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Animal Model for Central Serous Chorioretinopathy?
Author Response: Animal Model for Central Serous Chorioretinopathy?
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Jean-Claude Quintyn
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qjc76{at}hotmail.com Jean-Claude Quintyn
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We read with interest the article by Hui-Jin Chen and Zhi-Zhong Ma.1 They report that N-cadherin expression is increased in the retinal pigment epithelium in a rat model of retinal detachment (RD) and reattachment. We think this paper is interesting, but needs further clarification of the model. The authors specify that the RD is created by trans-scleral injection of 1.4% sodium hyaluronate into the subretinal space without producing retinal breaks. The experimental model is original and attractive. Can the authors specify the number of animals which were excluded because of intraocular hemorrhage? However, this model is much more similar to central serous chorioretinopathy than to RD. In central serous chorioretinopathy, the retinal pigment epithelium is altered,2 and the adhesion molecules could play an essential role in this pathology.3 Also, this model is not a model of proliferative vitreoretinopathy (PVR). Generally, cells are injected into the vitreous cavity to induce PVR.4 Although long duration of an RD is a clinical risk factor for PVR, it presumably does not alone produce PVR.5 This paper is very interesting, but it appears to us to be of greatest value in the understanding of the pathogenesis and in the treatment of central serous chorioretinopathy. Marie-Laure Ranty1 and Jean-Claude Quintyn2 1Department of Pathology, 2Department of Ophthalmology, C.H.U. Rangueil, Toulouse, France References 1. Chen HJ, Ma ZZ. N-cadherin expression in a rat model of retinal detachment and reattachment. Invest Ophthalmol Vis Sci. 2007;48:1832-1838. |
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Zhi-Zhong Ma
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puh3_yk{at}bjmu.edu.cn Zhi-Zhong Ma
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We thank Drs. Quintyn and Ranty for their interest in our article.1 There are several points made in the letter we would like to address. 1. We'd like to point out the distinction between the animal model in our experiment and the clinical condition named "central serous chorioretinopathy (CSC)." Although the complete pathogenesis of CSC remains unclear, it is generally accepted that the disruption of the pigment epithelial barrier and choroidal vascular hyperpermeability results in abnormal fluid movement and accumulation in the subretinal space and sub-RPE space.2,3 However, in our model, we made the separation between the neuroretina and the RPE first, and then observed the elevation of N-cadherin expression in RPE cells. In this model, the alteration of the adhesion molecules in RPE cells was the consequence of rather than the reason for retinal detachment (RD). Moreover, the decreased size of the detached retina with time in some degree indicated the function of the RPE pump was normal in this model. 2. We'd like to describe the procedure of our animal model creation more specifically. The conjunctiva was first penetrated with the needle from the nasal side until the needle tip could reach the equator of the sclera. When doing this, a slide was placed on the cornea by an assistant which allowed visualization of the fundus. A mound was seen created by the tip of the needle. The location of the needle tip was adjusted to find a good place to penetrate the globe. Once the tip of the needle was seen coming out of the choroid, the angle of the needle was changed (Fig. 1, from 1 to 2) to make sure the slope of the needle tip was parallel with the curve of the globe and the needle tip was advancing between the neuroretina and
the RPE. When part of the opening in the needle tip was located in the subretinal space, some viscoelastic was injected to enlarge the space and further advance the needle safely, and more viscoelastic was injected to create a RD without retinal breaks. The needle can't be too sharp, as it will easily penetrate the retina at the same time, and the needle can't be too blunt, as it will have difficulty penetrating the sclera and choroid. This is a relatively simple procedure with high success rate. There is no need to perform conjunctiva opening, sclerotomy, and choroid diathermy like what we are supposed to do for subretinal fluid drainage during the scleral buckling surgery. Our impression is that the choroid of the SD rat is much less susceptible to bleeding than the choroid of human being. In our experiment, only 1/10 of the animal developed choroidal hemorrhage and was excluded. However, it takes time to practice. The key point of the procedure is adjusting the angle of the needle and the force of the hand constantly. 3. We agree with your idea that RD alone does not inevitably induce proliferative vitreoretinopathy (PVR). PVR occurs when the proliferative factors overwhelm the anti-proliferative factors and the balance of growth is destroyed. However, we're fully convinced that RD is the initiating factor in the pathway.4 All subsequent events, including growth factor production, cell proliferation and migration, membrane formation and contraction are the results of RD. If the retina is successfully reattached, the cascade of PVR is interrupted. If RD is not treated and persists, PVR is just a matter of time. Based on this causal relationship between RD and PVR, it is advisable to investigate PVR from its very beginning, RD. Although the PVR model producing by intravitreal injection of fibroblasts has long been a popular procedure, there is limitation in this model. We have stated in our article that this model is not suitable for investigation of the molecular events in the early phase of PVR since it directly introduces the cell to the vitreous cavity and therefore surpasses the stage of cell proliferation and migration that is exactly what we want to observe. In the current study, we focused our interest on why chronic RD results in cell migration and finally leads to PVR and what are the molecular alterations that underlie this process. Therefore, we used a model of RD rather than the conventional PVR model. The dramatic difference of N-cadherin expression in response to RD and reattachment and the possible role it might play in RPE cell migration demonstrated N-cadherin is one of these molecules that drive the process from RD to PVR. Hui-Jin Chen and Zhi-Zhong Ma Peking University Third Hospital, Peking University Eye Center, Beijing, China References 1. Chen HJ, Ma ZZ. N-cadherin expression in a rat model of retinal detachment and reattachment. Invest Ophthalmol Vis Sci. 2007;48:1832-1838.
2. Ciardella AP, Guyer DR, Spitznas M, Yannuzzi LA. Central serous chorioretinopathy. In: Ryan SJ, ed. Retina. Vol 2. St. Louis, MO: Mosby; 2001:1153-1181. |
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