PMID- 36212172 OWN - NLM STAT- MEDLINE DCOM- 20221011 LR - 20221011 IS - 1875-8630 (Electronic) IS - 0278-0240 (Print) IS - 0278-0240 (Linking) VI - 2022 DP - 2022 TI - Identification of Significant Genes and Pathways for the Chronic and Subacute Cutaneous Lupus Erythematosus via Bioinformatics Analysis. PG - 9891299 LID - 10.1155/2022/9891299 [doi] LID - 9891299 AB - BACKGROUND: Chronic cutaneous lupus erythematosus (CCLE) and subacute cutaneous lupus erythematosus (SCLE) are both common variants of cutaneous lupus erythematosus (CLE) that mainly involve the skin and mucous membrane. Oral mucosal involvement is frequently observed in patients of CLE. Despite that they have different clinicopathological features, whether there is a significant difference in pathogenesis between them remains unclear. Herein, we investigated specific genes and pathways of SCLE and CCLE via bioinformatics analysis. METHODS: Microarray expression datasets of GSE109248 and GSE112943 were both retrieved from the GEO database. Differentially expressed genes (DEGs) between CCLE or SCLE skin tissues and health controls were selected by GEO2R. Common DEGs were picked out via the Venn diagram software. Then, functional enrichment and PPI network analysis were conducted, and the top 10 key genes were identified via Cytohubba. RESULTS: Totally, 176 DEGs of SCLE and 287 DEGs of CCLE were identified. The GO enrichment and KEGG analysis of DEGs of SCLE is significantly enriched in the response to virus, defense response to virus, response to IFN-gamma, cellular response to IFN-gamma, type I IFN signaling pathway, chemokine activity, chemokine receptor binding, NOD-like receptor signaling pathway, etc. The GO enrichment and KEGG analysis of DEGs of CCLE is significantly enriched in the response to virus, regulation of multiorganism process, negative regulation of viral process, regulation of lymphocyte activation, chemokine receptor binding, CCR chemokine receptor binding, NOD-like receptor signaling pathway, etc. The top 10 hub genes of SCLE and CCLE, respectively, include STAT1, CXCL10, IRF7, ISG15, and RSAD2 and CXCL10, IRF7, IFIT3, CTLA4, and ISG15. CONCLUSION: Our finding suggests that SCLE and CCLE have the similar potential key genes and pathways and majority of them belong to IFN signatures and IFN signaling pathway. Besides, the NOD-like receptor signaling pathway might also have an essential role in the pathogenesis of SCLE and CCLE. Together, the identified genes and signaling pathways have enhanced our understanding of the mechanism underlying the occurrence and development of both SCLE and CCLE. CI - Copyright (c) 2022 Yan Teng et al. FAU - Teng, Yan AU - Teng Y AD - Health Management Center, Department of Dermatology, Zhejiang Provincial People's Hospital, Affiliated People's Hospital of Hangzhou Medical College, Hangzhou 310014, China. FAU - Li, Sujing AU - Li S AD - Bengbu Medical College, Bengbu, China. FAU - Ding, Yang AU - Ding Y AD - Health Management Center, Department of Dermatology, Zhejiang Provincial People's Hospital, Affiliated People's Hospital of Hangzhou Medical College, Hangzhou 310014, China. FAU - Fan, Yibin AU - Fan Y AD - Health Management Center, Department of Dermatology, Zhejiang Provincial People's Hospital, Affiliated People's Hospital of Hangzhou Medical College, Hangzhou 310014, China. FAU - He, Miao AU - He M AD - Department of Orthopedics, Xiangya Hospital, Central South University, Changsha, 410008 Hunan, China. FAU - Li, Hengzhen AU - Li H AD - Department of Orthopedics, Xiangya Hospital, Central South University, Changsha, 410008 Hunan, China. FAU - Tao, Xiaohua AU - Tao X AD - Health Management Center, Department of Dermatology, Zhejiang Provincial People's Hospital, Affiliated People's Hospital of Hangzhou Medical College, Hangzhou 310014, China. FAU - Huang, Youming AU - Huang Y AUID- ORCID: 0000-0001-7871-1644 AD - Health Management Center, Department of Dermatology, Zhejiang Provincial People's Hospital, Affiliated People's Hospital of Hangzhou Medical College, Hangzhou 310014, China. LA - eng PT - Journal Article DEP - 20220929 PL - United States TA - Dis Markers JT - Disease markers JID - 8604127 RN - 0 (CTLA-4 Antigen) RN - 0 (Chemokines) RN - 0 (NLR Proteins) RN - 0 (Receptors, Chemokine) SB - IM MH - CTLA-4 Antigen MH - Chemokines MH - Computational Biology MH - *Graft vs Host Disease MH - Humans MH - *Lupus Erythematosus, Cutaneous/genetics/pathology MH - *Lupus Erythematosus, Discoid/genetics/pathology MH - NLR Proteins MH - Receptors, Chemokine PMC - PMC9537011 COIS- The authors declare no conflicting interests. EDAT- 2022/10/11 06:00 MHDA- 2022/10/12 06:00 PMCR- 2022/09/29 CRDT- 2022/10/10 04:07 PHST- 2022/07/04 00:00 [received] PHST- 2022/07/26 00:00 [revised] PHST- 2022/09/10 00:00 [accepted] PHST- 2022/10/10 04:07 [entrez] PHST- 2022/10/11 06:00 [pubmed] PHST- 2022/10/12 06:00 [medline] PHST- 2022/09/29 00:00 [pmc-release] AID - 10.1155/2022/9891299 [doi] PST - epublish SO - Dis Markers. 2022 Sep 29;2022:9891299. doi: 10.1155/2022/9891299. eCollection 2022.