Abstract：
To analyze the differential transcriptome expression in hypertrophic ligaments flavum (HLF) compared to normal ligaments.
A case-control study was conducted that included 15 patients with hypertrophy of LF and 15 controls. Samples of LF were obtained through a lumbar laminectomy and analyzed by DNA microarrays and histology. The dysregulated biological processes, signaling pathways, and pathological markers in the HLF were identified using bioinformatics tools.
The HLF had notable histological alterations, including hyalinosis, leukocyte infiltration, and disarrangement of collagen fibers. Transcriptomic analysis showed that up-regulated genes were associated with the signaling pathways of Rho GTPases, receptor tyrosine kinases (RTK), fibroblast growth factors (FGF), WNT, vascular endothelial growth factor, phosphoinositide 3-kinase (PIK3), mitogen-activated protein kinases, and immune system. The genes PIK3R1, RHOA, RPS27A, CDC42, VAV1, and FGF5, 9, 18, and 19 were highlighted as crucial markers in HLF. The down-expressed genes in the HLF had associations with the metabolism of RNA and proteins.
Our results suggest that abnormal processes in hypertrophied LF are mediated by the interaction of the Rho GTPase, RTK, and PI3K pathways, which have not been previously described in the HLF, but for which there are currently therapeutic proposals. More studies are required to confirm the therapeutic potential of the pathways and mediators described in our results.
A case-control study was conducted that included 15 patients with hypertrophy of LF and 15 controls. Samples of LF were obtained through a lumbar laminectomy and analyzed by DNA microarrays and histology. The dysregulated biological processes, signaling pathways, and pathological markers in the HLF were identified using bioinformatics tools.
The HLF had notable histological alterations, including hyalinosis, leukocyte infiltration, and disarrangement of collagen fibers. Transcriptomic analysis showed that up-regulated genes were associated with the signaling pathways of Rho GTPases, receptor tyrosine kinases (RTK), fibroblast growth factors (FGF), WNT, vascular endothelial growth factor, phosphoinositide 3-kinase (PIK3), mitogen-activated protein kinases, and immune system. The genes PIK3R1, RHOA, RPS27A, CDC42, VAV1, and FGF5, 9, 18, and 19 were highlighted as crucial markers in HLF. The down-expressed genes in the HLF had associations with the metabolism of RNA and proteins.
Our results suggest that abnormal processes in hypertrophied LF are mediated by the interaction of the Rho GTPase, RTK, and PI3K pathways, which have not been previously described in the HLF, but for which there are currently therapeutic proposals. More studies are required to confirm the therapeutic potential of the pathways and mediators described in our results.
摘要：
目的：分析肥大黄韧带（HLF）与正常韧带相比的差异转录组表达。
方法：进行了一项病例对照研究，包括15例LF肥大患者和15例对照。通过腰椎椎板切除术获得LF样品，并通过DNA微阵列和组织学进行分析。失调的生物过程，信号通路，使用生物信息学工具鉴定HLF中的病理标记物。
结果：HLF有明显的组织学改变，包括透明病,白细胞浸润,和胶原纤维的排列。转录组分析表明，上调基因与RhoGTPases的信号通路有关，受体酪氨酸激酶（RTK），成纤维细胞生长因子（FGF），WNT,血管内皮生长因子，磷酸肌醇3-激酶（PIK3），丝裂原活化蛋白激酶,和免疫系统。PIK3R1,RHOA,RPS27A,CDC42、VAV1和FGF5、9、18和19被突出显示为HLF中的关键标志物。HLF中的低表达基因与RNA和蛋白质的代谢有关。
结论：我们的结果表明，肥大型LF的异常过程是由RhoGTP酶的相互作用介导的，RTK,和PI3K通路，以前在HLF中没有描述过，但目前有治疗建议。需要更多的研究来证实我们结果中描述的途径和介质的治疗潜力。
方法：进行了一项病例对照研究，包括15例LF肥大患者和15例对照。通过腰椎椎板切除术获得LF样品，并通过DNA微阵列和组织学进行分析。失调的生物过程，信号通路，使用生物信息学工具鉴定HLF中的病理标记物。
结果：HLF有明显的组织学改变，包括透明病,白细胞浸润,和胶原纤维的排列。转录组分析表明，上调基因与RhoGTPases的信号通路有关，受体酪氨酸激酶（RTK），成纤维细胞生长因子（FGF），WNT,血管内皮生长因子，磷酸肌醇3-激酶（PIK3），丝裂原活化蛋白激酶,和免疫系统。PIK3R1,RHOA,RPS27A,CDC42、VAV1和FGF5、9、18和19被突出显示为HLF中的关键标志物。HLF中的低表达基因与RNA和蛋白质的代谢有关。
结论：我们的结果表明，肥大型LF的异常过程是由RhoGTP酶的相互作用介导的，RTK,和PI3K通路，以前在HLF中没有描述过，但目前有治疗建议。需要更多的研究来证实我们结果中描述的途径和介质的治疗潜力。
