Beta-nerve growth factor(β-NGF) is known to be a major leading cause of neuronal plasticity. To identify the possible action mechanisms of β-NGF gene therapy for sciatic nerve recovery, experimental dogs were random...Beta-nerve growth factor(β-NGF) is known to be a major leading cause of neuronal plasticity. To identify the possible action mechanisms of β-NGF gene therapy for sciatic nerve recovery, experimental dogs were randomly divided into control, pyridoxine, and pyridoxine + β-NGF groups. We observed chronological changes of morphology in the dorsal root ganglia in response to pyridoxine toxicity based on cresyl violet staining. The number of large neurons positive for cresyl violet was dramatically decreased after pyridoxine intoxication for 7 days in the dorsal root ganglia and the neuron number was gradually increased after pyridoxine withdrawal. In addition, we also investigated the effects of β-NGF gene therapy on neuronal plasticity in pyridoxine-induced neuropathic dogs. To accomplish this, tyrosine kinase receptor A(TrkA), βIII-tubulin and doublecortin(DCX) immunohistochemical staining was performed at 3 days after the last pyridoxine treatment. TrkA-immunoreactive neurons were dramatically decreased in the pyridoxine group compared to the control group, but strong TrkA immunoreactivity was observed in the small-sized dorsal root ganglia in this group. TrkA immunoreactivity in the dorsal root ganglia was similar between β-NGF and control groups. The numbers of βIII-tubulin-and DCX-immunoreactive cells decreased significantly in the pyridoxine group compared to the control group. However, the reduction of βIII-tubulin-and DCX-immunoreactive cells in the dorsal root ganglia in the β-NGF group was significantly ameliorated than that in the pyridoxine group. These results indicate that β-NGF gene therapy is a powerful treatment of pyridoxine-induced neuropathic damage by increasing the TrkA and DCX levels in the dorsal root ganglia. The experimental protocol was approved by the Institutional Animal Care and Use Committee(IACUC) of Seoul National University, South Korea(approval No. SNU-060623-1, SNU-091009-1) on June 23, 2006 and October 9, 2009, respectively.展开更多
目的探讨βⅢ-微管蛋白(βⅢ-tubulin,TUBB3)在反应性增生淋巴结和淋巴瘤中的表达,分析TUBB3在淋巴瘤诊断与鉴别诊断中的价值。方法采用免疫组化EnVision法检测20例反应性增生淋巴结和126例非霍奇金淋巴瘤(包括88例B细胞性淋巴瘤和38例...目的探讨βⅢ-微管蛋白(βⅢ-tubulin,TUBB3)在反应性增生淋巴结和淋巴瘤中的表达,分析TUBB3在淋巴瘤诊断与鉴别诊断中的价值。方法采用免疫组化EnVision法检测20例反应性增生淋巴结和126例非霍奇金淋巴瘤(包括88例B细胞性淋巴瘤和38例T细胞性和NK细胞性淋巴瘤)中TUBB3的表达,并复习相关文献。结果反应性增生淋巴结中,TUBB3高度局限于淋巴滤泡生发中心内。小淋巴细胞性淋巴瘤(small lymphocytic lymphoma,SLL)和结外黏膜相关性淋巴组织边缘区淋巴瘤(extranodal marginal zone lymphoma of mucosa-associated lymphoid tissue,MALToma)中,除了残留的淋巴滤泡表达TUBB3外,肿瘤细胞均不表达TUBB3。5例套细胞淋巴瘤(mantle cell lymphoma,MCL)中,1例表达TUBB3。24例低级别滤泡性淋巴瘤(follicular lymphoma,FL)中,8例表达TUBB3。39例弥漫大B细胞淋巴瘤(diffuse large B-cell lymphoma,DLBCL)中,15例表达TUBB3,TUBB3在生发中心样(germinal center B-like,GCB)型中的表达高于非生发中心样(non-germinal central B-like,non-GCB)型,但差异无统计学意义(P>0.05)。15例外周T细胞性淋巴瘤(非特指型)中,TUBB3阳性3例;15例NK/T细胞性淋巴瘤、3例间变性大细胞性淋巴瘤(anaplastic large cell lymphoma,ALCL)和5例血管免疫母细胞性T细胞性淋巴瘤(angioimmunoblastic T-cell lymphoma,AITL)均不表达TUBB3。TUBB3在DLBCL中的阳性率高于成熟性小B细胞性淋巴瘤(P<0.05)。TUBB3在B细胞性淋巴瘤中的阳性率明显高于其在NK细胞/T细胞性淋巴瘤中的阳性率(P<0.05)。结论TUBB3高度局限于反应性增生淋巴结的淋巴滤泡生发中心内,有助于低级别FL、SLL和MALToma的鉴别诊断。展开更多
