STC1 downregulation and CRIP1 upregulation associated with inflammatory Osteoarthritis
STC1 downregulation and CRIP1 upregulation associated with inflammatory Osteoarthritis
Maziar Oveisee,1,*Akram Gholipour,2Mahshid Malakootian,3
1. School of Medicine, Bam University of Medical Sciences, Bam 2. Cardiogenetic Research Center, Rajaie Cardiovascular Medical and Research Center, Iran University of Medical Sciences 3. Cardiogenetic Research Center, Rajaie Cardiovascular Medical and Research Center, Iran University of Medical Sciences
Introduction: Osteoarthritis (OA) is the most common form of arthritis and resulting in joint deterioration. OA synovial tissue typically displays a mild to moderate degree of inflammation. Synovial inflammation is present in the OA joint and has been associated with pain progression. In the present study, we aimed to detect critical genes with differential expression patterns in patients with Synovial inflammation.
Methods: The expression profiling array of patients with synovial cells from inflammatory (12 samples) and normal areas of osteoarthritis synovial membrane (12 samples) were obtained from the GEO database (GEO accession: GSE46750), and the samples were analyzed. Genes with differential expression patterns were isolated with the GEO2R by P.value < 0.05 and logFoldchange (logFC) ≠ 1 investigation. In addition, the biological process (BP) of differential expressed genes was analyzed using PANTHER17.0database.
Results: The result demonstrated that 101 genes upregulated and 149 genes downregulated. Of which stanniocalcin 1 (STC1) was the most downregulated with logFC = -2.544 and P.value = 0.00022177 and cysteine rich protein 1 (CRIP1) was the most upregulated ones with logFC = 1.467and P.value = 0.00065214. Further Biological process (BP) analysis revealed cellular process (GO:0009987) including cellular metabolic process, cellular response to stimulus and cell communication were the important process in pathophysiology of osteoarthritis.
Conclusion: All in all, STC1 downregulation and CRIP1 upregulation might play important role in pathophysiology of inflammatory OA. However, more experimental analysis is required to confirm the exact role of them in OA.