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Furthermore, these data imply that mi R-155 levels may reflect RA disease activity and could be a potential diagnostic or clinical disease activity biomarker for RA.Sphingosine kinases (SPHKs), SPHK1 and SPHK2, are isozymes that phosphorylate sphingosine into sphingosine-1- phosphate (S1P).The recruitment of effectors cells is an important step in RA progression and is mediated by chemokines and their receptors.
Of particular interest in the context of RA is mi R-155, which is upregulated in RA synovial macrophages where it regulates cytokine expression such as TNF-α.
Until now little was known about the role of mi R-155 in regulating monocyte migration.
Rheumatoid Arthritis (RA) is a common chronic autoimmune disease that is characterized by synovial tissue inflammation eventually leading to joint destruction with severe functional deterioration and increased mortality – the underlying pathogenesis of RA remains unsolved.
The principle of new therapeutic development is to define and characterize a molecular pathway both in terms of its basic biology and also its context-dependent effects in the synovial compartment.
These observations suggest that CCR2 and CCR7 were under the tight control of mi R-155 and that this regulation is preserved across the species; together suggesting that mi R-155 can act as an important regulator of these receptors.
We conclude that deregulation of mi R- 155 in RA monocytes contributes to monocyte retention at sites of inflammation due to induction of chemokine production and down-regulation of inflammatory chemokine receptors.
The copy number of mi R-155 expression was significantly increased in anti- citrullinated protein antibody (ACPA) positive RA compared with ACPA negative RA.
The RA PB monocyte mi R-155 copy number correlated positively and significantly with DAS28.
Until now however, no comprehensive analysis of expression of its components in RA has been performed.
My data show that S1P concentrations were significantly elevated in the serum of RA patients with active disease compared to RA patients in remission and in healthy controls.