Background Proneurotrophins such as the precursor of nerve growth factor （proNGF） and the precursor of brain-derived neurotrophic factor （proBDNF） interacted with sortilin and p75NTR to form a complex capable of a...Background Proneurotrophins such as the precursor of nerve growth factor （proNGF） and the precursor of brain-derived neurotrophic factor （proBDNF） interacted with sortilin and p75NTR to form a complex capable of activating an apoptotic signaling. We found that the expression of p75NTR and sortilin was increased in ischemic retina induced by elevated intraocular pressure （lOP）, but the protein expression changes of proNGF and proBDNF in the same situation were not clear. This study aimed to ascertain the protein expression changes of proNGF and proBDNF in ischemic retina induced by elevated lOP.展开更多
AIM： To determine if brain-derived neurotrophic factor （BDNF） could offer protention to retinal ganglion cells following a superior colliculus （SC） lesion in mice using pattern electroretinogram （PERG） and opti...AIM： To determine if brain-derived neurotrophic factor （BDNF） could offer protention to retinal ganglion cells following a superior colliculus （SC） lesion in mice using pattern electroretinogram （PERG） and optical coherence tomography （OCT） as a measures of ganglion cell response and retinal health. METHODS： Seven C57BIJ6J mice with BDNF protection were tested with PERG and OCT before and after SC lesions, RESULTS： Compared with baseline PERG, the amplitude of PERG decreased 11.7% after SC lesions, but not significantly（P〉0.05）. Through fast Fourier transform （FFT） analysis of the PERGs before and after SC lesions, it was found that dominant frequency of PERGs stayed unchanged, suggesting that the ganglion cells of the retina remained relatively healthy inspite of damage to the ends of the ganglion cell axons. Also, OCT showed no changes in retinal thickness after lesions. CONCLUSION： It was concluded that BDNF is essential component of normal retinal and helps retina keeping normal function. While retina lack of BDNF, ex vivo resource of BDNF provides protection to the sick retina. It implies that BDNF is a kind therapeutic neurotrophic factor to retina neurodegeneration diseases, such as glaucoma, age related macular degeneration.展开更多
Objective To investigate the distribution of bra in-derived neurotrophic factor(BDNF) protein in the rabbit retina. Methods Immune response material in the retina was observed using BDNF antibody by the method of i...Objective To investigate the distribution of bra in-derived neurotrophic factor(BDNF) protein in the rabbit retina. Methods Immune response material in the retina was observed using BDNF antibody by the method of immunohistochemistry. Results BDNF gene expression was mainly found in the RGCs, a lso in innernuclei cells and outernuclei cells in rabbit retina. Conclusion RGC is not only the target cell of BDNF, but also express the BDNF protein. BDNF from multi-sources participates in the regulati on of RGCs.展开更多
BACKGROUND： Exogenous brain-derived neurotrophic factor （BDNF） promotes retinal ganglion cell survival. However, the protective mechanisms remain unclear. OBJECTIVE： To investigate changes in retinal tyrosine kina...BACKGROUND： Exogenous brain-derived neurotrophic factor （BDNF） promotes retinal ganglion cell survival. However, the protective mechanisms remain unclear. OBJECTIVE： To investigate changes in retinal tyrosine kinase receptor B （trkB） expression and effects of exogenous BDNF on trkB activation in a rat model of acute high intraocular pressure （HtOP）. DESIGN, TIME AND SETTING： A randomized, controlled, animal experiment was performed at the Department of Anatomy and Neurobiology, Xiangya Medical School, Central South University from January 2004 to August 2006. MATERIALS： Rabbit anti-BDNF and anti-trkB.FL（full-length） polyclonal antibodies were purchased from Santa Cruz Biotechnology, USA; rabbit anti-p-trkB polyclonal antibodies were purchased from Cellsignal, USA. METHODS： A total of 48 healthy, adult, Sprague Dawiey rats were randomly assigned to acute HIOP （without BDNF pre-treatment） and BDNF pre-treated groups, with 24 animals in each group. In the BDNF pre-treated group, the left