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作 者:张彬[1] 陶谦[2] 黄洪章[1] 潘朝斌[1] 刘习强[1]
机构地区:[1]广州中山大学附属第二医院口腔颌面外科,510120 [2]中山大学光华口腔医学院口腔颌面外科
出 处:《实用口腔医学杂志》2006年第2期186-190,共5页Journal of Practical Stomatology
基 金:广东省自然科学基金资助项目(04300240);国家自然科学基金资助项目(30471896)
摘 要:目的探讨基质金属蛋白酶和Ⅳ型胶原与成釉细胞瘤复发、侵袭的关系。方法采用免疫组织化学LABC方法检测28例成釉细胞瘤组织中MMP-2、TIMP-2和Ⅳ型胶原的表达,并用RT-PCR方法检测MMP-2、TIMP-2和MT1-MMP在20例成釉细胞瘤的表达。结果MMP-2、TIMP-2和Ⅳ型胶原蛋白在成釉细胞瘤的阳性表达率分别为92.9%、75.0%和42.9%,Ⅳ型胶原阳性着色部位均位于基底膜及部分肿瘤细胞的胞质,MMP-2和TIMP-2阳性着色部位均位于细胞质,分布于瘤组织各层;复发性成釉细胞瘤Ⅳ型胶原的阳性表达率明显低于原发性成釉细胞瘤(P<0.01)。MMP-2、MT1-MMP、TIMP-2的mRNA在成釉细胞瘤组织中均有表达,复发性成釉细胞瘤的TIMP-2、MT1-MMP相对含量均显著高于原发性成釉细胞瘤(P<0.01)。结论基质金属蛋白酶MT1-MMP表达增加和Ⅳ型胶原在基底膜表达缺失与成釉细胞瘤的复发密切相关,MMP-2活性增加和基底膜Ⅳ型胶原降解增多可能是成釉细胞瘤局部侵袭的机制之一。Objective:To investigate the relationship between matrix metalloproteinase and collagen Ⅳexpression and ameloblastoma invasion and recurrence. Methods:Immunohistochemical LABC method was used in detecting the expression of matrix metalloproteinase -2 ( MMP-2 ), tissue inhibitor of metalloproteinase-2 ( TIMP-2 ) and collagen Ⅳ in 28 cases of ameloblastoma. Expression of MMP-2, TIMP-2 and membrane type 1-matrix metalloproteinase (MT1-MMP) in 20 cases of ameloblastoma was examined by RT-PCR. Results:The total positive expression rate of MMP-2, TIMP-2 and collagen Ⅳ in ameloblastoma was 92.9%, 75.0% and 42.9%, respectively. The positive ex- pression of collagen Ⅳ was mainly located in the basement membrane and the cytoplasm of some cells. The staining of MMP-2 and TIMP-2 was mainly located in the cytoplasm of all layers of the tumor. The positive expression rate of collagen Ⅳ in basement membrane of recurrent ameloblastoma was significantly lower than that of the primary( P 〈 0.01 ). All investigated cases expressed mRNA of MMP-2, MT1-MMP and TIMP-2. The mRNA levels of TIMP-2 and MT1-MMP in recurrent ameloblastoma were significantly higher than those in primary ameloblastoma respectively ( P 〈0.01 ). Conclusion: Increased expression of MT1-MMP and absent expression of collagen Ⅳ in basement membrane may be associated with the recurrent potentiality of ameloblastoma, and the augment in MMP-2 activity and degradation of collagen Ⅳ may be a reason of ameloblastoma invasion.
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