascular Diseases - epidemiology Cardiovascular Diseases - etiology Cell Adhesion Molecules - biosynthesis Cell Adhesion Molecules - genetics Cells, Cultured Coronary Disease - blood Coronary heart disease DNA, Complementary - genetics E-Selectin - biosynthesis E-Selectin - genetics Endothelium, Vascular - drug effects Endothelium, Vascular - metabolism Enzyme-Linked Immunosorbent Assay Female Gene Expression Regulation - drug effects Heart Humans Intercellular Adhesion Molecule-1 - biosynthesis Intercellular Adhesion Molecule-1 - genetics Intercellular Signaling Peptides and Proteins Male Medical sciences Middle Aged Monocytes - cytology Obesity - blood Obesity - complications Proteins - isolation & purification Proteins - pharmacology Proteins - physiology Risk Factors Tumor Necrosis Factor-alpha - antagonists & inhibitors Vascular Cell Adhesion Molecule-1 - biosynthesis Vascular Cell Adhesion Molecule-1 - genetics |
| Subtitle | Adipocyte-Derived Plasma Protein Adiponectin |
| Title | Novel Modulator for Endothelial Adhesion Molecules |
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