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1. The roles of serine racemase in excitotoxicity: implication in diabetic retinopathy | |||
Haiyan Jiang,He Zhang,Shengzhou Wu | |||
Clinical Medicine 17 April 2018 | |||
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Abstract:Excitotoxicity is a pathologic process when excitatory amino acids such as glutamate kill neurons or nerve; this process is largely ascribed to over-activation of glutamate receptors including the NMDA/non-NMDA receptors. Activation of the NMDA receptor is dependent on the binding of glutamate to GluN2 subunit and of D-serine/glycine to GluN1 subunit. Excitotoxicity accounts for neurodegeneration in stroke, traumatic brain injury, neurodegenerative diseases including Alzheimer\'s disease and amyotrophic lateral sclerosis, even in diabetic retinopathy (DR). DR is characterized with retinal neurodegeneration and retinal microvascular abnormalities; a plethora of data indicate that retinal neurodegeneration precedes microvascular abnormalities. In the last decade, neurodegeneration in DR has been highlighted; inflammation and oxidation due to hyperglycemia have been connected with retinal neuronal loss. Although the underlying mechanisms remain elusive, convincing data suggest the critical role of over-activation of NMDAR underlying retinal neurodegeneration. Recent data including ours demonstrate that overexpression of serine racemase and excessive D-serine contributes to neurodegeneration in DR; SR deficiency significantly rescues this retinal neuropathy. Herein, the role of serine racemase in excitotoxicity and the contribution to retinal neurodegeneration in DR have been reviewed. | |||
TO cite this article:Haiyan Jiang,He Zhang,Shengzhou Wu. The roles of serine racemase in excitotoxicity: implication in diabetic retinopathy[OL].[17 April 2018] http://en.paper.edu.cn/en_releasepaper/content/4744636 |
2. Color Doppler Ultrasonography as a Novel Diagnosis for Cyclodialysis Cleft | |||
Li Haibo,Cai Jinhong,Huang Yanming,Wu Duanxiao,Li Jianan,Huang Yunli,Mao Chunjie,Yan Hua | |||
Clinical Medicine 26 April 2017 | |||
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Abstract:Several techniques have been described to detect cyclodialysis clefts preoperatively or intraoperatively. We developed a novel tool which presented rapid, convenient images of the cyclodialysis cleft as well as the condition of posterior segment of eyeball using the color Doppler ultrasonography. The location of the cleft was verified using high frequency ultrasound biomicroscopy. | |||
TO cite this article:Li Haibo,Cai Jinhong,Huang Yanming, et al. Color Doppler Ultrasonography as a Novel Diagnosis for Cyclodialysis Cleft[OL].[26 April 2017] http://en.paper.edu.cn/en_releasepaper/content/4730030 |
3. Aberrant levels of circulating endothelial progenitor cells in type 2 diabetes mellitus patients with or without proliferative diabetic retinopathy | |||
Zhang Jingkai,Chen Qingzhong,Zhang Wei,Mao Chunjie,Zhang Zhuhong,Huang Bo,Yan Hua | |||
Clinical Medicine 22 April 2017 | |||
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Abstract:Purpose: To investigate the number and function of circulating endothelial progenitor cells (EPC) in patients with type 2 diabetes mellitus (T2DM) with or without proliferative diabetic retinopathy (PDR). Methods: Circulating EPCs were isolated from 30 T2DM patients with PDR (60 eyes), 30 T2DM patients without PDR (60 eyes), as well as age matched control subjects (n=20). EPCs isolated from peripheral blood were quantified using flow cytometric analysis to count the number of CD34+, CD133+and VEGF R2+ cells. Following isolation, the EPCs were cultured in vitro to evaluate proliferation, adhesion and migration. Results: The number of circulating EPCs was significantly decreased in T2DM patients with and without PDR when compared with the healthy control individuals. In addition, the number of EPCs in the cultured samples from T2DM patients with and without PDR was lower compared with the control individuals. Furthermore, impaired