eyes were intravitreally injected with 3 pg/kg BDNF 2 days prior to HIOP. Rats in the acute HIOP group were not pre-treated with BDNE HIOP models were established by increased intraocular pressure in the left eyes until the b-wave of flash electroretinogragh disappeared and pressure was maintained for 60 minutes. The right eyes of all rats were not treated and served as the normal controls. MAIN OUTCOME MEASURES： Retinal structure and cell numbers in the ganglion cell layer （GCL） were detected by Nissl staining; expression of trkB and phosphorylated trkB in the rat retina were determined by immunohistochemistry. RESULTS： A greater number of GCL neurons were observed in the pre-treated group compared to the acute HIOP group （P 〈 0.05）. TrkB expression was significantly increased following HIOP at days 1 and 3 （P 〈 0.05）, but expression varied between retinal areas. Although trkB expression decreased at 7 days, phosphorylated trkB dramatically decreased with increasing time （P 〈 0.展开更多
Several studies have investigated the protective functions of brain-derived neurotrophic factor（BDNF） in retinitis pigmentosa. However, a BDNF-based therapy for retinitis pigmentosa is not yet available. To develop ...Several studies have investigated the protective functions of brain-derived neurotrophic factor（BDNF） in retinitis pigmentosa. However, a BDNF-based therapy for retinitis pigmentosa is not yet available. To develop an efficient treatment for fundus disease, an eukaryotic expression plasmid was generated and used to transfect human 293 T cells to assess the expression and bioactivity of BDNF on acute retinal pigment epithelial-19（ARPE-19） cells, a human retinal epithelial cell line. After 96 hours of co-culture in a Transwell chamber, ARPE-19 cells exposed to BDNF secreted by 293 T cells were more viable than ARPE-19 cells not exposed to secreted BDNF. Western blot assay showed that Bax levels were downregulated and that Bcl-2 levels were upregulated in human ARPE-19 cells exposed to BDNF. Furthermore, 293 T cells transfected with the BDNF gene steadily secreted the protein. The powerful anti-apoptotic function of this BDNF may be useful for the treatment of retinitis pigmentosa and other retinal degenerative diseases.展开更多
基金This study was supported in part from grants of National Natural Science Foundation of China （No. 30973261 and No. 30571991）.
文摘Background Proneurotrophins such as the precursor of nerve growth factor （proNGF） and the precursor of brain-derived neurotrophic factor （proBDNF） interacted with sortilin and p75NTR to form a complex capable of activating an apoptotic signaling. We found that the expression of p75NTR and sortilin was increased in ischemic retina induced by elevated intraocular pressure （lOP）, but the protein expression changes of proNGF and proBDNF in the same situation were not clear. This study aimed to ascertain the protein expression changes of proNGF and proBDNF in ischemic retina induced by elevated lOP.
文摘AIM： To determine if brain-derived neurotrophic factor （BDNF） could offer protention to retinal ganglion cells following a superior colliculus （SC） lesion in mice using pattern electroretinogram （PERG） and optical coherence tomography （OCT） as a measures of ganglion cell response and retinal health. METHODS： Seven C57BIJ6J mice with BDNF protection were tested with PERG and OCT before and after SC lesions, RESULTS： Compared with baseline PERG, the amplitude of PERG decreased 11.7% after SC lesions, but not significantly（P〉0.05）. Through fast Fourier transform （FFT） analysis of the PERGs before and after SC lesions, it was found that dominant frequency of PERGs stayed unchanged, suggesting that the ganglion cells of the retina remained relatively healthy inspite of damage to the ends of the ganglion cell axons. Also, OCT showed no changes in retinal thickness after lesions. CONCLUSION： It was concluded that BDNF is essential component of normal retinal and helps retina keeping normal function. While retina lack of BDNF, ex vivo resource of BDNF provides protection to the sick retina. It implies that BDNF is a kind therapeutic neurotrophic factor to retina neurodegeneration diseases, such as glaucoma, age related macular degeneration.
