Role of long non-coding RNA RP11-288L9.1 in systemic lupus erythematosus and underlying mechanism
Objective To investigate the role of long non-coding RNA (lncRNA) RP11-288L9.1 in systemic lupus erythematosus (SLE) and its potential mechanism. Methods Transcriptome sequencing (RNA-seq) was used to screen the differentially expressed lncRNAs in peripheral blood mononuclear cells (PBMCs) of SLE pa...
Main Authors: | , , , , , , |
---|---|
Format: | Article |
Language: | zho |
Published: |
Editorial Office of Journal of Third Military Medical University
2021-07-01
|
Series: | Di-san junyi daxue xuebao |
Subjects: | |
Online Access: | http://aammt.tmmu.edu.cn/Upload/rhtml/202101010.htm |
_version_ | 1818649944304648192 |
---|---|
author | ZHAO Chenglei ZHAO Xingwang GUO Junkai WANG Juan ZHANG Min ZHANG Lian YOU Yi |
author_facet | ZHAO Chenglei ZHAO Xingwang GUO Junkai WANG Juan ZHANG Min ZHANG Lian YOU Yi |
author_sort | ZHAO Chenglei |
collection | DOAJ |
description | Objective To investigate the role of long non-coding RNA (lncRNA) RP11-288L9.1 in systemic lupus erythematosus (SLE) and its potential mechanism. Methods Transcriptome sequencing (RNA-seq) was used to screen the differentially expressed lncRNAs in peripheral blood mononuclear cells (PBMCs) of SLE patients, and the expression levels of these lncRNAs in 8 pairs of SLE patients and healthy controls were further verified by qRT-PCR. The knockdown as well as over-expression models of RP11-288L9.1 were constructed respectively by transfecting recombinant lentivirus into macrophages, and the transfection efficiency was determined subsequently. The subcellular distribution of RP11-288L9.1 was detected by fluorescence in situ hybridization (FISH) technique. Moreover, CCK-8 assay and Annexin V-FITC apoptosis detection kit were applied to examine the proliferation and apoptosis of macrophages in both models, and qRT-PCR was conducted to detect the expression of macrophage-related inflammatory cytokines, IL-1β, IL-6, IL-4, IL-10 and TGF-β1 after the transfection. Results Six differentially expressed lncRNAs were found (P < 0.05), in which RP11-288L9.1 was significantly up-regulated (P < 0.01), and mainly located in the cytoplasm of macrophages. The over-expression of RP11-288L9.1 promoted the apoptosis and inhibited the proliferation of macrophages (P < 0.05), increasing the levels of IL-1β and IL-6, and decreasing those of IL-4, IL-10 and TGF-β1 (P < 0.01). In contrast, the knockdown of RP11-288L9.1 significantly induced the proliferation of macrophages and inhibited the apoptosis (P < 0.05), with lowered levels of IL-1β and IL-6 and elevated IL-4, IL-10 and TGF-β1 (P < 0.01). Conclusion RP11-288L9.1 is highly expressed in the PBMCs of SLE patients, and regulates immune response in macrophages by affecting the synthesis of inflammatory cytokines, which may contribute to the occurrence of SLE. |
first_indexed | 2024-12-17T01:42:22Z |
format | Article |
id | doaj.art-91bd2a8b9f9948568c16e58b48bf5ea3 |
institution | Directory Open Access Journal |
issn | 1000-5404 |
language | zho |
last_indexed | 2024-12-17T01:42:22Z |
publishDate | 2021-07-01 |
publisher | Editorial Office of Journal of Third Military Medical University |
record_format | Article |
series | Di-san junyi daxue xuebao |
spelling | doaj.art-91bd2a8b9f9948568c16e58b48bf5ea32022-12-21T22:08:18ZzhoEditorial Office of Journal of Third Military Medical UniversityDi-san junyi daxue xuebao1000-54042021-07-0143131204121110.16016/j.1000-5404.202101010Role of long non-coding RNA RP11-288L9.1 in systemic lupus erythematosus and underlying mechanismZHAO Chenglei0ZHAO Xingwang1GUO Junkai2WANG Juan3 ZHANG Min4ZHANG Lian5YOU Yi6Department of Dermatology, First Affiliated Hospital, Army Medical University (Third Military Medical University), Chongqing, 400038, ChinaDepartment of Dermatology, First Affiliated Hospital, Army Medical University (Third Military Medical University), Chongqing, 400038, ChinaDepartment of Dermatology, First Affiliated Hospital, Army Medical University (Third Military Medical University), Chongqing, 400038, ChinaDepartment of Dermatology, First Affiliated Hospital, Army Medical University (Third Military Medical University), Chongqing, 400038, ChinaDepartment