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猪 Müller 细胞产生的牵拉力:人玻璃体中生长因子的刺激作用

Tractional force generation by porcine Müller cells: stimulation by growth factors in human vitreous.

作者信息

Hardwick C, Feist R, Morris R, White M, Witherspoon D, Angus R, Guidry C

机构信息

Department of Ophthalmology, Eye Foundation Hospital, University of Alabama at Birmingham, 35294, USA.

出版信息

Invest Ophthalmol Vis Sci. 1997 Sep;38(10):2053-63.

PMID:9331269
Abstract

PURPOSE

To examine the levels of Müller cell contraction-stimulating activity in human vitreous, correlate these levels with clinical presentation, and identify, the causative growth factors.

METHODS

Human vitreous was collected from patients undergoing pars plana vitrectomy (n = 84). Müller cells were isolated from porcine retina and maintained in tissue culture. Tractional forces generated by cells incubated on three-dimensional collagen gels were measured as changes in gel thickness. Contraction-stimulating activity in vitreous (VA) was calculated from the close-response profiles of gel contraction to vitreous protein. The contributions of individual growth factors to vitreous activity (n = 10) were assessed by inhibition with specific neutralizing antibodies.

RESULTS

The mean VA of patients with retinal detachment (3.65) and proliferative vitreoretinopathy stages A, B, and C (2.06) were elevated above that of patients without retinal pathology (vitreous activity = 0.23) or retinal defects alone (0.57). Mean activities in patients with epimacular proliferation (1.22) and vitreous hemorrhage (1.40) were also significantly elevated. The percentage of this activity attributable to insulin-like growth factor 1 (IGF-1) varied from 9.2% to 84.5% with a mean of 61.3%. Similarly, the percent contribution of platelet-derived growth factor (PDGF) ranged from 6.8% to 49.0% with a mean of 26.5%.

CONCLUSIONS

The vitreous of patients with retinal detachment, proliferative retinal disease, and vitreous hemorrhage contain varying amounts of growth factors that stimulate tractional force generation by Müller cells. The majority of the activity can be attributed to IGF-1 and a smaller proportion to PDGF.

摘要

目的

检测人玻璃体中 Müller 细胞收缩刺激活性水平,将这些水平与临床表现相关联,并鉴定致病生长因子。

方法

从接受玻璃体切割术的患者(n = 84)中收集人玻璃体。从猪视网膜分离 Müller 细胞并在组织培养中进行培养。测量在三维胶原凝胶上培养的细胞产生的牵拉力,以凝胶厚度变化表示。根据凝胶对玻璃体蛋白的收缩反应曲线计算玻璃体中的收缩刺激活性(VA)。通过用特异性中和抗体抑制来评估单个生长因子对玻璃体活性(n = 10)的贡献。

结果

视网膜脱离患者的平均 VA(3.65)以及增殖性玻璃体视网膜病变 A、B 和 C 期患者的平均 VA(2.06)高于无视网膜病变患者(玻璃体活性 = 0.23)或仅存在视网膜缺损患者(0.57)。黄斑前增殖患者(1.22)和玻璃体积血患者(1.40)的平均活性也显著升高。归因于胰岛素样生长因子 1(IGF-1)的该活性百分比从 9.2% 至 84.5% 不等,平均为 61.3%。同样,血小板衍生生长因子(PDGF)的贡献百分比范围为 6.8% 至 49.0%,平均为 26.5%。

结论

视网膜脱离、增殖性视网膜疾病和玻璃体积血患者的玻璃体含有不同量的生长因子,这些生长因子可刺激 Müller 细胞产生牵拉力。大部分活性可归因于 IGF-1,较小部分归因于 PDGF。

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