The Experts below are selected from a list of 4260 Experts worldwide ranked by ideXlab platform
J C Glorioso - One of the best experts on this subject based on the ideXlab platform.
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Herpes simplex virus vector-mediated delivery of neurturin rescues erectile dysfunction of cavernous nerve injury
Gene Therapy, 2009Co-Authors: R Kato, D Wolfe, C H Coyle, J B Wechuck, T Tsukamoto, J B Nelson, J C Glorioso, P Tyagi, M B Chancellor, N YoshimuraAbstract:Neurturin (NTN), a member of glial cell line-derived neurotrophic factor (GDNF) family, is known as an important neurotrophic factor for penis-projecting neurons. We recently demonstrated significant protection from erectile dysfunction (ED) following a replication-defective herpes simplex virus (HSV) vector-mediated GDNF delivery to the injured cavernous nerve. Herein, we applied HSV vector-mediated delivery of NTN to this ED model. Rat cavernous nerve was injured bilaterally using a clamp and dry ice. For HSV-treated groups, 20 μl of vector stock was administered directly to the damaged nerve. Delivery of an HSV vector expressing both green fluorescent protein and lacZ (HSV-LacZ) was used as a control. Intracavernous pressure along with systemic arterial pressure (ICP/AP) was measured 2 and 4 weeks after the nerve injury. Fluorogold (FG) was injected into the penile crus 7 days before being killed to assess neuronal survival. Four weeks after nerve injury, rats treated with HSV-NTN exhibited significantly higher ICP/AP compared with untreated or control vector-treated groups. The HSV-NTN group had more FG-positive major pelvic ganglion neurons than the control group following injury. HSV vector-mediated delivery of NTN could be a viable approach for the improvement of ED following cavernous nerve injury.
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Herpes simplex virus vector-mediated delivery of glial cell line-derived neurotrophic factor rescues erectile dysfunction following cavernous nerve injury
Gene Therapy, 2007Co-Authors: R Kato, D Wolfe, C H Coyle, S Huang, J B Wechuck, W F Goins, D M Krisky, T Tsukamoto, J B Nelson, J C GloriosoAbstract:Erectile dysfunction (ED) is frequently associated with injury to the cavernous nerve sustained during pelvic surgery. Functional recovery from cavernous nerve injury is generally incomplete and occurs over an extended time frame. We employed a therapeutic gene transfer approach with herpes simplex virus (HSV) vector expressing glial cell line-derived neurotrophic factor (GDNF). Rat cavernous nerve was injured bilaterally using a clamp and dry ice. For HSV-treated groups, 20 μ l of purified vector stock was administered directly to and around the damaged nerve. Delivery of an HSV vector expressing both green fluorescent protein (GFP) and lacZ (HSV-LacZ) was used as a control. Intracavernous pressure along with systemic arterial pressure (ICP/AP) was measured 2 and 4 weeks after the nerve injury. Fluorogold (FG) was injected into the penile crus 7 days before killing to assess nerve survival. Approximately 60% of major pelvic ganglion (MPG) cells were GFP positive after viral administration. At 4 weeks after nerve injury, rats treated with HSV-GDNF exhibited significant recovery of ICP/AP compared with control vector or untreated groups. The HSV-GDNF group also yielded more FG-positive MPG cells than the control vector group. HSV vector-mediated delivery of GDNF presents a viable approach for the treatment of ED following cavernous nerve injury.
R Kato - One of the best experts on this subject based on the ideXlab platform.
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Herpes simplex virus vector-mediated delivery of neurturin rescues erectile dysfunction of cavernous nerve injury
Gene Therapy, 2009Co-Authors: R Kato, D Wolfe, C H Coyle, J B Wechuck, T Tsukamoto, J B Nelson, J C Glorioso, P Tyagi, M B Chancellor, N YoshimuraAbstract:Neurturin (NTN), a member of glial cell line-derived neurotrophic factor (GDNF) family, is known as an important neurotrophic factor for penis-projecting neurons. We recently demonstrated significant protection from erectile dysfunction (ED) following a replication-defective herpes simplex virus (HSV) vector-mediated GDNF delivery to the injured cavernous nerve. Herein, we applied HSV vector-mediated delivery of NTN to this ED model. Rat cavernous nerve was injured bilaterally using a clamp and dry ice. For HSV-treated groups, 20 μl of vector stock was administered directly to the damaged nerve. Delivery of an HSV vector expressing both green fluorescent protein and lacZ (HSV-LacZ) was used as a control. Intracavernous pressure along with systemic arterial pressure (ICP/AP) was measured 2 and 4 weeks after the nerve injury. Fluorogold (FG) was injected into the penile crus 7 days before being killed to assess neuronal survival. Four weeks after nerve injury, rats treated with HSV-NTN exhibited significantly higher ICP/AP compared with untreated or control vector-treated groups. The HSV-NTN group had more FG-positive major pelvic ganglion neurons than the control group following injury. HSV vector-mediated delivery of NTN could be a viable approach for the improvement of ED following cavernous nerve injury.
