Title:MiR-223-3p Aggravates Ocular Inflammation in Sjögren’s Syndrome
Volume: 23
Issue: 8
Author(s): Xuan Qi*, Ronghua Wang, Lu Jin, Yu Tian, Hongtao Jin, Yuxiang Han, Chao Sun, Meng Ding and Huifang Guo*
Affiliation:
- Department of Rheumatism and Immunology, The Second Hospital of Hebei Medical University, Shijiazhuang, Hebei 050000,
P.R.China
- Department of Rheumatism and Immunology, The Second Hospital of Hebei Medical University, Shijiazhuang, Hebei 050000, P.R.China
Keywords:
miR-223-3p, ITPR3, NF-κB pathway, Sjögren’s syndrome, salivary gland epithelial cells, ocular inflammation.
Abstract:
Background and Objectives: Sjogren’s syndrome (SS) is a chronic autoimmune disease,
particularly involving the lacrimal and salivary glands, with dryness as the main symptom. To date, the
pathogenesis of SS is not fully understood. Recently, numerous miRNAs were implicated in SS etiology
and pathogenesis.
Methods: Ocular wash was collected from SS patients and healthy controls. INF-γ-treated salivary
gland epithelial cells (SGECs) were utilized as SS in vitro models. Expressions of miR-223-3p and
inositol 1,4,5-trisphosphate receptor type 3 (ITPR3) in ocular wash specimens and cells were measured
by RT-qPCR assay and western blot analysis, respectively. ELISA assay was exploited to detect IL-6,
IL-12, and TNF-γ levels. CCK-8, flow cytometry, and western blot assay were exploited to determine
cell viability, apoptosis, and apoptosis-related protein levels.
Results: ITPR3 was a direct downstream gene of miR-223-3p and negatively modulated by miR-223-
3p. MiR-223-3p increased while ITPR3 decreased in samples from SS patients and INF-γ-induced
SGECs. miR-223-3p knockdown facilitated INF-γ-induced SGECs cell viability and restrained apoptosis
and inflammation response through the NF-κB pathway.
Conclusion: MiRNA-223-3p is implicated in the process of SS initiation and development. It may become
one of the targets for the treatment of SS in the future, as well as a possible indicator for clinical
monitoring of disease activity.