Endothelial arginase II and atherosclerosis
Atherosclerotic vascular disease is the leading cause of morbidity and mortality in developed countries. While it is a complex condition resulting from numerous genetic and environmental factors, it is well recognized that oxidized low-density lipoprotein produces pro-atherogenic effects in endothel...
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| Format: | Article |
| Language: | English |
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Korean Society of Anesthesiologists
2011-07-01
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| Series: | Korean Journal of Anesthesiology |
| Subjects: | |
| Online Access: | http://ekja.org/upload/pdf/kjae-61-3.pdf |
| _version_ | 1819229142685581312 |
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| author | Sungwoo Ryoo Dan E. Berkowitz Hyun Kyo Lim |
| author_facet | Sungwoo Ryoo Dan E. Berkowitz Hyun Kyo Lim |
| author_sort | Sungwoo Ryoo |
| collection | DOAJ |
| description | Atherosclerotic vascular disease is the leading cause of morbidity and mortality in developed countries. While it is a complex condition resulting from numerous genetic and environmental factors, it is well recognized that oxidized low-density lipoprotein produces pro-atherogenic effects in endothelial cells (ECs) by inducing the expression of adhesion molecules, stimulating EC apoptosis, inducing superoxide anion formation and impairing protective endothelial nitric oxide (NO) formation. Emerging evidence suggests that the enzyme arginase reciprocally regulates NO synthase and NO production by competing for the common substrate L-arginine. As oxidized LDL (OxLDL) results in arginase activation/upregulation, it appears to be an important contributor to endothelial dysfunction by a mechanism that involves substrate limitation for endothelial NO synthase (eNOS) and NO synthesis. Additionally, arginase enhances production of reactive oxygen species by eNOS. Arginase inhibition in hypercholesterolemic (ApoE-/-) mice or arginase II deletion (ArgII-/-) mice restores endothelial vasorelaxant function, reduces vascular stiffness and markedly reduces atherosclerotic plaque burden. Furthermore, arginase activation contributes to vascular changes including polyamine-dependent vascular smooth muscle cell proliferation and collagen synthesis. Collectively, arginase may play a key role in the prevention and treatment of atherosclerotic vascular disease. |
| first_indexed | 2024-12-23T11:08:29Z |
| format | Article |
| id | doaj.art-b1d7728441a145b1b23096c993301b69 |
| institution | Directory Open Access Journal |
| issn | 2005-6419 2005-7563 |
| language | English |
| last_indexed | 2024-12-23T11:08:29Z |
| publishDate | 2011-07-01 |
| publisher | Korean Society of Anesthesiologists |
| record_format | Article |
| series | Korean Journal of Anesthesiology |
| spelling | doaj.art-b1d7728441a145b1b23096c993301b692022-12-21T17:49:25ZengKorean Society of AnesthesiologistsKorean Journal of Anesthesiology2005-64192005-75632011-07-0161131110.4097/kjae.2011.61.1.37203Endothelial arginase II and atherosclerosisSungwoo Ryoo0Dan E. Berkowitz1Hyun Kyo Lim2Division of Biology, Kangwon National University, Chuncheon, Korea.Department of Anesthesiology and Critical Medicine and Biomedical Engineering, The Johns Hopkins Medical Institutes, Baltimore, MD, USA.Department of Anesthesiology and Pain Medicine, Yonsei University Wonju College of Medicine, Wonju, Korea.Atherosclerotic vascular disease is the leading cause of morbidity and mortality in developed countries. While it is a complex condition resulting from numerous genetic and environmental factors, it is well recognized that oxidized low-density lipoprotein produces pro-atherogenic effects in endothelial cells (ECs) by inducing the expression of adhesion molecules, stimulating EC apoptosis, inducing superoxide anion formation and impairing protective endothelial nitric oxide (NO) formation. Emerging evidence suggests that the enzyme arginase reciprocally regulates NO synthase and NO production by competing for the common substrate L-arginine. As oxidized LDL (OxLDL) results in arginase activation/upregulation, it appears to be an important contributor to endothelial dysfunction by a mechanism that involves substrate limitation for endothelial NO synthase (eNOS) and NO synthesis. Additionally, arginase enhances production of reactive oxygen species by eNOS. Arginase inhibition in hypercholesterolemic (ApoE-/-) mice or arginase II deletion (ArgII-/-) mice restores endothelial vasorelaxant function, reduces vascular stiffness and markedly reduces atherosclerotic plaque burden. Furthermore, arginase activation contributes to vascular changes including polyamine-dependent vascular smooth muscle cell proliferation and collagen synthesis. Collectively, arginase may play a key role in the prevention and treatment of atherosclerotic vascular disease.http://ekja.org/upload/pdf/kjae-61-3.pdfarginaseatherosclerosisendothelial dysfunctionendothelial nitric oxide synthasevascular smooth muscle cell |
| spellingShingle | Sungwoo Ryoo Dan E. Berkowitz Hyun Kyo Lim Endothelial arginase II and atherosclerosis Korean Journal of Anesthesiology arginase atherosclerosis endothelial dysfunction endothelial nitric oxide synthase vascular smooth muscle cell |
| title | Endothelial arginase II and atherosclerosis |
| title_full | Endothelial arginase II and atherosclerosis |
| title_fullStr | Endothelial arginase II and atherosclerosis |
| title_full_unstemmed | Endothelial arginase II and atherosclerosis |
| title_short | Endothelial arginase II and atherosclerosis |
| title_sort | endothelial arginase ii and atherosclerosis |
| topic | arginase atherosclerosis endothelial dysfunction endothelial nitric oxide synthase vascular smooth muscle cell |
| url | http://ekja.org/upload/pdf/kjae-61-3.pdf |
| work_keys_str_mv | AT sungwooryoo endothelialarginaseiiandatherosclerosis AT daneberkowitz endothelialarginaseiiandatherosclerosis AT hyunkyolim endothelialarginaseiiandatherosclerosis |