INT165054
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
Susceptibility to Chlamydia trachomatis infections is 40% host based. microRNA-146a is a negative regulator of Tolllike receptor (TLR) signaling and possesses functional polymorphisms which decrease the production of premiR-146a and mature miR-146a. | |||||||||||||||
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He et al. also showed that miR-146, miR-221 and miR-222 distinguished unequivocally between papillary thyroid carcinoma (PTC) and normal thyroid. | |||||||||||||||
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MiR-150 has not been associated with the high expression of miR-146 and miR-155 in PBMC and synovium of RA in previous reports [24-26]. | |||||||||||||||
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In a previous report, accumulated CD3+ T cells were observed to express miR-146, thereby suggesting that miR-146 might play a role in the persistent inflammation in RA via a T cell network, which strongly supports that miR-146a thus expressed in Th17 cells [25]. | |||||||||||||||
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Indeed, previous reports demonstrated that miR-146a/b, miR-150 and miR-155 are expressed in PBMC or synovium in RA patients, which might include miRNAs which are expressed in IL-17 producing T cells. | |||||||||||||||
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The expression level of miR-146a was similar to that of IL-17. | |||||||||||||||
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The analysis of the synovium from RA and OA patients revealed that miR-146a/b, miR-150 and miR-155 were highly expressed in RA synovium with hyperplasia and infiltration of inflammatory cells including Th17 producing cells in poorly controlled patients with severe joint destruction (Figure 4A).
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Therefore, the expression pattern of miR-146a/b, miR-150, and miR-155 in the synovium of RA patients was examined using real time PCR. miR-146a, miR-146b, miR-150, and miR-155 were expressed intensely in RA in comparison to OA. | |||||||||||||||
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The synovium with high expression of miR-146a, miR-146b, miR-150 and miR-155 showed vigorous proliferation of synovial cells and infiltration of inflammatory cells and abundant IL-17 positive cells. | |||||||||||||||
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In a previous report, accumulated CD3+ T cells were observed to express miR-146, thereby suggesting that miR-146 might play a role in the persistent inflammation in RA via a T cell network, which strongly supports that miR-146a thus expressed in Th17 cells [25]. | |||||||||||||||
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The expression of miR-146a and miR-146b tended to increase with high disease activity, which was consistent with previous reports[24,25]. | |||||||||||||||
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There were significant differences between RA and OA patients in the expression level of miR-146a, miR-150 and miR-155. | |||||||||||||||
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MiR-146a was expressed intensely with IL-17 expression in PBMC from the patients with early stage of RA and high disease activity. miR-146a/b was associated with high disease activity, and miR-150 was intensely expressed in the patients with severe joint destruction. | |||||||||||||||
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The expression level of miR-26a, miR-146a/b, miR-150 and miR-155 in RA patients were significantly higher than in healthy subjects. | |||||||||||||||
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In addition, the miR-146a expression in the IL-17 producing T cells of the RA synovium was confirmed. | |||||||||||||||
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The expression of miR-146a and IL-17 was high in PBMC in patients with low score of Larsen grade and short disease duration in the current series. | |||||||||||||||
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Therefore, the high expression of miR-146a in PBMC was strongly associated with IL-17 expression, especially at the early stage of RA. | |||||||||||||||
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The synovium from RA patients exhibit increased expression of miR-146a,b, 150, and 155 | |||||||||||||||
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The expression level of miR-146a and IL-17 in patient RA1 and RA4 was high in comparison to the other patients. miR-146a expressed intensely with IL-17 expression in PBMC from the patients with early stage of RA and high disease activity (Figure 2B).
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The expression level of miR-146a and IL-17 in patient RA1 and RA4 was high in comparison to the other patients. miR-146a expressed intensely with IL-17 expression in PBMC from the patients with early stage of RA and high disease activity (Figure 2B).
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