PMID- 21532752 OWN - NLM STAT- MEDLINE DCOM- 20110830 LR - 20211020 IS - 1932-6203 (Electronic) IS - 1932-6203 (Linking) VI - 6 IP - 4 DP - 2011 Apr 12 TI - Chemokine (C-C motif) ligand 2 (CCL2) in sera of patients with type 1 diabetes and diabetic complications. PG - e17822 LID - 10.1371/journal.pone.0017822 [doi] LID - e17822 AB - BACKGROUND: Chemokine (C-C motif) ligand 2 (CCL2), commonly known as monocyte chemoattractant protein-1 (MCP-1), has been implicated in the pathogenesis of many diseases characterized by monocytic infiltration. However, limited data have been reported on MCP-1 in type 1 diabetes (T1D) and the findings are inconclusive and inconsistent. METHODS: In this study, MCP-1 was measured in the sera from 2,472 T1D patients and 2,654 healthy controls using a Luminex assay. The rs1024611 SNP in the promoter region of MCP-1 was genotyped for a subset of subjects (1764 T1D patients and 1323 controls) using the TaqMan-assay. RESULTS: Subject age, sex or genotypes of MCP-1 rs1024611SNP did not have a major impact on serum MCP-1 levels in either healthy controls or patients. While hemoglobin A1c levels did not have a major influence on serum MCP-1 levels, the mean serum MCP-1 levels are significantly higher in patients with multiple complications (mean = 242 ng/ml) compared to patients without any complications (mean = 201 ng/ml) (p = 3.5x10(-6)). Furthermore, mean serum MCP-1 is higher in controls (mean = 261 ng/ml) than T1D patients (mean = 208 ng/ml) (p<10(-23)). More importantly, the frequency of subjects with extremely high levels (>99(th) percentile of patients or 955 ng/ml) of serum MCP-1 is significantly lower in the T1D group compared to the control group (odds ratio = 0.11, p<10(-33)). CONCLUSION: MCP-1 may have a dual role in T1D and its complications. While very high levels of serum MCP-1 may be protective against the development of T1D, complications are associated with higher serum MCP-1 levels within the T1D group. FAU - Guan, Ruili AU - Guan R AD - Institute of Translational Medicine and School of Pharmaceutical Sciences, Nanjing University of Technology, Nanjing, Jiangsu, People's Republic of China. FAU - Purohit, Sharad AU - Purohit S FAU - Wang, Hongjie AU - Wang H FAU - Bode, Bruce AU - Bode B FAU - Reed, John Chip AU - Reed JC FAU - Steed, R Dennis AU - Steed RD FAU - Anderson, Stephen W AU - Anderson SW FAU - Steed, Leigh AU - Steed L FAU - Hopkins, Diane AU - Hopkins D FAU - Xia, Chun AU - Xia C FAU - She, Jin-Xiong AU - She JX LA - eng GR - R21 HD050196/HD/NICHD NIH HHS/United States GR - R01 HD037800/HD/NICHD NIH HHS/United States GR - 4R33-DK069878/DK/NIDDK NIH HHS/United States GR - 4R33HD050196/HD/NICHD NIH HHS/United States GR - R33 DK069878/DK/NIDDK NIH HHS/United States GR - 2R01HD37800/HD/NICHD NIH HHS/United States GR - R21 DK069878/DK/NIDDK NIH HHS/United States GR - R33 HD050196/HD/NICHD NIH HHS/United States PT - Journal Article PT - Research Support, N.I.H., Extramural PT - Research Support, Non-U.S. Gov't DEP - 20110412 PL - United States TA - PLoS One JT - PloS one JID - 101285081 RN - 0 (CCL2 protein, human) RN - 0 (Chemokine CCL2) SB - IM MH - Case-Control Studies MH - Chemokine CCL2/*blood/genetics MH - Diabetes Mellitus, Type 1/*blood/complications MH - Genotype MH - Humans MH - Polymerase Chain Reaction MH - Polymorphism, Single Nucleotide MH - Promoter Regions, Genetic PMC - PMC3075244 COIS- Competing Interests: The authors have declared that no competing interests exist. EDAT- 2011/05/03 06:00 MHDA- 2011/08/31 06:00 PMCR- 2011/04/12 CRDT- 2011/05/03 06:00 PHST- 2010/11/23 00:00 [received] PHST- 2011/02/12 00:00 [accepted] PHST- 2011/05/03 06:00 [entrez] PHST- 2011/05/03 06:00 [pubmed] PHST- 2011/08/31 06:00 [medline] PHST- 2011/04/12 00:00 [pmc-release] AID - PONE-D-10-05398 [pii] AID - 10.1371/journal.pone.0017822 [doi] PST - epublish SO - PLoS One. 2011 Apr 12;6(4):e17822. doi: 10.1371/journal.pone.0017822.