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Herpes simplex virus vector-mediated delivery of glial cell line-derived neurotrophic factor rescues erectile dysfunction following cavernous nerve injury
Gene Therapy, 2007Co-Authors: R Kato, D Wolfe, C H Coyle, S Huang, J B Wechuck, W F Goins, D M Krisky, T Tsukamoto, J B Nelson, J C GloriosoAbstract:Erectile dysfunction (ED) is frequently associated with injury to the cavernous nerve sustained during pelvic surgery. Functional recovery from cavernous nerve injury is generally incomplete and occurs over an extended time frame. We employed a therapeutic gene transfer approach with herpes simplex virus (HSV) vector expressing glial cell line-derived neurotrophic factor (GDNF). Rat cavernous nerve was injured bilaterally using a clamp and dry ice. For HSV-treated groups, 20 μ l of purified vector stock was administered directly to and around the damaged nerve. Delivery of an HSV vector expressing both green fluorescent protein (GFP) and lacZ (HSV-LacZ) was used as a control. Intracavernous pressure along with systemic arterial pressure (ICP/AP) was measured 2 and 4 weeks after the nerve injury. Fluorogold (FG) was injected into the penile crus 7 days before killing to assess nerve survival. Approximately 60% of major pelvic ganglion (MPG) cells were GFP positive after viral administration. At 4 weeks after nerve injury, rats treated with HSV-GDNF exhibited significant recovery of ICP/AP compared with control vector or untreated groups. The HSV-GDNF group also yielded more FG-positive MPG cells than the control vector group. HSV vector-mediated delivery of GDNF presents a viable approach for the treatment of ED following cavernous nerve injury.
Joanna Lewinkowalik - One of the best experts on this subject based on the ideXlab platform.
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Fluorogold labeled organotypic retinal explant culture for neurotoxicity screening studies
Oxidative Medicine and Cellular Longevity, 2018Co-Authors: A Smedowski, Marita Pietruchadutczak, Ruchi Maniar, Michael Ajeleti, Iwona Matuszek, Joanna LewinkowalikAbstract:Preclinical toxicity screening of the new retinal compounds is an absolute requirement in the pathway of further drug development. Since retinal neuron cultivation and in vivo studies are relatively expensive and time consuming, we aimed to create a fast and reproducible ex vivo system for retinal toxicity screening. For this purpose, we used rat retinal explant culture that was retrogradely labeled with the Fluorogold before the isolation. Explants were exposed to a toxic concentration of gentamicin and ciliary neurotrophic factor (CNTF), a known neuroprotective agent. The measured outcomes showed the cell density in retinal ganglion cell layer (GCL) and the activity of lactate dehydrogenase (LDH) in the culture medium. Gentamicin-induced oxidative stress resulted in retinal cell damage and rapid LDH release to the culture medium (). Additional CNTF supplementation minimized the cell damage, and the increase of LDH release was insignificant when compared to LDH levels before gentamicin insult (). As well as this, the LDH activity was directly correlated with the cell count in GCL (, ), making a sensitive marker of retinal neuron damage. The FLOREC protocol could be considered as a fast, reproducible, and sensitive method to detect neurotoxicity in the screening studies of the retinal drugs.
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Fluorogold labeled organotypic retinal explant culture florec for neurodegeneration and neurotoxicity screening studies
Acta Ophthalmologica, 2017Co-Authors: Michael Ajeleti, A Smedowski, Marita Pietruchadutczak, Ruchi Maniar, Iwona Matuszek, Joanna LewinkowalikAbstract:Purpose To create a fast and reproducible system for retinal drugs toxicity screening. Methods In this study, we used retinal explants culture from 4 weeks old Wistar rats (n = 16). First, to determine the effect of Fluorogold (FG) on explants quality, we used 8 animals. FG was injected into midbrain of rats (n = 4) 5 days before euthanasia. Each retina after isolation was divided into 2 parts. In this way, we prepared 16 retinal explants with FG labeling and 16 explants without FG. Explants were cultured in supplemented Neurobasal A medium in Millicell culture inserts. After 7 days of culture, the explants were fixed, stained with s3-tubulin and processed for stereology. The culture medium was used to evaluate LDH release. The other group of 8 rats was processed in a similar way, but the culture medium was additionally supplemented with CNTF or toxic concentration of Gentamycin. Results We did not observe differences between FG and no-FG explants for s3-tubulin-positive cell count and LDH release after 7 days of culture. The number of s3-tubulin-positive cells was similar to FG-labelled cells (57 ± 23; 58 ± 17 cells respectively, p > 0.5). Gentamycin treatment resulted in retinal cell damage expressed in rapid LDH release to culture medium. After 7 days of culture, the levels of LDH in medium increased up to 157 ± 57% and 144 ± 27% when compared to the corresponding LDH levels before Gentamycin exposure in no-FG (p 0.5) and FG (p > 0.05) explants respectively. Conclusions The FLOREC protocol could be considered as a fast, reproducible and sensitive method to detect neurotoxicity and neuroprotection in the screening studies of the retinal drugs.