of Dermatology, First Affiliated Hospital, Army Medical University (Third Military Medical University), Chongqing, 400038, ChinaDepartment of Dermatology, First Affiliated Hospital, Army Medical University (Third Military Medical University), Chongqing, 400038, ChinaDepartment of Dermatology, First Affiliated Hospital, Army Medical University (Third Military Medical University), Chongqing, 400038, ChinaObjective To investigate the role of long non-coding RNA (lncRNA) RP11-288L9.1 in systemic lupus erythematosus (SLE) and its potential mechanism. Methods Transcriptome sequencing (RNA-seq) was used to screen the differentially expressed lncRNAs in peripheral blood mononuclear cells (PBMCs) of SLE patients, and the expression levels of these lncRNAs in 8 pairs of SLE patients and healthy controls were further verified by qRT-PCR. The knockdown as well as over-expression models of RP11-288L9.1 were constructed respectively by transfecting recombinant lentivirus into macrophages, and the transfection efficiency was determined subsequently. The subcellular distribution of RP11-288L9.1 was detected by fluorescence in situ hybridization (FISH) technique. Moreover, CCK-8 assay and Annexin V-FITC apoptosis detection kit were applied to examine the proliferation and apoptosis of macrophages in both models, and qRT-PCR was conducted to detect the expression of macrophage-related inflammatory cytokines, IL-1β, IL-6, IL-4, IL-10 and TGF-β1 after the transfection. Results Six differentially expressed lncRNAs were found (P < 0.05), in which RP11-288L9.1 was significantly up-regulated (P < 0.01), and mainly located in the cytoplasm of macrophages. The over-expression of RP11-288L9.1 promoted the apoptosis and inhibited the proliferation of macrophages (P < 0.05), increasing the levels of IL-1β and IL-6, and decreasing those of IL-4, IL-10 and TGF-β1 (P < 0.01). In contrast, the knockdown of RP11-288L9.1 significantly induced the proliferation of macrophages and inhibited the apoptosis (P < 0.05), with lowered levels of IL-1β and IL-6 and elevated IL-4, IL-10 and TGF-β1 (P < 0.01). Conclusion RP11-288L9.1 is highly expressed in the PBMCs of SLE patients, and regulates immune response in macrophages by affecting the synthesis of inflammatory cytokines, which may contribute to the occurrence of SLE.http://aammt.tmmu.edu.cn/Upload/rhtml/202101010.htmsystemic lupus erythematosuslong non-coding rnarp11-288l9.1macrophages |
spellingShingle | ZHAO Chenglei ZHAO Xingwang GUO Junkai WANG Juan ZHANG Min ZHANG Lian YOU Yi Role of long non-coding RNA RP11-288L9.1 in systemic lupus erythematosus and underlying mechanism Di-san junyi daxue xuebao systemic lupus erythematosus long non-coding rna rp11-288l9.1 macrophages |
title | Role of long non-coding RNA RP11-288L9.1 in systemic lupus erythematosus and underlying mechanism |
title_full | Role of long non-coding RNA RP11-288L9.1 in systemic lupus erythematosus and underlying mechanism |
title_fullStr | Role of long non-coding RNA RP11-288L9.1 in systemic lupus erythematosus and underlying mechanism |
title_full_unstemmed | Role of long non-coding RNA RP11-288L9.1 in systemic lupus erythematosus and underlying mechanism |
title_short | Role of long non-coding RNA RP11-288L9.1 in systemic lupus erythematosus and underlying mechanism |
title_sort | role of long non coding rna rp11 288l9 1 in systemic lupus erythematosus and underlying mechanism |
topic | systemic lupus erythematosus long non-coding rna rp11-288l9.1 macrophages |
url | http://aammt.tmmu.edu.cn/Upload/rhtml/202101010.htm |
work_keys_str_mv | AT zhaochenglei roleoflongnoncodingrnarp11288l91insystemiclupuserythematosusandunderlyingmechanism AT zhaoxingwang roleoflongnoncodingrnarp11288l91insystemiclupuserythematosusandunderlyingmechanism AT guojunkai roleoflongnoncodingrnarp11288l91insystemiclupuserythematosusandunderlyingmechanism AT wangjuan roleoflongnoncodingrnarp11288l91insystemiclupuserythematosusandunderlyingmechanism AT zhangmin roleoflongnoncodingrnarp11288l91insystemiclupuserythematosusandunderlyingmechanism AT zhanglian roleoflongnoncodingrnarp11288l91insystemiclupuserythematosusandunderlyingmechanism AT youyi roleoflongnoncodingrnarp11288l91insystemiclupuserythematosusandunderlyingmechanism |