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Xun Xu

Publications and source records attributed to Xun Xu.

At least 37 records · Page 2Linked to original sources

Purification, characterization and cDNA cloning of a novel lipopolysaccharide-binding lectin from the shrimp Penaeus monodon.

In invertebrates, C-type lectin plays an important role in innate immunity by mediating the recognition of pathogens to host cells and clearing microinvaders. A few C-type lectins have been identified from shrimps, but none of their gene or protein sequences is known to date. In this paper, a C-type lectin (named PmLec) specific for bacterial lipopolysaccharide was purified from the serum of the shrimp Penaeus monodon. The binding of PmLec to lipopolysaccharide was mainly mediated through the O-antigen. PmLec had a strong hemagglutinating and bacterial-agglutinating activity as well as an opsonic effect that enhances hemocyte phagocytosis. The PmLec cDNA sequence was obtained from the cDNA library of P. monodon by polymerase chain reaction with the degenerated primer designed according to the amino-terminal residue sequence of purified PmLec. A 546-bp open reading frame was found to encode a putative protein comprising 182 amino acids and containing a preceding signal peptide of 17 amino acids. A C-type lectin domain existed in PmLec, but no glycosylation site was found. The recombinant PmLec protein expressed in Escherichia coli also showed the same agglutinating activity and opsonic effect as that of the native protein. This is the first report of a lectin cDNA from the shrimp. PmLec functions as a pattern-recognition protein and an opsonin in the shrimp, and it provides a clue to elucidate the role of lectin in the innate immunity of aquatic invertebrates at the molecular level.

Animals↗

LEF1 is a critical epithelial survival factor during tooth morphogenesis.

LEF1 is a cell-type-specific transcription factor and mediates Wnt signaling pathway by association with its co-activator beta-catenin. Wnt signaling is known to be critical for the specification of cranial neural crest (CNC) cells and may regulate the fate diversity of the CNC during craniofacial morphogenesis. Loss of Lef1 results in arrested tooth development at the late bud stage and LEF1 is required for a relay of a Wnt signaling to a cascade of FGF signaling activities to mediate the epithelial-mesenchymal interaction during tooth morphogenesis. It remains unclear, however, what is the cellular mechanism of LEF1 signaling in regulating tooth morphogenesis. To test the hypothesis that LEF1 signaling regulates the fate of the dental epithelial and the CNC-derived mesenchymal cells during tooth morphogenesis, we investigated and compared the cellular migration, proliferation, and apoptotic activity within the tooth germ between the wild-type and Lef1 null mutant mice. Using the Wnt1-Cre/R26R transgenic system for indelibly marking the progenies of CNC cells, we show that there is no CNC migration defect in the Lef1 null mutant mice, indicating that the arrest in tooth development is not the result of shortage of the CNC contribution into the first branchial arch in the Lef1 mutant. Furthermore, there is no alteration in cell proliferation or condensation of the CNC-derived dental mesenchyme in the Lef1 null mutant, suggesting that LEF1 may not affect the cell cycle progression of the multipotential CNC cells during tooth morphogenesis. Importantly, apoptotic activity is significantly increased within the dental epithelium in the Lef1 null mutant mice. As the result of this increased cell death, the bud stage tooth germ fails to advance to the cap stage in the absence of Lef1. Inhibition of apoptotic activity by FGF4 rescues the tooth development in the Lef1 null mutant. Our studies suggest that LEF1 is a critical survival factor for the dental epithelial cells during tooth morphogenesis.

Animals↗

PDGFR-alpha signaling is critical for tooth cusp and palate morphogenesis.

