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INNOSC Theranostics and
Pharmacological Sciences Transcriptome-based RNA sequencing

Table 2. (Continued)
S. No. Purpose Study pattern Sample type Methodology Justification Year of References
study
8 The most prevalent The aim of this study Synovium The study used the A total of 206 genes with 2021 53
internal alteration was to identify different MH7A cell line to detect differentially regulated
found in eukaryotic amounts of m6A m6A methylation in RA, m6A methylation were
mRNAs is methylation in human confirming the expression detected using m6A-
N6-methyladenosine RA using two high- levels in MH7A cells and seq, of which 118 had
(m6A), and it exerts throughput sequencing synovial tissues of AA rats. substantially elevated m6A
a direct effect on the techniques. methylation and 88 had
development and significantly decreased
course of several m6A methylation.
diseases, particularly In MH7A cells, the
tumors. This study transcriptional mapping
investigated the of m6A was performed,
relationship between and a possible correlation
m6A methylation between the RNA
and RA using methylation alteration
transcriptomic and RA-related genes was
RNA-seq. noted.
Abbreviations: RNA-seq: RNA sequencing; RA: Rheumatoid arthritis.

poor quality. To identify the differentially expressed genes with MTX being the first-line treatment in 40 – 60% of
(DEGs) based on fold change and statistical significance cases. 35,36
criteria, techniques such as DEseq2 and limma-voom
are used. Moreover, it performs DEG annotation using 3.5. Immune dysregulation
databases and bioinformatics tools, and DEG maps are Analyzing gene expression in immune cells and the
used to identify pathways that are enriched in dysregulated synovium can assist in identifying dysregulated pathways
genes according to predetermined criteria. Bar plots, and RA etiology using RNA sequencing. The expression
bubble plots, and network diagrams are useful for patterns of cytokines and chemokines in the synovium and
showing the most important pathways. 33,34 Dysregulated other tissues of patients with RA were also examined. Tumor
pathways in RA include T-cell receptor signaling, altered necrosis factor-alpha, interleukin-6, and other chemokines
B-cell receptor signaling, autoantibodies, and the Toll- can be used to identify the pathophysiology of RA. RNA-
like receptor. Type I IFN signaling is activated in RA, seq enables the profiling of autoantigens, immunological
contributing to inflammation and joint destruction. The tolerance, and autoantibodies. Autoimmune problems are
signal transducer and activator of transcription (STAT) significant for patients with RA. Combining all omics data
regulates inflammation and the immune response, helps in the study of immune dysregulation (genomics and
whereas nuclear factor-κB regulates gene expression. proteomics). 37-39
Abnormal expression of the Janus kinase–STAT pathway
and the mitogen-activated protein kinase (MAPK) signal 4. Transcriptomic profiling of synovial
transduction pathway also contribute to RA pathogenesis. tissue and fluid in patients with RA

3.4. Personalized medicine The synovium, a thin tissue layer, aids in the function
40
of diarthrodial joints by lining the fibrous capsule.
The traditional treatment for RA involves medication,
psychotherapy, and rehabilitation to maintain the In healthy joints, it generates lubricin and hyaluronate
for synovial fluid, supporting flexion and load-bearing
locomotor system and reduce discomfort, inflammation, without compromising bone and cartilage integrity. The
and osteoporosis. Weak opioids, muscle relaxants, and
analgesics are used to manage pain, whereas strong opioids inflammatory synovium in RA exhibits tissue hyperplasia,
such as morphine are considered in certain cases. RNA- angiogenesis, and leukocyte infiltration, with fibroblasts
playing a vital role in cartilage destruction, leukocyte
seq profiling can predict prognosis, treatment response, 41
and disease progression. Synthetic disease-modifying influx and outflow, and bone damage.
antirheumatic medications include cyclosporine A, In RA, proinflammatory chemicals such as IL-6
leflunomide, azathioprine, methotrexate (MTX), and CCL5 are generated, synovium fibroblasts are
sulfasalazine (SSZ), and cyclophosphamide. RA is diverse, constantly active, and matrix remodeling enzymes such

Volume 8 Issue 1 (2025) 23 doi: 10.36922/itps.4449