impact factor, citescore
logo
 

Full Papers

 

Long non-coding RNA expression profiles in neutrophils revealed potential biomarker for rapidly progressive interstitial lung disease in MDA5+ dermatomyositis


1, 2, 3, 4, 5, 6

 

  1. Department of Rheumatology, Shanghai Jiao Tong University School of Medicine Affiliated Renji Hospital, Shanghai, China.
  2. Department of Rheumatology, Shanghai Jiao Tong University School of Medicine Affiliated Renji Hospital, Shanghai, China.
  3. Department of Rheumatology, Shanghai Jiao Tong University School of Medicine Affiliated Renji Hospital, Shanghai, China.
  4. Vision Academy, Shanghai, China.
  5. Department of Rheumatology, Shanghai Jiao Tong University School of Medicine Affiliated Renji Hospital, Shanghai, China. xia_nana0914@163.com
  6. Department of Rheumatology, Shanghai Jiao Tong University School of Medicine Affiliated Renji Hospital; and Department of Rheumatology, Jiading District Central Hospital Affiliated Shanghai University of Medicine & Health Sciences, Shanghai, China. bluedescent@126.com

CER19136
Full Papers

purchase article

Received: 25/07/2025
Accepted : 12/01/2026
In Press: 04/05/2026

Abstract

OBJECTIVES:
The long non-coding RNAs play important roles in the pathogenesis of autoimmune rheumatic diseases. This study aims to screen and identify dysregulated lncRNAs in neutrophils of anti-melanoma differentiation-associated gene 5 positive dermatomyositis (MDA5+DM) and explore the relationship between candidate lncRNA levels and well-recognised disease activity-related indicators.
METHODS:
RNA-Seq was used to identify differentially expressed lncRNAs in neutrophils from MDA5+DM, Jo1+ASyS and healthy controls. Following the screening process, levels of the candidate lncRNAs were confirmed using real-time quantitative polymerase chain reaction in 280 participants, including 103 MDA5+DM, 85 Jo1+ASyS, 12 MDA5−DM, 26 SLE, 54 healthy controls.
RESULTS:
LncRNA expression profiling analysis identified 412 up-regulated and 201 down-regulated lncRNAs in neutrophils of MDA5+DM compared to healthy controls. Moreover, 144 lncRNAs were up-regulated, and 191 lncRNAs were down-regulated between MDA5+DM and Jo1+ASyS. RT-qPCR assay confirmed that the level of Lnc-ZCCHC13-18:1 was significantly higher in neutrophils of MDA5+DM compared to MDA5−DM, Jo1+ASyS, SLE, and healthy controls (all p-values <0.001). Notably, Lnc-ZCCHC13-18:1 (OR: 9.94, 95%CI: 2.71–47.12, p=0.001) was identified as an independent risk factor for RPILD, along with other well-recognised risk factors, such as the percentage of predicted diffusing capacity for carbon monoxide (OR: 6.23, 95%CI: 1.88–24.29, p=0.004), Krebs von den Lungen-6 (OR: 4.26, 95%CI: 1.31–15.63, p=0.02), serum ferritin (OR: 6.14, 95%CI: 1.75–26.41, p=0.008) and age at admission (OR: 1.07, 95%CI: 1.01–1.13, p=0.031).
CONCLUSIONS:
LncRNA expression profiling in neutrophils of MDA5+DM revealed differentially expressed lncRNAs. Lnc-ZCCHC13-18:1 has been identified as a possible biomarker for RPILD in MDA5+DM.

Rheumatology Article

Rheumatology Addendum