Platelet-derived growth factor receptor alpha (PDGFR-alpha) and PDGF ligands are key regulators for embryonic development. Although Pdgfralpha is spatially expressed in the cranial neural crest (CNC)-derived odontogenic mesenchyme, mice deficient for Pdgfralpha are embryonic lethal, making it impossible to investigate the functional significance of PDGF signaling in regulating the fate of CNC cells during tooth morphogenesis. Taking advantage of the kidney capsule assay, we investigated the biological function of PDGF signaling in regulating tooth morphogenesis. Pdgfralpha and Pdgfa are specifically and consistently expressed in the CNC-derived odontogenic mesenchyme and the dental epithelium, respectively, throughout all stages of tooth development, suggesting a paracrine function of PDGF signaling in regulating tooth morphogenesis. Highly concentrated expression patterns of Pdgfralpha and Pdgfa are associated with the developing dental cusp, suggesting possible functional importance of PDGF signaling in regulating cusp formation. Loss of the Pdgfralpha gene does not affect proper odontoblasts proliferation and differentiation in the CNC-derived odontogenic mesenchyme but perturbs the formation of extracellular matrix and the organization of odontoblast cells at the forming cusp area, resulting in dental cusp growth defect. Pdgfralpha-/- mice have complete cleft palate. We show that the cleft palate in Pdgfralpha mutant mice results from an extracellular matrix defect within the CNC-derived palatal mesenchyme. The midline epithelium of the mutant palatal shelf remains functionally competent to mediate palatal fusion once the palatal shelves are placed in close contact in vitro. Collectively, our data suggests that PDGFRalpha and PDGFA are critical regulators for the continued epithelial-mesenchymal interaction during tooth and palate morphogenesis. Disruption of PDGFRalpha signaling disturbs the growth of dental cusp and interferes with the critical extension of palatal shelf during craniofacial development.

Animals↗

Differential profile of genes expressed in hemocytes of White Spot Syndrome Virus-resistant shrimp (Penaeus japonicus) by combining suppression subtractive hybridization and differential hybridization.

White Spot Syndrome Virus (WSSV) is the major viral pathogen of culture shrimp. Although remarkable progress has been made in characterizing the WSSV genome, information concerning the antiviral process of host is still limited. To identify the genes differentially expressed along with their expression profile in the hemocytes of the virus-resistant shrimp, suppression subtractive hybridization (SSH) and differential hybridization (DH) were employed. Relying on the sequences identified in the subtractive cDNA library, 30 genes were characterized to be involved in the antiviral process as defense-relevant, among them, 22 are found for the first time in penaeid shrimp. The most interesting finding is that the interferon-like protein (IntlP) and (2'-5') oligo(A) synthetase-like protein (data not shown) known as the antiviral factors showed increased expression in virus-resistant shrimp and the non-specific antiviral activity of IntlP protein was verified by cytotoxicity experiment. A number of proteins with certain similarities to the components of the complement and cytokines system in vertebrates were also found in the subtracted library. The high expression of redox-related factors (NADH dehydrogenase, glutathione peroxidase and transcription factor AP-1 precursor), plasma defensive protein (C-type lectin and laminin-like protein) and translationally controlled tumor protein (TCTP) in the virus-resistant shrimp suggested that they are essential components participating in the antiviral process. Our work provides a wide array of genes differentially expressed in the virus-resistant shrimp, and a framework for further studies aimed at antiviral mechanism in shrimp.

Animals↗

Differential gene expression profile in hepatopancreas of WSSV-resistant shrimp (Penaeus japonicus) by suppression subtractive hybridization.

In order to find the immune-relevant factors responsible for the virus resistance in the WSSV-resistant shrimp, a suppression subtractive hybridization method was employed to identify differentially expressed genes and their expression profile in the hepatopancreas of the virus-resistant penaeid shrimp. Thirty five genes were identified from more than 400 clones, of which eight are found for the first time in penaeid shrimp. betaGBP is the most abundant gene in our subtractive library except hemocyanin. Lectin, ferritin, oxygenase and chitinase of the virus-resistant shrimp all showed up-regulation in expression compared with those of normal shrimp. In addition, Ranbp, Rho and Rab were found in the subtractive library. This is the first evidence indicating that small GTPases are involved in the signal transduction in shrimp defense response. Furthermore, a number of genes encoding apoptotic-related proteins and antioxidant enzymes were expressed at a higher level in the virus-resistant shrimp. In short, the high expression of immuno-related genes in response to the virus infection and the involvement of small GTPases in the antiviral response provide a new insight for further study in the crustacean innate immunity.

