The Experts below are selected from a list of 303 Experts worldwide ranked by ideXlab platform
Bao Han Pan - One of the best experts on this subject based on the ideXlab platform.
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the lateral thoracic nerve and the cutaneous maximus muscle a novel in vivo model system for nerve Degeneration and regeneration studies
Experimental Neurology, 2012Co-Authors: Thien Nguyen, Bao Han Pan, Benedikt Grunewald, Mohamed H Farah, Michael Polydefkis, John W Mcdonald, Lawrence P Schramm, Klaus V ToykaAbstract:We report a novel in vivo mouse model system to study regeneration of injured motor nerve and spatiotemporal pattern of denervation in experimental nerve diseases. The lateral thoracic nerve (LTN), as a pure motor nerve, innervates the cutaneous maximus muscle (CMM) by some of the shortest and the longest motor nerve fibers in the mouse body. Its branches and nerve terminals can be imaged in whole mount preparations. Here we describe the branching pattern of the LTN and its innervation of the CMM, and characterize Degeneration and regeneration over time after a LTN crush by morphological and electrophysiological analyses. We demonstrate the utility of this model in a well-established neurotoxicity paradigm and in a genetic disease model of the peripheral neuropathy. Furthermore, this system enables punch biopsies that allow repeated and multi-location examinations for LTN regeneration and CMM reinnervation over time. The presence of the LTN and the CMM in a variety of species and its easy accessibility suggests that this in vivo model system offers considerable promise for future nerve Degeneration and regeneration research.
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The lateral thoracic nerve and the cutaneous maximus muscle—A novel in vivo model system for nerve Degeneration and regeneration studies
Experimental neurology, 2012Co-Authors: Bao Han Pan, Thien Nguyen, Benedikt Grunewald, Mohamed H Farah, Michael Polydefkis, John W Mcdonald, Lawrence P Schramm, Klaus V Toyka, Ahmet Hoke, John W. GriffinAbstract:We report a novel in vivo mouse model system to study regeneration of injured motor nerve and spatiotemporal pattern of denervation in experimental nerve diseases. The lateral thoracic nerve (LTN), as a pure motor nerve, innervates the cutaneous maximus muscle (CMM) by some of the shortest and the longest motor nerve fibers in the mouse body. Its branches and nerve terminals can be imaged in whole mount preparations. Here we describe the branching pattern of the LTN and its innervation of the CMM, and characterize Degeneration and regeneration over time after a LTN crush by morphological and electrophysiological analyses. We demonstrate the utility of this model in a well-established neurotoxicity paradigm and in a genetic disease model of the peripheral neuropathy. Furthermore, this system enables punch biopsies that allow repeated and multi-location examinations for LTN regeneration and CMM reinnervation over time. The presence of the LTN and the CMM in a variety of species and its easy accessibility suggests that this in vivo model system offers considerable promise for future nerve Degeneration and regeneration research.
Enhua Shao - One of the best experts on this subject based on the ideXlab platform.
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regeneration of the zebrafish retinal pigment epithelium after widespread genetic ablation
PLOS Genetics, 2019Co-Authors: Nicholas J Hanovice, Lyndsay L Leach, Kayleigh Slater, Ana E Gabriel, Dwight K Romanovicz, Enhua Shao, Ross F Collery, Edward A Burton, Kira L LathropAbstract:The retinal pigment epithelium (RPE) is a specialized monolayer of pigmented cells within the eye that is critical for maintaining visual system function. Diseases affecting the RPE have dire consequences for vision, and the most prevalent of these is atrophic (dry) age-related macular Degeneration (AMD), which is thought to result from RPE dysfunction and Degeneration. An intriguing possibility for treating RPE degenerative diseases like atrophic AMD is the stimulation of endogenous RPE regeneration; however, very little is known about the mechanisms driving successful RPE regeneration in vivo. Here, we developed a zebrafish transgenic model (rpe65a:nfsB-eGFP) that enabled ablation of large swathes of mature RPE. RPE ablation resulted in rapid RPE Degeneration, as well as Degeneration of Bruch’s membrane and underlying photoreceptors. Using this model, we demonstrate for the first time that zebrafish are capable of regenerating a functional RPE monolayer after RPE ablation. Regenerated RPE cells first appear at the periphery of the RPE, and regeneration proceeds in a peripheral-to-central fashion. RPE ablation elicits a robust proliferative response in the remaining RPE. Subsequently, proliferative cells move into the injury site and differentiate into RPE. BrdU incorporation assays demonstrate that the regenerated RPE is likely derived from remaining peripheral RPE cells. Pharmacological disruption using IWR-1, a Wnt signaling antagonist, significantly reduces cell proliferation in the RPE and impairs overall RPE recovery. These data demonstrate that the zebrafish RPE possesses a robust capacity for regeneration and highlight a potential mechanism through which endogenous RPE regenerate in vivo.
