<b>Objectives:</b> To explore the genetic interaction between Wnt/β-catenin signalling pathway genes and ankylosing spondylitis (AS) in the Chinese population.<b>Methods:</b> Six single-nucleotide polymorphisms (SNPs) in DKK1, LRP5, LRP6, and SOST genes were genotyped in 673 AS patients and 687 healthy controls by using SNPs can Technic.
After transfection of miR-451 synthetic mimic or FAM-labelled negative control mimic to AS PBMCs, MIF and cytokine levels were determined using quantitative real-time PCR or ELISA.
The expressions of miR-495 and DVL-2 were negative corrected in AS. miR-495 and si-DVL-2 did not affect the cell viability. miR-495 and si-DVL-2 obviously inhibited inflammatory response by down-regulating tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β) and IL-6 levels, and facilitated bone differentiation by up-regulating osteoprotegerin (OPG) and receptor activator for nuclear factor-κB ligand (RANKL) levels in HFLS cells.
Genetic polymorphism (rs1800693) of TNFRSF1A (type 1 tumour necrosis factor receptor) encodes a potentially anti-inflammatory soluble truncated form of the p55 receptor, which is associated with predisposition to multiple sclerosis but protection against ankylosing spondylitis (AS).
In the DCE-MRI follow-up treatment imaging of 48 patients with AS (192 parts), the TIC curve type recorded was as follows: 43.75% (84/192) of type II, 56.25% (108/192) of type III, and type I curve was not seen.
Increased BMPR1A expression induces abnormal ASMSC adipogenic differentiation, potentially contributing to fat metaplasia and thus new bone formation in patients with AS.
Genetic polymorphism (rs1800693) of TNFRSF1A (type 1 tumour necrosis factor receptor) encodes a potentially anti-inflammatory soluble truncated form of the p55 receptor, which is associated with predisposition to multiple sclerosis but protection against ankylosing spondylitis (AS).
Genetic polymorphism (rs1800693) of TNFRSF1A (type 1 tumour necrosis factor receptor) encodes a potentially anti-inflammatory soluble truncated form of the p55 receptor, which is associated with predisposition to multiple sclerosis but protection against ankylosing spondylitis (AS).
We provide evidence for the predisposition of miR-335-5p, miR-27a and miR-218 to syndesmophytes in AS patients, indicating a contributory role of miRNAs in the pathogenesis of syndesmophytes.Further validation is warranted.
Six studies used "single CD25-positive" cells as Tregs, which revealed a significant increase in AS patients compared with healthy blood donors [0.736, (0.138, 1.334), <i>p</i> = 0.016, <i>I</i><sup>2</sup> = 80.7%].
In conclusion, our findings reveal a role of the miR-17-5p-ANKH axis in the regulation of heterotopic ossification, which is essential for therapeutic intervention in heterotopic ossification in AS.
Carrying HLA-B*27 was associated with robust hypomethylation of HCP5, tubulin folding cofactor A (TBCA) and phospholipase D Family Member 6 (PLD6) in ankylosing spondylitis patients.
We have identified a novel integrin-expressing mature CD8+ T cell population (CD49a+CD103+β7+CD29+) that appears to be more prevalent in AS SF than RA SF.
Carrying HLA-B*27 was associated with robust hypomethylation of HCP5, tubulin folding cofactor A (TBCA) and phospholipase D Family Member 6 (PLD6) in ankylosing spondylitis patients.
Genetic polymorphism (rs1800693) of TNFRSF1A (type 1 tumour necrosis factor receptor) encodes a potentially anti-inflammatory soluble truncated form of the p55 receptor, which is associated with predisposition to multiple sclerosis but protection against ankylosing spondylitis (AS).
In the DCE-MRI follow-up treatment imaging of 48 patients with AS (192 parts), the TIC curve type recorded was as follows: 43.75% (84/192) of type II, 56.25% (108/192) of type III, and type I curve was not seen.
Despite the lower basal expression of TLRs, AS-MSCs were as sensitive or more sensitive to TLR agonists as compared with HD-MSCs in terms of activation of p38 and ERK MAPK signaling pathways.