Amino Acid Sequence↗

Role of protein kinase C on the alteration of retinal endothelin-1 in streptozotocin-induced diabetic rats.

Activation of protein kinase C (PKC) has been implicated in the pathogenesis of diabetic retinopathy. The purpose of this study was to investigate the role of PKC on the alteration of retinal endothelin-1 in 2-week streptozotocin (STZ)-induced diabetic rats. The measurement of retinal PKC activities from membranous and cytosolic fractions was conducted by ELISA. Retinal tissues were analysed for the expression of endothelin-1 (ET-1), endothelin-3 (ET-3), endothelin-A (ET-A), and endothelin-B (ET-B) mRNA by means of semi-quantitative RT-PCR. Retinal vasculature isolated by trypsin digest technique was immunostained for ET-1. We followed the alteration of retinal ET-1 after intravitreal injection of a general PKC inhibitor, GF109203X, in 2-week diabetic rats. Retinal PKC specific activities were significantly increased by 37% (P=0.027) in the membranous fraction in diabetic rats compared with normal rats, whereas PKC specific activities in the cytosolic fraction were unchanged. The retina from the diabetic rats showed increased ET-1 mRNA expression after 2 weeks, while no changes were found for ET-3, ET-A and ET-B. ET-1 immunoreactivity was also increased in the retinal vasculature of diabetic rats. Retinal ET-1 expression was decreased after intravitreal injection of GF109203X (10(-5), 10(-6), 10(-7) M) in a dose-dependent manner. The results from this study showed that the enhanced ET-1 expression associated with the activation of PKC has occurred in early diabetes, and PKC inhibitor could reverse the up regulation of ET-1.

Animals↗

PVD following plasmin but not hyaluronidase: implications for combination pharmacologic vitreolysis therapy.

PURPOSE: To study whether intravitreal injection of plasmin + hyaluronidase safely induces posterior vitreous detachment (PVD). METHODS: Rabbits were randomized into three groups: (A) 20 rabbits, intravitreal injection of plasmin 1 U + hyaluronidase 20 U in balanced salt solution (BSS) 0.1 mL into one eye; (B) 12 rabbits, plasmin alone; (C) 12 rabbits, hyaluronidase alone. The fellow eye of each rabbit was injected BSS 0.1 mL. In Group A, scanning electron microscopy (SEM) was done in four rabbits at 0.5 hour and in four rabbits at 1 hour. After 7 days, all the remaining 36 rabbits received electroretinography, SEM was examined in eight of each group, and immunohistochemistry was done in four of each group. RESULTS: SEM disclosed the eyes of Group A had complete PVD (8/8), Group B partial PVD (7/8), and Group C (8/8) and all the control eyes (24/24) no PVD after 7 days. Partial PVD was found in 4/4 at 0.5 hour and complete PVD was seen in 3/4 at 1 hour in Group A. Immunohistochemistry showed that the amounts of laminin and fibronectin in the vitreoretinal interface were decreased in Group A and B versus the control eyes (P <0.001), but not in Group C versus the control eyes (P >0.05). Electroretinography showed no changes in any group (P >0.05). CONCLUSION: Vitreous injection of plasmin + hyaluronidase induced complete PVD with no obvious toxicity. Plasmin induced partial PVD, but hyaluronidase had no effects.

Animals↗

[Prevalence study of age-related macular degeneration in Caojiadu blocks, Shanghai].