基金supported by Basic Science Research Program through the National Research Foundation of Korea(NRF)funded by the Ministry of Science,ICT&Future Planning(No.NRF-2017R1A1A1A05000762)Cooperative Research Program for Agriculture Science and Technology Development,Rural Development Administration,Republic of Korea(No.PJ01395602 both to JYC)
文摘Beta-nerve growth factor(β-NGF) is known to be a major leading cause of neuronal plasticity. To identify the possible action mechanisms of β-NGF gene therapy for sciatic nerve recovery, experimental dogs were randomly divided into control, pyridoxine, and pyridoxine + β-NGF groups. We observed chronological changes of morphology in the dorsal root ganglia in response to pyridoxine toxicity based on cresyl violet staining. The number of large neurons positive for cresyl violet was dramatically decreased after pyridoxine intoxication for 7 days in the dorsal root ganglia and the neuron number was gradually increased after pyridoxine withdrawal. In addition, we also investigated the effects of β-NGF gene therapy on neuronal plasticity in pyridoxine-induced neuropathic dogs. To accomplish this, tyrosine kinase receptor A(TrkA), βIII-tubulin and doublecortin(DCX) immunohistochemical staining was performed at 3 days after the last pyridoxine treatment. TrkA-immunoreactive neurons were dramatically decreased in the pyridoxine group compared to the control group, but strong TrkA immunoreactivity was observed in the small-sized dorsal root ganglia in this group. TrkA immunoreactivity in the dorsal root ganglia was similar between β-NGF and control groups. The numbers of βIII-tubulin-and DCX-immunoreactive cells decreased significantly in the pyridoxine group compared to the control group. However, the reduction of βIII-tubulin-and DCX-immunoreactive cells in the dorsal root ganglia in the β-NGF group was significantly ameliorated than that in the pyridoxine group. These results indicate that β-NGF gene therapy is a powerful treatment of pyridoxine-induced neuropathic damage by increasing the TrkA and DCX levels in the dorsal root ganglia. The experimental protocol was approved by the Institutional Animal Care and Use Committee(IACUC) of Seoul National University, South Korea(approval No. SNU-060623-1, SNU-091009-1) on June 23, 2006 and October 9, 2009, respectively.
文摘目的探讨βⅢ-微管蛋白(βⅢ-tubulin,TUBB3)在反应性增生淋巴结和淋巴瘤中的表达,分析TUBB3在淋巴瘤诊断与鉴别诊断中的价值。方法采用免疫组化EnVision法检测20例反应性增生淋巴结和126例非霍奇金淋巴瘤(包括88例B细胞性淋巴瘤和38例T细胞性和NK细胞性淋巴瘤)中TUBB3的表达,并复习相关文献。结果反应性增生淋巴结中,TUBB3高度局限于淋巴滤泡生发中心内。小淋巴细胞性淋巴瘤(small lymphocytic lymphoma,SLL)和结外黏膜相关性淋巴组织边缘区淋巴瘤(extranodal marginal zone lymphoma of mucosa-associated lymphoid tissue,MALToma)中,除了残留的淋巴滤泡表达TUBB3外,肿瘤细胞均不表达TUBB3。5例套细胞淋巴瘤(mantle cell lymphoma,MCL)中,1例表达TUBB3。24例低级别滤泡性淋巴瘤(follicular lymphoma,FL)中,8例表达TUBB3。39例弥漫大B细胞淋巴瘤(diffuse large B-cell lymphoma,DLBCL)中,15例表达TUBB3,TUBB3在生发中心样(germinal center B-like,GCB)型中的表达高于非生发中心样(non-germinal central B-like,non-GCB)型,但差异无统计学意义(P>0.05)。15例外周T细胞性淋巴瘤(非特指型)中,TUBB3阳性3例;15例NK/T细胞性淋巴瘤、3例间变性大细胞性淋巴瘤(anaplastic large cell lymphoma,ALCL)和5例血管免疫母细胞性T细胞性淋巴瘤(angioimmunoblastic T-cell lymphoma,AITL)均不表达TUBB3。TUBB3在DLBCL中的阳性率高于成熟性小B细胞性淋巴瘤(P<0.05)。TUBB3在B细胞性淋巴瘤中的阳性率明显高于其在NK细胞/T细胞性淋巴瘤中的阳性率(P<0.05)。结论TUBB3高度局限于反应性增生淋巴结的淋巴滤泡生发中心内,有助于低级别FL、SLL和MALToma的鉴别诊断。