proliferation, adhesion and migration were observed in the cultured EPCs from T2DM patients with and without PDR. Notably, increased numbers and aggravated dysfunction of EPCs were detected in T2DM patients with PDR compared with T2DM patients without PDR. In addition, a positive correlation was identified between the EPC number and PDR duration in T2DM patients with PDR.Conclusion: Reduced number and impaired function of circulating EPCs were observed in T2DM patients with or without PDR. In conclusion, EPC levels and aggravated EPC dysfunction in patients with PDR compared with patients without PDR may contribute to the pathogenesis of PDR in T2DM patients. EPC levels may be used as indicators in order to monitor PDR. | |||
TO cite this article:Zhang Jingkai,Chen Qingzhong,Zhang Wei, et al. Aberrant levels of circulating endothelial progenitor cells in type 2 diabetes mellitus patients with or without proliferative diabetic retinopathy[OL].[22 April 2017] http://en.paper.edu.cn/en_releasepaper/content/4728085 |
4. The Effects of Pleiotrophin in Proliferative Vitreoretinopathy | |||
Ding Xue,Bai Yujing,Zhu Xuemei,Li Tianqi,Jin Enzhong,Huang Lvzhen,Yu Wenzhen,Zhao Mingwei | |||
Clinical Medicine 09 December 2016 | |||
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Abstract:Purpose: The purpose of our study was to investigate the effects of pleiotrophin (PTN) in proliferative vitreoretinopathy (PVR) both in vitro and in vivo. Methods: Immunofluorescence was used to observe the PTN expression in periretinal membrane samples from PVR patients and controls. ARPE-19 cells were exposed to TGF-β1. The epithelial-to-mesenchymal transition (EMT) of the ARPE-19 cells was confirmed by observed morphological changes and the increased expression of α-SMA and fibronectin at both the mRNA and protein levels. We used specific small interfering (si)RNA to knockdown the expression of PTN. The subsequent effects of PTN inhibition were assessed regarding the EMT, migration, proliferation, cytoskeletal arrangement, TGF-β signaling, PTN signaling, integral tight junction protein expression (e.g., claudin-1 and occludin), p38 MAPK and p-p38 MAPK levels. Additionally, a PVR rat model was established by the intravitreal injection of ARPE-19 cells transfected with PTN-siRNA and evaluated accordingly. Results: PTN was highly expressed in PVR membranes compared to the controls. PTN knockdown attenuated the TGF-β1-induced migration, proliferation, cytoskeletal rearrangement, and expression of EMT markers, such as α-SMA and fibronectin, in the ARPE-19 cells, and these effects may have been mediated through p38 MAPK signaling pathway activation. PTN silencing inhibited the up-regulation of claudin-1 and occludin stimulated by TGF-β1, and PTN knockdown inhibited the proliferative aspects of severe PVR in vivo. Conclusions: PTN is involved in the process of the EMT induced by TGF-β1 in human ARPE-19 cells in vitro, and PTN knockdown attenuated the progression of experimental PVR in vivo. These findings provide new insights into the pathogenesis of PVR. | |||
TO cite this article:Ding Xue,Bai Yujing,Zhu Xuemei, et al. The Effects of Pleiotrophin in Proliferative Vitreoretinopathy[OL].[ 9 December 2016] http://en.paper.edu.cn/en_releasepaper/content/4713698 |
5. Pirfenidone inhibits migration, differentiation, and proliferation of human retinal pigment epithelial cells in vitro | |||
WANG Jing,YANG Yangfan,XU Jiangang,LIN Xianchai,WU Kaili,YU Minbin | |||
Clinical Medicine 13 June 2016 | |||