OBJECTIVE: To investigate the prevalence of age-related maculopathy (AMD) in Shanghai residents older than 50 years. METHODS: 1023 individuals were examined in the years 2002 and 2003 for clinical and subjective signs of dry and exudative AMD. A interview concerning clinical symptoms of AMD as also a complete eye exam was performed. Non-mydriatic retinoscopy was done by use of a direct opthalmoscopy. Fundus photography was used to confirm and document the diagnosis. The diagnosis of both forms of AMD was made according to the criteria of the Sub-society of Fundus Disease, Chinese Ophthalmological Society. RESULTS: 15.5% of the included population had AMD and 19 of them were exudative AMD. The prevalences of AMD in the age groups of 50-59, 60-69, 70-79 and more than 80 were identified as 5.7%, 13.5%, 20.2% and 23.5%, respectively (chi(2) = 27.97, P < 0.01). No statistical differences were found concerning atrophic and exudative AMD related to gender, education, daily focus time, smoking, alcohol consumption and systematic diseases. In the AMD patients, 5.1% and 36.2% of the eyes were identified as blind or with low vision. In exudative AMD patients, 23.3% and 63.3% of the eyes were identified as blind or with low vision. The visual acuity of eyes with exudative AMD was significantly lower than the visual acuity of atrophic AMD eyes. (chi(2) = 15.4, P < 0.01). CONCLUSIONS: The prevalence of AMD is high, and increasing with aging. The AMD, especially the exudative AMD, leads to severe visual impairment.

Age Factors↗

[Actuality and challenge of the clinical basic researches related to ocular fundus diseases].

The visual loss caused by fundus diseases such as age related macular degeneration and inherited retinal diseases is one of the toughest subjects in preventing blindness. The level of basic researches determines the progress of diagnosis and treatment for them. Although some fruits have been got these years in the fields of stem cell identification, transplantation and differentiation, local environment of survival cells and replacement of retinal pigment epithelium by iris pigment epithelium, many questions still remain to be elucidated about the regulation of gene expression and developmental environment. These answers will benefit the development of novel therapeutic approaches for refractory fundus dysfunctions finally.

Humans↗

[The effect of freezing and low molecular weight heparin treatment on the production of hepatocyte growth factor of human RPE cells].

OBJECTIVE: This study is to investigate the human hepatocyte growth factor (HGF) level and proliferation of cultured human retinal pigment epithelial cells (RPE), treated with freezing, or Tedelparin (low molecular weight heparin), or both. METHOD: Cultured human RPE cells were placed at -80 degrees C freezer for 15 and 60 seconds respectively. One group of freezing-treated cells was kept in culture for another 3 d or 6 d, with or without Tedelparin (25 microl/ml). Another group of freezing-treated cells was injected into the vitreous of rabbits immediately, and 3 d or 6 d later the vitreous of injected rabbits were harvested and put into the medium of cultured human RPE cells, with or without Tedelparin (25 microl/ml). The level of HGF in culture medium and vitreous was measured by ELISA, and the cell proliferation was examined by MTT assay. RESULTS: The HGF concentration was increased on day 3 in culture medium of freezing-treated human RPE cells (F = 27.36, P < 0.01), and in the rabbit vitreous injected with freezing-treated human RPE cells (F = 6.24, P < 0.01). Tedelparin can reduce the HGF concentration in culture medium of freezing-treated human RPE cells at day 3 and 6 (F = 179.50, P < 0.01). The rabbit vitreous injected with freezing-treated RPE cells can promote the proliferation of normal RPE cells (P < 0.01), which was suppressed by 48 h treatment of Tedelparin (F = 44.90, P < 0.05). CONCLUSION: Freezing may increase the expression of HGF, or promote the proliferation of RPE cells. Tedelparin may suppress the proliferation of RPE cells by inhibiting HGF production.

Animals↗

[Development and evaluation of psychometric tests of the Chinese-version of low vision quality of life questionnaire].

