Muller cell production of insulin-like growth factor-binding proteins in vitro: modulation with phenotype and growth factor stimulation.
Muller cell production of insulin-like growth factor-binding proteins in vitro: modulation with phenotype and growth factor stimulation.
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Muller 细胞在体外产生胰岛素样生长因子结合蛋白：通过表型和生长因子刺激进行调节。
DOI：
10.1167/iovs.04-0447
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发表时间：
2004
影响因子：
4.4
通讯作者：
Guidry,Clyde
中科院分区：
文献类型：
--
作者：
King,JefferyL;Guidry,Clyde
目的。Müler细胞存在于糖尿病纤维收缩眼组织中，并对胰岛素样生长因子产生牵引力。最近的研究表明，糖尿病患者玻璃体中胰岛素样生长因子活性的增加部分是由于胰岛素样生长因子结合蛋白(IGFBPs)的变化。本研究的目的是评估Müler细胞作为IGFBPs的来源，并表征与已知存在于糖尿病玻璃体中的细胞表型和生长因子刺激相关的变化。从正常猪视网膜分离的Müler细胞在培养1周和5周后，产生了被描述为增殖性和肌成纤维细胞的表型。用反转录聚合酶链式反应和Northern印迹杂交分析了猪肝、视网膜和Müler细胞培养物中的核糖核酸。Mü培养上清液和洗涤剂提取蛋白的Western配体和Western印迹分析证实了IGFBP的产生。对正常视网膜、增殖和肌纤维母细胞的Müler细胞的分子生物学分析没有检测到IGFBP-1的消息，但发现IGFBP-2、-3、-4和-6的消息丰度逐渐增加。IGFBP-5在所有样本中均可检测到，但在肌成纤维细胞Müler细胞中含量最低。胰岛素样生长因子-I和胰岛素样生长因子II刺激肌成纤维细胞Müler细胞，但不刺激血小板衍生生长因子，进一步增加胰岛素样生长因子结合蛋白-2、-4、-5和-6的信息丰度和产生，但不增加胰岛素样生长因子结合蛋白-3。Müler细胞产生的IGFBPs随表型而变化，在大多数情况下，在最有可能参与纤维收缩视网膜疾病的细胞中，IGFBPs的产量最高。IGF-I和IGF-II进一步增加了这些细胞的IGFBP的产生，这两种生长因子在增殖性玻璃体视网膜病变中存在并活跃，这表明Müler细胞在涉及该细胞类型的疾病中是玻璃体IGFBP的潜在来源。
purpose. Müller cells are present in diabetic fibrocontractive ocular tissues and generate tractional forces in response to insulin-like growth factors. Recent studies indicate that diabetes-associated increases in vitreous insulin-like growth factor activity are, in part, attributable to changes in insulin-like growth factor binding proteins (IGFBPs). The objectives of this study were to evaluate Müller cells as a source of IGFBPs and characterize changes associated with cell phenotype and growth factor stimuli known to be present in diabetic vitreous.methods. Müller cells isolated from normal porcine retina were maintained in culture for 1 and 5 weeks, yielding phenotypes described as proliferative and myofibroblastic. RNA preparations from porcine liver, retina, and Müller cell cultures were evaluated by RT-PCR and Northern blot analysis. IGFBP production was verified by Western ligand and Western blot analysis of Müller-cell–conditioned media and detergent-extracted proteins.results. Molecular biological analyses of RNA from normal retina and from proliferative and myofibroblastic Müller cells did not detect message for IGFBP-1, but revealed progressive increases in message abundance for IGFBP-2,-3,-4, and-6. IGFBP-5 message was detected in all samples, but was least abundant in myofibroblastic Müller cells. Stimulation of myofibroblastic Müller cells by IGF-I and-II, but not PDGF, further increased message abundance and production of IGFBP-2,-4,-5, and-6, but not IGFBP-3.conclusions. Müller cell production of IGFBPs changes with phenotype and, in most cases, is highest in the cells most likely to participate in fibrocontractive retinal disease. IGFBP production by these cells is further increased by IGF-I and-II, growth factors known to be present and active in proliferative vitreoretinal disorders, suggesting that Müller cells represent a potential source of vitreous IGFBPs in disorders involving this cell type.
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影响因子：
14.9
作者：
Patterson,TA;Dean,M
通讯作者：
Dean,M
DOI：
10.1073/pnas.75.5.2458
发表时间：
1978-01-01
影响因子：
11.1
作者：
COLLINS, SJ;RUSCETTI, FW;GALLO, RC
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DOI：
--
发表时间：
1984
期刊：
影响因子：
--
作者：
Ruddle Fh
通讯作者：
Ruddle Fh
DOI：
10.1073/pnas.84.22.8006
发表时间：
1987-11-01
影响因子：
11.1
作者：
BARKER, D;GREEN, P;DONISKELLER, H
通讯作者：
DONISKELLER, H
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DOI：
10.1126/science.2544027
发表时间：
1989
期刊：
Science (New York, N.Y.)
影响因子：
--
作者：
Brownstein,BH;Silverman,GA;Little,RD;Burke,DT;Korsmeyer,SJ;Schlessinger,D;Olson,MV
通讯作者：
Olson,MV