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作 者:李真珍[1] 文建国[1] 张红[1] 张国贤[1] 王焱[1] 王庆伟[1]
机构地区:[1]郑州大学第一附属医院小儿外科尿动力学中心河南省高等学校临床医学重点学科开放实验室,河南郑州450052
出 处:《临床儿科杂志》2009年第4期337-341,共5页Journal of Clinical Pediatrics
基 金:国家自然科学基金(No.30571931);河南省高校杰出科研人才创新工程(No.2001KYCX004);河南省杰出青年科学基金(No.02120001100);河南省医学科技攻关资助项目(No.20081002);郑州市技术研究与开发经费支付项目(No.074SGHH32262)
摘 要:目的探讨小儿先天性积水肾脏(hydronephrotic kidney,HnK)不同病理改变水通道蛋白(aquaporins,AQPs)1~4及其mRNA的表达情况。方法收集26例接受肾盂成形术和肾造瘘术的肾盂输尿管连接部狡窄(PUJO)患儿的肾组织标本,按其病理学变化程度分为轻度肾积水组(12例,病理学分级Ⅱ-Ⅲ级)和重度肾积水组(14例,病理学分级Ⅳ-Ⅴ级)2组。10例正常肾脏组织标本来自于肾母细胞瘤周围正常肾组织。免疫组织化学技术检测AQP1~4在正常肾脏和积水肾脏中的表达与定位,逆转录-聚合酶链反应(RT-PCR)检测AQP1~4 mRNA在正常肾脏和积水肾脏中的表达水平。结果免疫组化显示先天性积水肾脏中AQP1~4表达强度弱于正常对照组肾脏;半定量RT-PCR显示重度肾积水中AQP1~4的相对表达量显著低于轻度肾积水和正常肾组织(P均<0.01)。结论小儿先天性积水肾脏中AQP1~4蛋白及其mRNA水平的表达均下调,且随积水肾脏病理改变程度而变化。AQP1~4表达水平的变化可能在先天性肾积水的病理发展过程中发挥一定作用。Objective To investigate the expression of aquaporin-1, -2, -3 and -4 (AQP1-4) in children with the different degree of pathology of congenital hydronephrotic kidneys (HnK) due to pelviureteral junction obstruction (PUJO). Methods Twenty-six hydronephrotic kidney samples were collected during the surgery of pyeloplasty and nephrostomy and divided into two groups according to histopathologic changes, mild HnK group (n = 12, including grades Ⅱ-Ⅲ) and severe HnK group (n = 14, grades Ⅳ-Ⅴ). Ten normal kidney samples were collected from normal part of kidney with Wilm's tumor. The expressions and localizations of AQP1-4 were determined by immunohistochemistry in the kidneys. The expression levels of AQPI-4 mRNA were determined by semi-quantitative reverse transcription-polymerase chain reaction (RT-PCR). The PCR products were cloned and sequenced. Results In HnK, the abundance of AQP1-4 labeling was gradually decreased according to the degree of hydronephrosis. The expression of AQPI-4 mRNA was significantly decreased in the severe HnK group compared with the mild HnK group and normal group (P 〈 0.01 ). Conclusions The expression of AQP1-4 is down-regulated in children with HnK at the mRNA and protein level, which depend on the degree of hydronephrosis. These changes in AQP1-4 expression may play a role in pathogenesis in children with congenital HnK.
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