N Yoshimura - One of the best experts on this subject based on the ideXlab platform.
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Herpes simplex virus vector-mediated delivery of neurturin rescues erectile dysfunction of cavernous nerve injury
Gene Therapy, 2009Co-Authors: R Kato, D Wolfe, C H Coyle, J B Wechuck, T Tsukamoto, J B Nelson, J C Glorioso, P Tyagi, M B Chancellor, N YoshimuraAbstract:Neurturin (NTN), a member of glial cell line-derived neurotrophic factor (GDNF) family, is known as an important neurotrophic factor for penis-projecting neurons. We recently demonstrated significant protection from erectile dysfunction (ED) following a replication-defective herpes simplex virus (HSV) vector-mediated GDNF delivery to the injured cavernous nerve. Herein, we applied HSV vector-mediated delivery of NTN to this ED model. Rat cavernous nerve was injured bilaterally using a clamp and dry ice. For HSV-treated groups, 20 μl of vector stock was administered directly to the damaged nerve. Delivery of an HSV vector expressing both green fluorescent protein and lacZ (HSV-LacZ) was used as a control. Intracavernous pressure along with systemic arterial pressure (ICP/AP) was measured 2 and 4 weeks after the nerve injury. Fluorogold (FG) was injected into the penile crus 7 days before being killed to assess neuronal survival. Four weeks after nerve injury, rats treated with HSV-NTN exhibited significantly higher ICP/AP compared with untreated or control vector-treated groups. The HSV-NTN group had more FG-positive major pelvic ganglion neurons than the control group following injury. HSV vector-mediated delivery of NTN could be a viable approach for the improvement of ED following cavernous nerve injury.
D Wolfe - One of the best experts on this subject based on the ideXlab platform.
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Herpes simplex virus vector-mediated delivery of neurturin rescues erectile dysfunction of cavernous nerve injury
Gene Therapy, 2009Co-Authors: R Kato, D Wolfe, C H Coyle, J B Wechuck, T Tsukamoto, J B Nelson, J C Glorioso, P Tyagi, M B Chancellor, N YoshimuraAbstract:Neurturin (NTN), a member of glial cell line-derived neurotrophic factor (GDNF) family, is known as an important neurotrophic factor for penis-projecting neurons. We recently demonstrated significant protection from erectile dysfunction (ED) following a replication-defective herpes simplex virus (HSV) vector-mediated GDNF delivery to the injured cavernous nerve. Herein, we applied HSV vector-mediated delivery of NTN to this ED model. Rat cavernous nerve was injured bilaterally using a clamp and dry ice. For HSV-treated groups, 20 μl of vector stock was administered directly to the damaged nerve. Delivery of an HSV vector expressing both green fluorescent protein and lacZ (HSV-LacZ) was used as a control. Intracavernous pressure along with systemic arterial pressure (ICP/AP) was measured 2 and 4 weeks after the nerve injury. Fluorogold (FG) was injected into the penile crus 7 days before being killed to assess neuronal survival. Four weeks after nerve injury, rats treated with HSV-NTN exhibited significantly higher ICP/AP compared with untreated or control vector-treated groups. The HSV-NTN group had more FG-positive major pelvic ganglion neurons than the control group following injury. HSV vector-mediated delivery of NTN could be a viable approach for the improvement of ED following cavernous nerve injury.
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Herpes simplex virus vector-mediated delivery of glial cell line-derived neurotrophic factor rescues erectile dysfunction following cavernous nerve injury
Gene Therapy, 2007Co-Authors: R Kato, D Wolfe, C H Coyle, S Huang, J B Wechuck, W F Goins, D M Krisky, T Tsukamoto, J B Nelson, J C GloriosoAbstract:Erectile dysfunction (ED) is frequently associated with injury to the cavernous nerve sustained during pelvic surgery. Functional recovery from cavernous nerve injury is generally incomplete and occurs over an extended time frame. We employed a therapeutic gene transfer approach with herpes simplex virus (HSV) vector expressing glial cell line-derived neurotrophic factor (GDNF). Rat cavernous nerve was injured bilaterally using a clamp and dry ice. For HSV-treated groups, 20 μ l of purified vector stock was administered directly to and around the damaged nerve. Delivery of an HSV vector expressing both green fluorescent protein (GFP) and lacZ (HSV-LacZ) was used as a control. Intracavernous pressure along with systemic arterial pressure (ICP/AP) was measured 2 and 4 weeks after the nerve injury. Fluorogold (FG) was injected into the penile crus 7 days before killing to assess nerve survival. Approximately 60% of major pelvic ganglion (MPG) cells were GFP positive after viral administration. At 4 weeks after nerve injury, rats treated with HSV-GDNF exhibited significant recovery of ICP/AP compared with control vector or untreated groups. The HSV-GDNF group also yielded more FG-positive MPG cells than the control vector group. HSV vector-mediated delivery of GDNF presents a viable approach for the treatment of ED following cavernous nerve injury.