Retinal Pigment Epithelium and Müller Progenitor Cell Interaction Increase Müller Progenitor Cell Expression of PDGFRα and Ability to Induce Proliferative Vitreoretinopathy in a Rabbit Model.
Retinal Pigment Epithelium and Müller Progenitor Cell Interaction Increase Müller Progenitor Cell Expression of PDGFRα and Ability to Induce Proliferative Vitreoretinopathy in a Rabbit Model.
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DOI：
10.1155/2012/106486
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发表时间：
2012
影响因子：
4.3
通讯作者：
Young MJ
中科院分区：
文献类型：
--
作者：
Velez G;Weingarden AR;Tucker BA;Lei H;Kazlauskas A;Young MJ
目的.增生性玻璃体视网膜病变（PVR）是视网膜脱离的并发症，其特征在于由于膜形成和收缩导致的视网膜再脱离。多种视网膜细胞，包括视网膜色素上皮细胞（RPE）和Müller神经胶质细胞，以及生长因子可能是负责的。血小板衍生生长因子受体α（PDGFR α）在PVR膜中大量存在，是兔模型中PVR发展的内在因素。本研究探讨了PDGFR在RPE和Müller细胞共培养物中随时间的表达，以研究这两种细胞类型如何在PVR的发展中合作。我们还研究了PDGFR α表达的变化如何改变Müller细胞的致病性。方法.在跨膜共培养系统中研究了人MIO-M1 Müller祖细胞（MPC）和ARPE 19细胞。免疫细胞化学和Western blot检测PDGFR α、PDGFR β和GFAP的表达。生成表达PDGFR α（MIO-M1 α）的转染MPC系细胞系，并在兔模型中检测其诱导PVR的能力。结果与ARPE 19细胞共培养的MIO-M1 MPC中PDGFR α和PDGFR β的表达上调; GFAP的表达轻微降低。在兔模型中，MIO-M1细胞系中PDGFR α表达增加导致致病性增加和诱导PVR的能力增强。结论. Müller和RPE细胞相互作用可导致PDGFR α上调和Müller细胞致病性增加。Müller细胞可能在PVR膜的发育中发挥比以前认为的更积极的作用，特别是当受到富含RPE细胞的环境刺激时。需要对人体样本和动物模型进行进一步研究。
Purpose. Proliferative vitreoretinopathy (PVR) is a complication of retinal detachment characterized by redetachment of the retina as a result of membrane formation and contraction. A variety of retinal cells, including retinal pigment epithelial (RPE) and Müller glia, and growth factors may be responsible. Platelet-derived growth factor receptor alpha (PDGFRα) is found in large quantities in PVR membranes, and is intrinsic to the development of PVR in rabbit models. This study explores the expression of PDGFR in cocultures of RPE and Müller cells over time to examine how these two cell types may collaborate in the development of PVR. We also examine how changes in PDGFRα expression alter Müller cell pathogenicity. Methods. Human MIO-M1 Müller progenitor (MPC) and ARPE19 cells were studied in a transmembrane coculture system. Immunocytochemistry and Western blot were used to look at PDGFRα, PDGFRβ, and GFAP expression. A transfected MPC line cell line expressing the PDGFRα (MIO-M1α) was generated, and tested in a rabbit model for its ability to induce PVR. Results. The expression of PDGFRα and PDGFRβ was upregulated in MIO-M1 MPCs cocultured with ARPE19 cells; GFAP was slightly decreased. Increased expression of PDGFRα in the MIO-M1 cell line resulted in increased pathogenicity and enhanced ability to induce PVR in a rabbit model. Conclusions. Müller and RPE cell interaction can lead to upregulation of PDGFRα and increased Müller cell pathogenicity. Müller cells may play a more active role than previously thought in the development of PVR membranes, particularly when stimulated by an RPE-cell-rich environment. Additional studies of human samples and in animal models are warranted.
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影响因子：
3.4
作者：
Cui, Jing;Lei, Hetian;Samad, Arif;Basavanthappa, Sreenivasa;Maberley, David;Matsubara, Joanne;Kazauskas, Andrius
通讯作者：
Kazauskas, Andrius
影响因子：
4.1
作者：
Tian, Chunyu;Zhao, Tongtao;Yin, Zheng Qin
通讯作者：
Yin, Zheng Qin
DOI：
10.1007/bf00927264
发表时间：
1990-01-01
影响因子：
2.7
作者：
OKADA, M;MATSUMURA, M;HONDA, Y
通讯作者：
HONDA, Y
影响因子：
4.2
作者：
MACHEMER, R;AABERG, TM;MICHELS, RM
通讯作者：
MICHELS, RM
影响因子：
3.4
作者：
Johnsen, Erik O.;Froen, Rebecca C.;Moe, Morten C.
通讯作者：
Moe, Morten C.