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Abstract:Purpose: To investigate the effects of pirfenidone (PFD) on the migration, differentiation, and proliferation of retinal pigment epithelial (RPE) cells and demonstrate whether the drug induces cytotoxicity. Methods: Human RPE cells (line D407) were treated with various concentrations of PFD. Cell migration was measured by scratch assay. The protein levels of fibronectin (FN), connective tissue growth factor (CTGF), α-smooth muscle actin (α-SMA), transforming growth factor beta (TGFβS), and Smads were assessed by Western blot analyses. Levels of mRNA of TGFβS, FN, and Snail1 were analyzed using reverse transcriptase-polymerase chain reaction (RT-PCR). Cell apoptosis was detected by flow cytometry using Annexin V/PI Apoptosis Kit and the percentages of cells labeled in different apoptotic stage were compared. A trypan blue assay was used to assess cell viability. Results: PFD inhibited RPE cells migration. Western blot analyses showed that PFD inhibited the expression of FN, α-SMA, CTGF, TGFβ1, TGFβ2, Smad2/3, and Smad4. Similarly, PFD also down-regulated mRNA levels of Snail1, FN, TGFβ1, TGFβ2. No significant differences were observed in cell apoptosis or viability between the control and PFD-treated groups. Conclusions: PFD inhibited RPE cell migration, differentiation, and proliferation in vitro and caused no significant cytotoxicity. | |||
TO cite this article:WANG Jing,YANG Yangfan,XU Jiangang, et al. Pirfenidone inhibits migration, differentiation, and proliferation of human retinal pigment epithelial cells in vitro[OL].[13 June 2016] http://en.paper.edu.cn/en_releasepaper/content/4692614 |
6. β-Ⅲ-Tubulin: A Reliable Marker for Retinal Ganglion Cell Labeling in Experimental Models of Glaucoma | |||
Jiang Shanming,Zeng Jihong,Li Ni,Chen Xiaoming,Wei Xin | |||
Clinical Medicine 11 May 2014 | |||
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Abstract:Purpose: To evaluate the reliability of β-III-Tubulin protein as a RGC marker in the experimental glaucoma model. Method: Glaucoma mouse models were established by injecting polystyrene microbeads into the anterior chamber of C57BL/6J mice, then their retinas were obtained 14 days and 28days after the intraocular pressure (IOP) was elevated. Retinal flat mounts and sections were double-labeled by fluorogold (FG) and β-III-Tubulin antibody or single-labeled by β-III-Tubulin antibody, then retinal ganglion cells (RGC) were counted and compared respectively. Result: IOP of the injected eyes were elevated significantly and reached the peak at 22.8±0.7 mmHg by day 14 after injection, then dropped to 11.3±0.7 mmHg by day 28. RGC numbers counted by FG labeling and β-III-Tubulin antibody labeling were 64807±4930 and 64614±5054 respectively in the control group, with no significant difference. By day 14, RGCs in the experimental group decreased significantly compared to the control group, but there was no significant difference between the FG labeling counting and the β-III-Tubulin antibody labeling counting either in the experimental group or in the control group. The result was similar by day 28, with further RGC loss. Conclusion: The β-III-Tubulin protein was not affected by IOP elevation and can be used as a reliable marker for RGC in experimental models of glaucoma.????? | |||
TO cite this article:Jiang Shanming,Zeng Jihong,Li Ni, et al. β-Ⅲ-Tubulin: A Reliable Marker for Retinal Ganglion Cell Labeling in Experimental Models of Glaucoma[OL].[11 May 2014] http://en.paper.edu.cn/en_releasepaper/content/4596882 |
7. Tetrandrine protects mouse retinal ganglion cells from ischemic injury | |||
LI Weiyi,XU Yongsheng,DANG Yalong,YU Haiyan,Wu Wentao,ZHANG Chun | |||
Clinical Medicine 26 February 2014 | |||
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Abstract:This study aimed to determine the protective effects of tetrandrine (Tet) on murine ischemia-injured retinal ganglion cells (RGCs). For this, we used serum deprivation and glutamate and hydrogen peroxide-induced RGC-5 cell death models and staurosporine-differentiated neuron-like RGC-5 in vitro. We also investigated cell survival of purified primary-cultured RGCs treated with Tet. An in vivo retinal ischemia/reperfusion model was used to examine RGC survival after Tet administration 1 day before ischemia. We found that Tet affected RGC-5 survival in a dose- and time-dependent manner. Compared to dimethyl sulfoxide treatment, Tet increased the numbers of RGC-5 cells by 30% at 72 h. After 48 h, Tet protected staurosporine-induced RGC-5 cells from serum deprivation-induced