Article: Induction of MCP1, CCR2, and iNOS expression in THP-1 macrophages by serum of children late after kawasaki disease
| Title | Induction of MCP1, CCR2, and iNOS expression in THP-1 macrophages by serum of children late after kawasaki disease |
|---|---|
| Authors | Cheung, YF2 Karmin, O1 Tam, SCF3 Siow, YL1 |
| Issue Date | 2005 |
| Publisher | Lippincott Williams & Wilkins. The Journal's web site is located at http://www.pedresearch.org/ |
| Citation | Pediatric Research, 2005, v. 58 n. 6, p. 1306-1310 [How to Cite?] DOI: http://dx.doi.org/10.1203/01.pdr.0000183360.79872.1c |
| Abstract | Evidence of premature atherosclerosis late after Kawasaki disease (KD) is accumulating. Given the potential roles of monocyte chemoattractant protein-1 (MCP-1), chemokine receptor CCR-2, and inducible nitric oxide synthase (iNOS) in atherogenesis, we sought to determine whether serum obtained from children late after KD would induce expression of these genes in macrophages in vitro. A total of 79 subjects were studied, which comprised 57 KD patients, 33 of whom had coronary aneurysms, and 22 age-matched controls. Expression of MCP-1, CCR2, and iNOS mRNA in THP-1 macrophages in the presence of patient and control serum was quantified as a ratio to β-actin mRNA and expressed as a percentage of control. MCP-1 expression was significantly increased in the presence of serum from patients with coronary aneurysms. Expression of CCR2 and iNOS was significantly increased when THP-1 macrophages were incubated with serum from patients with and without coronary aneurysms. The magnitude of induction of MCP-1, CCR2, and iNOS or in combinations correlated positively with serum high-sensitivity C-reactive protein (hs-CRP), and low-density lipoprotein (LDL) cholesterol levels and negatively with high-density lipoprotein (HDL) cholesterol level. In conclusion, the serum of patients with a history of KD induces expression of MCP-1, CCR2, and iNOS in THP-1 macrophages in vitro. Induction of these genes in vivo may be related to chronic inflammation and may have important implications for premature atherosclerosis. Copyright © 2005 International Pediatric Research Foundation, Inc. |
| ISSN | 0031-3998 2011 Impact Factor: 2.7 2011 SCImago Journal Rankings: 0.238 |
| DOI | http://dx.doi.org/10.1203/01.pdr.0000183360.79872.1c |
| References | References in Scopus |
| dc.contributor.author | Cheung, YF |
|---|---|
| dc.contributor.author | Karmin, O |
| dc.contributor.author | Tam, SCF |
| dc.contributor.author | Siow, YL |
| dc.date.accessioned | 2012-10-30T06:07:44Z |
| dc.date.available | 2012-10-30T06:07:44Z |
| dc.date.issued | 2005 |
| dc.description.abstract | Evidence of premature atherosclerosis late after Kawasaki disease (KD) is accumulating. Given the potential roles of monocyte chemoattractant protein-1 (MCP-1), chemokine receptor CCR-2, and inducible nitric oxide synthase (iNOS) in atherogenesis, we sought to determine whether serum obtained from children late after KD would induce expression of these genes in macrophages in vitro. A total of 79 subjects were studied, which comprised 57 KD patients, 33 of whom had coronary aneurysms, and 22 age-matched controls. Expression of MCP-1, CCR2, and iNOS mRNA in THP-1 macrophages in the presence of patient and control serum was quantified as a ratio to β-actin mRNA and expressed as a percentage of control. MCP-1 expression was significantly increased in the presence of serum from patients with coronary aneurysms. Expression of CCR2 and iNOS was significantly increased when THP-1 macrophages were incubated with serum from patients with and without coronary aneurysms. The magnitude of induction of MCP-1, CCR2, and iNOS or in combinations correlated positively with serum high-sensitivity C-reactive protein (hs-CRP), and low-density lipoprotein (LDL) cholesterol levels and negatively with high-density lipoprotein (HDL) cholesterol level. In conclusion, the serum of patients with a history of KD induces expression of MCP-1, CCR2, and iNOS in THP-1 macrophages in vitro. Induction of these genes in vivo may be related to chronic inflammation and may have important implications for premature atherosclerosis. Copyright © 2005 International Pediatric Research Foundation, Inc. |
| dc.description.nature | Link_to_subscribed_fulltext |
| dc.identifier.citation | Pediatric Research, 2005, v. 58 n. 6, p. 1306-1310 [How to Cite?] DOI: http://dx.doi.org/10.1203/01.pdr.0000183360.79872.1c |
| dc.identifier.doi | http://dx.doi.org/10.1203/01.pdr.0000183360.79872.1c |
| dc.identifier.epage | 1310 |
| dc.identifier.issn | 0031-3998 2011 Impact Factor: 2.7 2011 SCImago Journal Rankings: 0.238 |
| dc.identifier.issue | 6 |
| dc.identifier.pmid | 16306213 |
| dc.identifier.scopus | eid_2-s2.0-27644468219 |
| dc.identifier.spage | 1306 |
| dc.identifier.uri | http://hdl.handle.net/10722/170352 |
| dc.identifier.volume | 58 |
| dc.language | eng |
| dc.publisher | Lippincott Williams & Wilkins. The Journal's web site is located at http://www.pedresearch.org/ |
| dc.publisher.place | United States |
| dc.relation.ispartof | Pediatric Research |
| dc.relation.references | References in Scopus |
| dc.subject.mesh | Atherosclerosis - Genetics |
| dc.subject.mesh | Cells, Cultured |
| dc.subject.mesh | Chemokine Ccl2 - Genetics |
| dc.subject.mesh | Child |
| dc.subject.mesh | Female |
| dc.subject.mesh | Gene Expression |
| dc.subject.mesh | Humans |
| dc.subject.mesh | Lipids - Blood |
| dc.subject.mesh | Macrophages - Metabolism |
| dc.subject.mesh | Male |
| dc.subject.mesh | Mucocutaneous Lymph Node Syndrome - Complications - Genetics - Immunology |
| dc.subject.mesh | Nitric Oxide Synthase Type Ii - Genetics |
| dc.subject.mesh | Receptors, Ccr2 |
| dc.subject.mesh | Receptors, Chemokine - Genetics |
| dc.subject.mesh | Serum - Metabolism |
| dc.subject.mesh | Up-Regulation - Genetics |
| dc.title | Induction of MCP1, CCR2, and iNOS expression in THP-1 macrophages by serum of children late after kawasaki disease |
| dc.type | Article |
Author Affiliations
- University of Manitoba
- The University of Hong Kong
- Queen Mary Hospital Hong Kong

