PMID- 25902044
OWN - NLM
STAT- MEDLINE
DCOM- 20160119
LR  - 20181113
IS  - 1932-6203 (Electronic)
IS  - 1932-6203 (Linking)
VI  - 10
IP  - 4
DP  - 2015
TI  - Genetic variation in the Mcp-1 gene promoter associated with the risk of 
      polycystic ovary syndrome.
PG  - e0123045
LID - 10.1371/journal.pone.0123045 [doi]
LID - e0123045
AB  - Monocyte chemoattractant protein-1 (MCP-1) is a pivotal chemokine in the 
      inflammatory response, which plays an important role in recruiting monocytes to 
      sites of injury and infection. However, the exact mechanism of Mcp-1 associated 
      with PCOS risk was unknown. In this study, we explored whether the Mcp-1 -2518G>A 
      polymorphism increases the risk of PCOS. We performed a comparative study of 
      -2518G>A polymorphism of the Mcp-1 gene with PCOS. In addition, luciferase 
      reporter assay was performed to evaluate the Mcp-1 transcriptional activity. A 
      strong association was observed between the -2518G>A polymorphism of Mcp-1 gene 
      and PCOS (p-value = 0.016, odd ratio (OR) = 0.693). A p-value under 0.05 is 
      considered statistically significant. The genotype and allelic frequencies were 
      assumed to be in Hardy-Weinberg equilibrium (HWE). The luciferase assays in 2 
      cell lines showed that the Mcp-1 -2518G>A substitution can increase the 
      expression of Mcp-1. MCP-1 levels in serum for PCOS group were significantly 
      higher than those in serum for controls (p-value = 0.02). Furthermore, the 
      patients carrying a genotype A/A had significantly increased levels of MCP-1 in 
      serum compared with levels of the MCP-1 of the patients with genotypes G/G and 
      G/A (p-value = 0.031). This is the first study on the genetic variation of the 
      Mcp-1 gene and PCOS. This finding suggests that the Mcp-1 -2518G>A polymorphism 
      is associated with PCOS risk by affecting transcriptional activity, leading to an 
      increased expression level of Mcp-1.
FAU - Li, Lan
AU  - Li L
AD  - Department of Biomedical Science, CHA University, Bundang CHA Hospital, 
      Gyeonggi-do, Republic of Korea.
FAU - Ryoo, Ji Eun
AU  - Ryoo JE
AD  - Hankuk Academy of Foreign Studies, Yongin, Republic of Korea.
FAU - Lee, Kyung-Ju
AU  - Lee KJ
AD  - Department of Gynecology and Obstetrics, CHA University, CHA General Hospital, 
      Seoul, Republic of Korea.
FAU - Choi, Bum-Chae
AU  - Choi BC
AD  - Department of Obstetrics and Gynecology, CL Women's Hospital, Gwangju, Republic 
      of Korea.
FAU - Baek, Kwang-Hyun
AU  - Baek KH
AD  - Department of Biomedical Science, CHA University, Bundang CHA Hospital, 
      Gyeonggi-do, Republic of Korea.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20150422
PL  - United States
TA  - PLoS One
JT  - PloS one
JID - 101285081
RN  - 0 (CCL2 protein, human)
RN  - 0 (Chemokine CCL2)
SB  - IM
MH  - Adult
MH  - Chemokine CCL2/*genetics
MH  - Female
MH  - Genetic Predisposition to Disease/*genetics
MH  - Humans
MH  - Polycystic Ovary Syndrome/*genetics
MH  - *Polymorphism, Single Nucleotide
MH  - Promoter Regions, Genetic/*genetics
MH  - Transcription, Genetic/genetics
PMC - PMC4406762
COIS- Competing Interests: The authors have declared that no competing interests exist.
EDAT- 2015/04/23 06:00
MHDA- 2016/01/20 06:00
PMCR- 2015/04/22
CRDT- 2015/04/23 06:00
PHST- 2014/09/30 00:00 [received]
PHST- 2015/02/18 00:00 [accepted]
PHST- 2015/04/23 06:00 [entrez]
PHST- 2015/04/23 06:00 [pubmed]
PHST- 2016/01/20 06:00 [medline]
PHST- 2015/04/22 00:00 [pmc-release]
AID - PONE-D-14-43481 [pii]
AID - 10.1371/journal.pone.0123045 [doi]
PST - epublish
SO  - PLoS One. 2015 Apr 22;10(4):e0123045. doi: 10.1371/journal.pone.0123045. 
      eCollection 2015.