OBJECTIVE: To develop and evaluate a Chinese language vision health related quality-of-life (VRQoL) questionnaire. METHODS: The low vision quality of life questionnaire (LVQOL) was translated and adapted into the Chinese-version low vision quality of life questionnaire (CLVQOL). The systematic protocols were set as 3 forward translations, 2 committee reviews and 1 back-ward translation. The CLVQOL was performed in 100 randomly selected people with low vision (primary group) and 100 people with normal vision (control group). Ninety-four participants from the primary group completed the CLVQOL and repeated 2 weeks later (test-retest group). The results were compared with patient demographics and the internal consistency reliability, test-retest reliability, item-internal consistency, item-discrimination validity, construct validity and discrimination validity of the CLVQOL were calculated. RESULTS: The review committee agreed that the CLVQOL replicated the meaning of the LVQOL and was sensitive to cultural adaptations. The Cronbach alpha coefficient and the split-half coefficient for the four scales and total CLVQOL scales were 0.75 to 0.97. The test-retest reliability as estimated by intraclass correlation coefficient was 0.69 to 0.95. Item-internal consistency was > 0.4 and item-discrimination validity was generally < 0.40. The varimax rotation factor analysis of the CLVQOL identified four principal factors. All of the scores of four subscales and the total score of CLVQOL of the primary group were lower than those of the control group, both in patients and local residents. CLVQOL scores were highly correlated with visual acuity. CONCLUSIONS: The CLVQOL is a culturally specific VRQOL measure instrument. CLVQOL can satisfy conventional psychometric criteria, can discriminate visually healthy populations from low vision patients and is valuable in the clinical practice and in the screening of the community populations.

Adult↗

Identification of genes involved in the response of haemocytes of Penaeus japonicus by suppression subtractive hybridization (SSH) following microbial challenge.

Penaeus japonicus were injected with a heat-killed microorganism suspension and 291 randomly selected cDNA fragments generated by suppression subtractive hybridization (SSH) were sequenced. A total of 71 cDNA clones corresponding to 25 genes were found to have enhanced expression, of which eight are found for the first time in shrimp. The most abundant gene in the subtractive library was Kunitz-type protease inhibitor, clearly indicating this protease inhibitor in the response. A number of genes encoding signaling molecules, such as Ras-related nuclear protein (Ran), growth factor receptor bound protein (Grb), TGF-beta receptor interacting protein, integrin binding protein and interferon receptor bound protein were found for the first time in the shrimp, and they may be involved in the regulation of the host defense against the injected microbes. Furthermore, cDNAs of chaperonin, proteasome, antioxidant as well as genes associated with actin reorganization, which may be necessary for phagocytosis and encapsulation, were also expressed at a higher level after the challenge. These results may facilitate the understanding of shrimp immune responses.

Amino Acid Sequence↗

Blood-retinal barrier breakdown induced by activation of protein kinase C via vascular endothelial growth factor in streptozotocin-induced diabetic rats.

PURPOSE: To investigate (1) the mechanism of blood-retinal barrier breakdown induced by protein kinase C (PKC) activation (2) the relationship between PKC activation and vascular endothelial growth factor (VEGF) in 2-week streptozotocin-induced diabetes. METHODS: Retinal PKC activities, retinal and vitreous concentration of VEGF protein were conducted by enzyme-linked immunoabsorbent assay (ELISA). Retinal VEGF mRNA expression was analyzed by semi-quantitative reverse transcription-polymerase chain reaction (RT-PCR). Blood-retinal barrier breakdown was quantified using the Evans blue technique. Alteration of retinal VEGF and blood-retinal barrier were observed after intravitreal injection of PKC inhibitor, GF109203X, in 2-week diabetic rats. RESULTS: Two weeks of diabetes in rats resulted in elevation of retinal PKC specific activities, retinal and vitreous VEGF, and retinal vascular permeability. Retinal VEGF and retinal vascular permeability were decreased after intravitreal injection of GF109203X (10(-5), 10(-6) mol/L) in a dose-dependent manner. CONCLUSIONS: The results from this study showed that enhanced expression of VEGF and PKC in early diabetes and the blood-retinal barrier breakdown of early diabetic retinopathy induced by PKC activation may be partly due to the upregulation of VEGF. PKC inhibitor could reverse the blood-retinal barrier breakdown.

Animals↗

Safety and efficacy of dispase and plasmin in pharmacologic vitreolysis.