cell death and significantly increased the relative number of cells cultured with hydrogen peroxide (P < 0.01). Several concentrations of Tet significantly prevented 25-mM-glutamate-induced cell death in a dose-dependent manner. Tet also increased primary RGC survival after 72 and 96 h. Tet administration (10 μM, 2 μL) 1 day before retinal ischemia showed RGC layer (GCL) loss (greater survival), which was less than those in groups with PBS intravitreal injection + ischemia in the central (P = 0.005, n = 6), middle (P = 0.018, n = 6), and peripheral (P = 0.017, n = 6) parts of the retina, respectively. Thus, Tet conferred protective effects on serum deprivation models of staurosporine-differentiated neuron-like RGC-5 cells and primary cultured murine RGCs. Furthermore, Tet showed greater in vivo protective effects on RGCs 1 day after ischemia. Tet and CNTF maintained the mitochondrial transmembrane potential (ΔΨm) of primary cultured RGCs and inhibited the expression of activated Caspase-3 and Bcl-2 in I/R-insult retinas. | |||
TO cite this article:LI Weiyi,XU Yongsheng,DANG Yalong, et al. Tetrandrine protects mouse retinal ganglion cells from ischemic injury[OL].[26 February 2014] http://en.paper.edu.cn/en_releasepaper/content/4587640 |
8. Effect of conjunctival extracellular matrix on reconstructing conjunctival defects | |||
WEN Dan,WANG Hua,LIU Hua | |||
Clinical Medicine 13 February 2014 | |||
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Abstract:Objectives: To investigate the characteristics and effects of allogeneic conjunctiva and conjunctival extracellular matrix (ECM) as the substitute of conjunctival tissues. Methods: The bulbar conjunctivas of 6 out of 30 rabbits were prepared into a conjunctival defect model, and the remaining rabbits were randomly divided into 2 groups (n = 12). The conjunctivas of the trial group were repaired by transplanting conjunctival ECM prepared by tissue engineering technology, and the control group received fresh conjunctival allograft. Thereafter, the postoperative conjunctival reconstruction was observed. Their conjunctivas were examined by naked eye, microscope, immunohistochemical and lymphocyte toxicity tests. Results: Blood vessels of the trial group began to grow into the graft after one week, and the conjunctivas appeared almost normal without immune rejection after 8 weeks. The transplanted conjunctival epitheliums were observed to recover after 4 weeks under light microscope. A large number of invasive inflammatory cells were found in the grafts of the control group 2 weeks after surgery. Conclusion: Conjunctival ECM is an ideal substitute for conjunctiva, which can be used for the effective surface reconstruction of conjunctiva. | |||
TO cite this article:WEN Dan,WANG Hua,LIU Hua. Effect of conjunctival extracellular matrix on reconstructing conjunctival defects[OL].[13 February 2014] http://en.paper.edu.cn/en_releasepaper/content/4585382 |
9. In vivo confocal microscopic observation of lamellar corneal transplantation in the rabbit using xenogenic acellular corneal scaffolds as a substitute | |||
Feng Yun,wang wei | |||
Clinical Medicine 10 February 2014 | |||
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Abstract:Background: The limiting factor to corneal transplantation is the availability of donors. Research has suggested that xenogenic acellular corneal scaffolds (XACS) may be a possible alternative to transplantation. This study investigates the viability of performing lamellar corneal transplantation (LCT) in rabbits using canine XACS. Method: Fresh dog corneas were decellularized by serial digestion and LCT was performed on rabbit eyes using xenogeneic decellularized corneal matrix. Cellular and morphological changes were observed by slit-lamp, light, and scanning electron microscopy at 7, 30 and 90 days postoperatively. Immunocytochemical staining for specific markers such as keratin 3, vimentin and MUC5AC, was used to identify cells in the graft. Nerve regeneration was studied using gold chloride staining and HRT II in vivo