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Sjögren’s syndrome-associated microRNAs may suppress transforming growth factor-beta signaling
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Recently published results showed transforming growth factor-beta signaling may be suppressed collectively by Sjögren’s syndrome-associated micro ribonucleic acid as opposed to pro-inflammatory interleukin-12 and toll-like receptor/nuclear factor-kappa beta pathways in Sjögren’s syndrome pathogenesis.
Researchers isolated peripheral blood cluster of differentiation 14+ (CD14+) monocytes for micro ribonucleic acid (miRNA) microarray analysis and extracted total RNA from healthy controls and patients with either Sjögren’s syndrome, systemic lupus erythematosus or rheumatoid arthritis. Using quantitative reverse transcription-polymerase chain reaction (PCR), researchers evaluated the original cohort and a new cohort of monocyte RNA samples from healthy controls and patients with either Sjögren’s syndrome, systemic lupus erythematosus or rheumatoid arthritis to validate select miRNA from the microarray analysis.
Compared with controls, results showed Sjögren’s syndrome monocytes had predominately upregulated miRNAs. Co-regulation of miR-34b-3p, miR-4701-5p, miR-609, miR-300, miR3162-3p and miR-877-3p in Sjögren’s syndrome monocytes was supported by quantitative reverse transcription-PCR confirmations vs. systemic lupus erythematosus and rheumatoid arthritis, according to results. Researchers found Sjögren’s syndrome-associated miRNAs appear to preferentially target the canonical transforming growth factor-beta signaling pathway as opposed to pro-inflammatory interleukin-12 and toll-like receptor/nuclear factor-kappa beta pathways, as identified by miRNA-target pathway predictions. – by Casey Tingle
Disclosure: The researchers report no relevant financial disclosures.
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