PURPOSE: To evaluate the safety and efficacy of dispase and plasmin when inducing posterior vitreous detachment (PVD) by intravitreous injection in rabbit eyes. METHODS: Forty-eight young pigmented rabbits were randomized into six groups. Groups 1 and 5 received 0.025 U dispase in test eyes; group 2, 0.1 U dispase; groups 3 and 6, 1 U plasmin; and group 4, 4 U plasmin. All groups received PBS in control eyes. Groups 5 and 6 were euthanatized 15 minutes after surgery for ocular histologic examination. The remaining groups (groups 1-4) received indirect ophthalmoscope and biomicroscopy 15 and 30 minutes; 1, 2, and 8 hours; and 1, 3, and 7 days after surgery. Ultrasonography and electroretinogram were performed 1 hour and 1 and 7 days after surgery. The eyes then were examined by scanning and transmission electron microscopy. RESULTS: Partial or complete PVDs were observed in the eyes that received dispase and plasmin, confirmed by the results of scanning electron microscopy. Light microscopy showed inflammation in both dispase- and plasmin-treated eyes of groups 5 and 6. However, whereas in plasmin-treated eyes the ERG and cell ultrastructure showed no significant changes, in dispase-treated eyes, the amplitudes of ERG showed a significant reduction from baseline and ultrastructural damage to the retina was detected by transmission electron microscopy. Cell damage, preretinal hemorrhage, and cataract were also observed in these eyes. No changes were observed in the control eyes. CONCLUSIONS: Intravitreal injection of dispase at 0.025 U or more can induce PVD, but it is not safe. Plasmin (1-4 U) is safer, except for the potential risk of inducing intraocular inflammation.

Animals↗

PmAV, a novel gene involved in virus resistance of shrimp Penaeus monodon.

Diseases caused by viruses especially by white spot syndrome virus (WSSV) are the greatest challenge to worldwide shrimp aquaculture. The innate immunity of shrimp has attracted extensive attention, but no factor involved in the virus resistance has been reported. Here we report for the first time the identification of an antiviral gene from shrimp Penaeus monodon. A differential cDNA (designated as PmAV) cloned from virus-resistant shrimp P. monodon by differential display (DD) was found to have an open reading frame (ORF) encoding a 170 amino acid peptide with a C-type lectin-like domain (CTLD). The PmAV gene was expressed in Escherichia coli and the protein was purified. Recombinant PmAV protein displayed a strong antiviral activity in inhibiting virus-induced cytopathic effect in fish cell in vitro. Moreover, native PmAV protein was isolated from shrimp hemolymph by immuno-affinity chromatography and confirmed by Western blot. No agglutination activity was observed both in recombinant and native PmAV protein. Immunohistological study showed that PmAV protein was located mainly in the cytoplasm, and not bound to the shrimp WSSV. It implies that the antiviral mechanism of PmAV protein is not by inhibiting the attachment of virus to target host cell. The discovery of PmAV gene might provide a clue to elucidate the innate immunity of marine invertebrates and would be helpful to shrimp viral disease control.

Amino Acid Sequence↗

Developmental expression of Smad1-7 suggests critical function of TGF-beta/BMP signaling in regulating epithelial-mesenchymal interaction during tooth morphogenesis.

Members of the transforming growth factor-beta family (e.g. TGF-beta, BMP and activin) are critical regulators of tooth morphogenesis. The basic TGF-beta signaling engine consists of a receptor complex that activates Smads and a Smad-containing complex that controls transcription of the downstream target genes. Little is known about the expression of endogenous Smads during tooth morphogenesis. Using a cRNA probe or antibody which specifically recognizes the expression of each Smad molecule, we provide a comprehensive endogenous Smad expression analysis during tooth morphogenesis. BMP signaling is transmitted through Smad1 and 5 which are first expressed within the dental lamina and later expand into condensed dental mesenchyme at the bud stage. As tooth development advances into the cap and bell stage, BMP signaling Smads are strongly localized within the inner enamel epithelium (IEE) and cranial neural crest derived dental mesenchyme (DM), indicating their critical role in regulating epithelial-mesenchyme interaction during tooth morphogenesis. Smad2 and 3 are responsible for transmitting TGF-beta/activin signaling and show unique expression patterns during tooth morphogenesis. They are localized within the nuclei of both IEE and DM, suggesting that TGF-beta-activated Smads are critical for regulating tooth development. Smad4, the common Smad, is expressed in both dental epithelium and mesenchyme throughout all stages of tooth morphogenesis. The expression of inhibitory Smads (Smad6 and 7) largely overlaps with receptor regulated Smads, indicating that negative feedback on BMP/TGF-beta signaling is critical throughout all stages of tooth morphogenesis. Our results suggest that both receptor-regulated and inhibitory Smads are important regulators of tooth morphogenesis. The selective activation of Smad, as indicated by nucleartranslocation, may suggest selective activation of different members of the TGF-beta superfamily during tooth development.