microscopic studies. Results: Decellularized xenogenic corneal matrix remained transparent for about 1 month after LCT. The recipient cells were able to survive and proliferate into the grafts. Three months after transplantation, grafts had merged with host tissue, and graft epithelialization and vascularization had occurred. Corneal nerve fibers were able to grow into the graft in rabbits transplanted with XACS. Conclusion: XACS can maintain the transparency of corneal grafts about 1 month and permit growth of cells and nerve fibers, and is therefore a potential substitute or carrier for a replacement cornea. | |||
TO cite this article:Feng Yun,wang wei. In vivo confocal microscopic observation of lamellar corneal transplantation in the rabbit using xenogenic acellular corneal scaffolds as a substitute[OL].[10 February 2014] http://en.paper.edu.cn/en_releasepaper/content/4584752 |
10. Preliminary studies on tissue-engineered corneal graft using rabbit bone marrow mesenchymal stem cells and dog xenogenic decellularized corneal matrix in vitro | |||
Feng Yun,Wang Wei | |||
Clinical Medicine 10 February 2014 | |||
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Abstract:Objective. To study the growth pattern of rabbit bone marrow mesenchymal stem cells (MSCs) in vitro and to explore the growth of engineered corneal grafts constructed using rabbit bone marrow MSCs as seed cells and the dog xenogenic decellularized corneal matrix (XDCM) as the carrier. Methods. The MSCs were isolated from adult rabbit bone marrow and cultured for passages, then observed by inverted microscope and evaluated by marked BrdU monoclonal antibody. Flow cytometric analysis was used to examine the expression of CD29 and CD90. The XDCM was generated from dog corneas. Passaged MSCs with strong proliferation ability were selected and grown in XDCS to construct the tissue-engineered cornea. The growth and proliferation of the engineered corneal graft were observed using the electron microscope and confocal microscope. Immunofluorescence staining and flow cytometry were used to detect CD29, K3. Results. The rabbit MSCs showed adherent growth shortly after culturing. At. one week, colony formation was visible. Subculturing showed that the cell morphology was mostly consistent with scaffolding with fusiform appearance, arranged in parallel or concentric growth patterns. The proliferation ability of the MSCs was strong before 5 passages. On the 7th day, most MSC nuclei showed positive expression by marked BrdU monoclonal antibody. The flow-cytometry detection indicated that the markers of CD29 and CD90 showed positive expression. MSCs showed adherent growth on the first day of tissue-engineered corneal graft being constructed. The distribution was not uniform in XDCM. Scanning electron microscopy (SEM) showed many more hypertrophic cells, with a rough surface with visible prominences and a large number of villi-like structures. Frozen section showed positive staining of CD29 and K3, but negative staining of MUC5AC. Confocal microscopy found that part of CD29 was positively stained, and part of cell corneal epithelial marker K3 was positively stained when MSCs had been planted into XDCM for 14 days. Conclusion. A high purity of MSCs can be obtained by using Percoll cell isolation medium and cell adherent method in vitro. MSCs had strong proliferation ability at about the 7th day before 5 passages. At this time, MSCs should be chosen and implanted into XDCM. When MSCs had been planted into XDCM for 14 days, MSCs expressed partially corneal epithelial cell surface markers. This indicates that 14 days is likely the best time to transplant engineered corneal graft contributed by rabbit MSCs and dog XDCM. | |||
TO cite this article:Feng Yun,Wang Wei. Preliminary studies on tissue-engineered corneal graft using rabbit bone marrow mesenchymal stem cells and dog xenogenic decellularized corneal matrix in vitro[OL].[10 February 2014] http://en.paper.edu.cn/en_releasepaper/content/4584929 |
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