2014
DOI: 10.3109/14397595.2013.854077
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Elevated miR-29a expression is not correlated with disease activity index in PBMCs of patients with ankylosing spondylitis

Abstract: We report for the first time elevated miR-29a expression in PBMCs of patients with ankylosing spondylitis, and miR-29a might be used as a useful diagnostic marker in new bone formation but cannot reflect disease activity.

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Cited by 42 publications
(32 citation statements)
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“…Notably, the function and downstream molecular pathways of several crucial deregulated miRNAs, including miR‐16, miR‐29a, miR‐146, miR‐155, miR‐210, and miR‐221 remain to be illuminated. Dysregulation of these miRNAs has been corroborated with a reasonably large sample size (Huang, Song, et al, ; Lai et al, ; Qian et al, ). Considering that miRNAs exert their function in a complicated network, other contributing factors that affect these molecules, like other miRNAs and epigenetic regulatory mechanisms as well as SNPs, should be evaluated alongside with mere evaluation of miRNA transcript levels.…”
Section: Resultsmentioning
confidence: 86%
See 1 more Smart Citation
“…Notably, the function and downstream molecular pathways of several crucial deregulated miRNAs, including miR‐16, miR‐29a, miR‐146, miR‐155, miR‐210, and miR‐221 remain to be illuminated. Dysregulation of these miRNAs has been corroborated with a reasonably large sample size (Huang, Song, et al, ; Lai et al, ; Qian et al, ). Considering that miRNAs exert their function in a complicated network, other contributing factors that affect these molecules, like other miRNAs and epigenetic regulatory mechanisms as well as SNPs, should be evaluated alongside with mere evaluation of miRNA transcript levels.…”
Section: Resultsmentioning
confidence: 86%
“…miR‐29a expression was regulated by TNF‐α in vitro (Roderburg et al, ). Furthermore, Huang, Song, Yin, Luo, & Ye () for the first time reported the increased miR‐29a expression in PBMCs of patients with AS. Recently Li, Zhang, & Gu () indicated that miR‐29a controls TNF‐α mediated bone loss mostly by targeting dickkopf WNT signaling pathway inhibitor 1 (DKK1) and glycogen synthase kinase 3 beta (GSK3β), through activating the Wnt/β‐catenin pathway.…”
Section: Biogenesis Of Mirnasmentioning
confidence: 97%
“…11 Subsequent studies suggest that miR-146, miR-155, and miR-223 are thought to regulate the acute inflammatory response after the recognition of pathogens by Toll-like receptors, [12][13][14] whereas miR-155 and miR-181a are involved in B-cell and T-cell response. 17 The pathogenesis of AS has been reported because human leukocyte antigen B27 (HLA-B27), a class I major histocompatibility complex gene, was proven to be the strongest predisposing factor of AS. 17 The pathogenesis of AS has been reported because human leukocyte antigen B27 (HLA-B27), a class I major histocompatibility complex gene, was proven to be the strongest predisposing factor of AS.…”
mentioning
confidence: 99%
“…Huang et al 41 studied the miR-29a expression levels in the PBMCs (peripheral blood mononuclear cells) of the AS, rheumatoid arthritis, and healthy controls by using real-time PCR. They found that there was a higher miR-29a expression was found in the PBMCs of AS patients compared to that in the rheumatoid arthritis patients or healthy controls.…”
Section: Resultsmentioning
confidence: 99%