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Myofibroblast in the ligamentum flavum hypertrophic activity

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dc.contributor.authorJunseok W. Hur-
dc.contributor.authorTaegeun Bae-
dc.contributor.authorSunghyeok Ye-
dc.contributor.authorJoo-Hyun Kim-
dc.contributor.authorSunhye Lee-
dc.contributor.authorKyoungmi Kim-
dc.contributor.authorSeung-Hwan Lee-
dc.contributor.authorJin-Soo Kim-
dc.contributor.authorJang-Bo Lee-
dc.contributor.authorTai-Hyoung Cho-
dc.contributor.authorJung-Yul Park-
dc.contributor.authorJunho K. Hur-
dc.date.available2017-12-06T05:04:06Z-
dc.date.created2017-09-25-
dc.date.issued2017-08-
dc.identifier.issn0940-6719-
dc.identifier.urihttps://pr.ibs.re.kr/handle/8788114/4011-
dc.description.abstractMajority of the previous studies compared lumbar spinal stenosis (LSS) and lumbar disc herniation (LDH) patients for analyses of LFH. However, the separation of normal/hypertrophied LF has often been ambiguous and the severity of hypertrophic activity differed. Here, we present a novel analysis scheme for LFH in which myofibroblast is proposed as a major etiological factor for LFH study. Seventy-one LF patient tissue samples were used for this study. Initially, mRNA levels of the samples were assessed by qRT-PCR: angiopoietin-like protein-2 (ANGPTL2), transforming growth factor-beta1 (TGF-beta 1), vascular endothelial growth factor (VEGF), interleukin-6, collagen-1, 3, 4, 5, and 11, and elastin. Myofibroblasts were detected by immune stain using alpha-smooth muscle actin (alpha SMA) as a marker. To study the myofibroblast in TGF-beta pathway, LF tissues were analyzed for protein levels of alpha SMA/TGF-beta 1 by Western blot. In addition, from LF cells cultured with exogenous TGF-beta 1 conditioned medium, expression of alpha SMA/collagen-1 was assessed and the cell morphology was identified. The comparative analysis of mRNA expression levels (LSS vs LDH) failed to show significant differences in TGF-beta 1 (p = 0.08); however, we found a significant positive correlation among ANGPTL2, VEGF, TGF-beta 1, and collagen-1 and 3, which represent common trends in hypertrophic activity (p < 0.05). We detected myofibroblast in the patient samples by alpha SMA staining, and the protein levels of alpha SMA were positively correlated with TGF-beta 1. In LF cell culture, exogenous TGF-beta 1 upregulated alpha SMA/collagen-1 mRNA levels and facilitated trans-differentiation to myofibroblast. We conclude that the transition of fibroblast to myofibroblasts via TGF-beta pathway is a key linker between inflammation and fibrosis in LFH mechanism. (c) Springer-Verlag Berlin Heidelberg 2017-
dc.description.uri1-
dc.language영어-
dc.publisherSPRINGER-
dc.subjectLigamentum flavum-
dc.subjectHypertrophy-
dc.subjectMyofibroblasts-
dc.subjectAlpha-smooth muscle actin-
dc.subjectTransforming growth factor beta1-
dc.titleMyofibroblast in the ligamentum flavum hypertrophic activity-
dc.typeArticle-
dc.type.rimsART-
dc.identifier.wosid000407369400005-
dc.identifier.scopusid2-s2.0-85011856655-
dc.identifier.rimsid60225ko
dc.date.tcdate2018-10-01-
dc.contributor.affiliatedAuthorJunseok W. Hur-
dc.contributor.affiliatedAuthorTaegeun Bae-
dc.contributor.affiliatedAuthorSunghyeok Ye-
dc.contributor.affiliatedAuthorKyoungmi Kim-
dc.contributor.affiliatedAuthorSeung-Hwan Lee-
dc.contributor.affiliatedAuthorJin-Soo Kim-
dc.identifier.doi10.1007/s00586-017-4981-2-
dc.identifier.bibliographicCitationEUROPEAN SPINE JOURNAL, v.26, no.8, pp.2021 - 2030-
dc.citation.titleEUROPEAN SPINE JOURNAL-
dc.citation.volume26-
dc.citation.number8-
dc.citation.startPage2021-
dc.citation.endPage2030-
dc.date.scptcdate2018-10-01-
dc.description.wostc2-
dc.description.scptc3-
dc.description.journalClass1-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.subject.keywordPlusSPINAL-CANAL STENOSIS-
dc.subject.keywordPlusTISSUE-
dc.subject.keywordPlusPATHOGENESIS-
dc.subject.keywordPlusDISEASES-
dc.subject.keywordPlusFIBROSIS-
dc.subject.keywordAuthorLigamentum flavum-
dc.subject.keywordAuthorHypertrophy-
dc.subject.keywordAuthorMyofibroblasts-
dc.subject.keywordAuthorAlpha-smooth muscle actin-
dc.subject.keywordAuthorTransforming growth factor beta1-
Appears in Collections:
Center for Genome Engineering(유전체 교정 연구단) > 1. Journal Papers (저널논문)
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