PMID- 34752683 OWN - NLM STAT- MEDLINE DCOM- 20220404 LR - 20220531 IS - 2050-4527 (Electronic) IS - 2050-4527 (Linking) VI - 10 IP - 2 DP - 2022 Feb TI - The MCP-1 rs1024611 and MTHFR rs1801133 gene variations and expressions in alopecia areata: A pilot study. PG - 209-217 LID - 10.1002/iid3.564 [doi] AB - BACKGROUND: Monocyte chemoattractant protein-1 (MCP-1) is highly expressed by lymphocytes at skin sites affected by alopecia areata (AA). Variations in MCP-1 as well as in methylene-tetrahydrofolate reductase (MTHFR), a key enzyme related to many inflammatory pathologies, have been associated with several autoimmune disorders. This study was designed to test a possible association between MCP-1 and MTHFR variations and altered expression of their genes and the risk of AA. METHODS: Blood samples of patients (60) suffering from AA as well as healthy subjects (60) were collected. Gene expression levels of MCP-1 and MTHFR were evaluated by real-time reverse-transcription polymerase chain reaction analysis. Moreover, MCP-1 rs1024611 (A-2518G) and MTHFR rs1801133 (C677T) polymorphisms were genotyped by using polymerase chain reaction-restriction fragment length polymorphism assays. RESULTS: In contrast to MCP-1, the MTHFR gene expression was found to be significantly higher in patients than in controls. Further stratification of the patients revealed that polymorphic genotypes in MCP-1 (AG + GG) and MTHFR (CT + TT) could significantly alter gene expression levels. Elevation of MCP-1 expression was significantly associated with the total number of variant MCP-1 and MTHFR alleles. However, no statistically significant difference was noticed in the genotypic distribution of MCP-1 and MTHFR variations between patients and controls. CONCLUSION: In summary, despite MCP-1 rs1024611 and MTHFR rs1801133 variations are not associated with AA risk, they may implicate the disease pathogenesis by influencing MCP-1 activity. CI - (c) 2021 The Authors. Immunity, Inflammation and Disease published by John Wiley & Sons Ltd. FAU - Tabatabaei-Panah, Pardis-Sadat AU - Tabatabaei-Panah PS AD - Department of Biology, East Tehran Branch, Islamic Azad University, Tehran, Iran. FAU - Moravvej, Hamideh AU - Moravvej H AD - Skin Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran. FAU - Hajihasani, Mahsa AU - Hajihasani M AD - Department of Biology, East Tehran Branch, Islamic Azad University, Tehran, Iran. FAU - Mousavi, Mahsa AU - Mousavi M AD - Department of Biology, East Tehran Branch, Islamic Azad University, Tehran, Iran. FAU - Ludwig, Ralf J AU - Ludwig RJ AD - Lubeck Institute of Experimental Dermatology, University of Lubeck, Germany. FAU - Akbarzadeh, Reza AU - Akbarzadeh R AUID- ORCID: 0000-0001-7668-702X AD - Skin Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran. AD - Lubeck Institute of Experimental Dermatology, University of Lubeck, Germany. AD - Institute of Clinical Chemistry and Laboratory Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, Germany. LA - eng PT - Journal Article DEP - 20211109 PL - England TA - Immun Inflamm Dis JT - Immunity, inflammation and disease JID - 101635460 RN - 0 (CCL2 protein, human) RN - 0 (Chemokine CCL2) RN - EC 1.5.1.20 (MTHFR protein, human) RN - EC 1.5.1.20 (Methylenetetrahydrofolate Reductase (NADPH2)) SB - IM MH - *Alopecia Areata/genetics MH - *Chemokine CCL2/genetics MH - Genetic Predisposition to Disease MH - Humans MH - *Methylenetetrahydrofolate Reductase (NADPH2)/genetics MH - Pilot Projects MH - Polymorphism, Single Nucleotide PMC - PMC8767509 OTO - NOTNLM OT - MCP-1 OT - MTHFR OT - alopecia areata OT - gene expression OT - polymorphism COIS- The authors declare that there are no conflict of interests. EDAT- 2021/11/10 06:00 MHDA- 2022/04/05 06:00 PMCR- 2021/11/09 CRDT- 2021/11/09 17:38 PHST- 2021/10/31 00:00 [revised] PHST- 2021/08/02 00:00 [received] PHST- 2021/11/02 00:00 [accepted] PHST- 2021/11/10 06:00 [pubmed] PHST- 2022/04/05 06:00 [medline] PHST- 2021/11/09 17:38 [entrez] PHST- 2021/11/09 00:00 [pmc-release] AID - IID3564 [pii] AID - 10.1002/iid3.564 [doi] PST - ppublish SO - Immun Inflamm Dis. 2022 Feb;10(2):209-217. doi: 10.1002/iid3.564. Epub 2021 Nov 9.