Animals↗

[Neuroprotection of nerve growth factor in experiment retinal detachment].

OBJECTIVE: To study the neuroprotection by nerve growth factor (NGF) in retina in experimental retinal detachment (RD). METHODS: Thirty one Sprague-Dawley rats were used as RD animal model by injected 0.1% sodium hyaluronate into the sub-neuroretina space. Those rats were divided into NGF experimental group, placebo group, normal control groups and pathologic control group. NGF 1 g/L/eye was injected into vitreous every 4 days in NGF experimental group and 5 micro l of PBS intravitreal injection was used as control after RD. On postoperative time 1/2 d, 1 d, 2 d, 4 d, 8 d, 16 d, 32 d, rats were sacrificed and eyes were enucleated. The effect of NGF on retina was assessed by electron, light microscopy and cell counters. RESULTS: Histology studies showed markedly changes in photoreceptor cells, bipolar cells and ganglion cells after RD, included depletion and shorten of inner and outer segments, disturbance and thinness of inner and outer nuclear layer and swelling of ganglion cells in NGF treated group and control. Changes in the microscopic examination in NGF group showed significantly less than that in control groups, especially in inner and outer segments of photoreceptor cells. In reattached retina, the tissue structure and cell morphology showed more close to normal in NGF group than that in RD control groups. Cell counters showed the cell numbers decreased both in NGF groups and RD control groups. When retina reattached, the cell number in experimental groups showed significantly lower than that in normal control group (P < 0.05). Nuclear number of outernuclear layer and ganglion cell layer in NGF groups was greater than that in RD control groups (P < 0.05). CONCLUSION: Intravitreal injection exogenous NGF partly protects retinal cells from degeneration in experimental RD and help recovery of retinal cells after retina reattached.

Animals↗

[Exogenous advanced glycosylation end products induce diabetes-like vascular dysfunction in normal rats: a factor for occurrence of diabetic retinopathy].

OBJECTIVE: To disclose the relationship between the deposition of advanced glycosylation end products (AGE) in the retinal vascular tissues and damage of retinal vessels in diabetic retinopathy. METHODS: Sixteen SD rats aged 2 months were divided into 4 groups, with 4 rats in each group. Rats in normal group received no treatment. Diabetes was induced by AGE in the diabetes group. Rat serum albumin (RSA, 40 mg/kg weight) was administered daily to healthy non-diabetic rats through tail veins for 2 weeks (RSA group). AGE-modified RSA was injected to rats in another group at the same route and dosage (AGE-RSA group). The number of pericytes in retinal capillary vessels was counted 2 weeks later. RESULTS: After two weeks continuous AGE treatment, the average amount of pericytes of capillary vessel per 10 microscope visual field (x 100 magnification) in AGE group (4.31 +/- 0.34) was significantly less than that of RSA group (5.80 +/- 0.48) (P < 0.01). Meanwhile, in the AGE-RSA group, AGE were identified in the retinal vascular tissues by immunohistochemical staining. CONCLUSION: Injection of exogenous AGE into healthy rats induces vascular changes resembling those find in the diabetic retinopathy. AGE might be one of the independent pathogenic factors in the occurrence of diabetic retinopathy.

Animals↗