文摘Objective To investigate the distribution of bra in-derived neurotrophic factor(BDNF) protein in the rabbit retina. Methods Immune response material in the retina was observed using BDNF antibody by the method of immunohistochemistry. Results BDNF gene expression was mainly found in the RGCs, a lso in innernuclei cells and outernuclei cells in rabbit retina. Conclusion RGC is not only the target cell of BDNF, but also express the BDNF protein. BDNF from multi-sources participates in the regulati on of RGCs.
基金the National Natural Science Foundation of China, No. 30100098, 30570979
文摘BACKGROUND： Exogenous brain-derived neurotrophic factor （BDNF） promotes retinal ganglion cell survival. However, the protective mechanisms remain unclear. OBJECTIVE： To investigate changes in retinal tyrosine kinase receptor B （trkB） expression and effects of exogenous BDNF on trkB activation in a rat model of acute high intraocular pressure （HtOP）. DESIGN, TIME AND SETTING： A randomized, controlled, animal experiment was performed at the Department of Anatomy and Neurobiology, Xiangya Medical School, Central South University from January 2004 to August 2006. MATERIALS： Rabbit anti-BDNF and anti-trkB.FL（full-length） polyclonal antibodies were purchased from Santa Cruz Biotechnology, USA; rabbit anti-p-trkB polyclonal antibodies were purchased from Cellsignal, USA. METHODS： A total of 48 healthy, adult, Sprague Dawiey rats were randomly assigned to acute HIOP （without BDNF pre-treatment） and BDNF pre-treated groups, with 24 animals in each group. In the BDNF pre-treated group, the left eyes were intravitreally injected with 3 pg/kg BDNF 2 days prior to HIOP. Rats in the acute HIOP group were not pre-treated with BDNE HIOP models were established by increased intraocular pressure in the left eyes until the b-wave of flash electroretinogragh disappeared and pressure was maintained for 60 minutes. The right eyes of all rats were not treated and served as the normal controls. MAIN OUTCOME MEASURES： Retinal structure and cell numbers in the ganglion cell layer （GCL） were detected by Nissl staining; expression of trkB and phosphorylated trkB in the rat retina were determined by immunohistochemistry. RESULTS： A greater number of GCL neurons were observed in the pre-treated group compared to the acute HIOP group （P 〈 0.05）. TrkB expression was significantly increased following HIOP at days 1 and 3 （P 〈 0.05）, but expression varied between retinal areas. Although trkB expression decreased at 7 days, phosphorylated trkB dramatically decreased with increasing time （P 〈 0.
基金supported by the National Natural Science Foundation of China,No.81271046the Joint Program of Beijing Municipal Natural Science Foundation(category B)Beijing Educational Committee(key project),No.KZ201510025025
文摘Several studies have investigated the protective functions of brain-derived neurotrophic factor（BDNF） in retinitis pigmentosa. However, a BDNF-based therapy for retinitis pigmentosa is not yet available. To develop an efficient treatment for fundus disease, an eukaryotic expression plasmid was generated and used to transfect human 293 T cells to assess the expression and bioactivity of BDNF on acute retinal pigment epithelial-19（ARPE-19） cells, a human retinal epithelial cell line. After 96 hours of co-culture in a Transwell chamber, ARPE-19 cells exposed to BDNF secreted by 293 T cells were more viable than ARPE-19 cells not exposed to secreted BDNF. Western blot assay showed that Bax levels were downregulated and that Bcl-2 levels were upregulated in human ARPE-19 cells exposed to BDNF. Furthermore, 293 T cells transfected with the BDNF gene steadily secreted the protein. The powerful anti-apoptotic function of this BDNF may be useful for the treatment of retinitis pigmentosa and other retinal degenerative diseases.