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regeneration of the zebrafish retinal pigment epithelium after widespread genetic ablation
bioRxiv, 2018Co-Authors: Nicholas J Hanovice, Lyndsay L Leach, Kayleigh Slater, Ana E Gabriel, Dwight K Romanovicz, Enhua Shao, Ross F Collery, Edward A BurtonAbstract:ABSTRACT The retinal pigment epithelium (RPE) is a specialized monolayer of pigmented cells within the eye that is critical for maintaining visual system function. Diseases affecting the RPE have dire consequences for vision, and the most prevalent of these is atrophic (dry) age-related macular Degeneration (AMD), which is thought to result from RPE dysfunction and Degeneration. An intriguing possibility for treating RPE degenerative diseases like atrophic AMD is the stimulation of endogenous RPE regeneration; however, very little is known about the mechanisms driving successful RPE regeneration in vivo. Here, we developed a zebrafish transgenic model (rpe65a:nfsB-GFP) that enabled ablation of large swathes of mature RPE. RPE ablation resulted in rapid RPE Degeneration, as well as Degeneration of Bruch’s membrane and underlying photoreceptors. Using this model, we demonstrate for the first time that larval and adult zebrafish are capable of regenerating a functional RPE monolayer after RPE ablation. Regenerated RPE cells first appear at the periphery of the RPE, and regeneration proceeds in a peripheral-to-central fashion. RPE ablation elicits a robust proliferative response in the remaining RPE. Subsequently, proliferative cells move into the injury site and differentiate into RPE. BrdU pulse-chase analyses demonstrate that the regenerated RPE is likely derived from remaining peripheral RPE cells. Pharmacological inhibition of Wnt signaling significantly reduces cell proliferation in the RPE and delays overall RPE recovery. These data demonstrate that the zebrafish RPE possesses a robust capacity for regeneration and highlight a potential mechanism through which endogenous RPE regenerate in vivo. SIGNIFICANCE STATEMENT Diseases resulting in RPE Degeneration are among the leading causes of blindness worldwide, and no therapy exists that can replace RPE or restore lost vision. One intriguing possibility is the development of therapies focused on stimulating endogenous RPE regeneration. For this to be possible, we must first gain a deeper understanding of the mechanisms underlying RPE regeneration. Here, we ablate mature RPE in zebrafish and demonstrate that zebrafish regenerate RPE after widespread injury. Injury-adjacent RPE proliferate and regenerate RPE, suggesting that they are the source of regenerated tissue. Finally, we demonstrate that Wnt signaling is required for RPE regeneration. These findings establish an in vivo model through which the molecular and cellular underpinnings of RPE regeneration can be further characterized.
Klaus V Toyka - One of the best experts on this subject based on the ideXlab platform.
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the lateral thoracic nerve and the cutaneous maximus muscle a novel in vivo model system for nerve Degeneration and regeneration studies
Experimental Neurology, 2012Co-Authors: Thien Nguyen, Bao Han Pan, Benedikt Grunewald, Mohamed H Farah, Michael Polydefkis, John W Mcdonald, Lawrence P Schramm, Klaus V ToykaAbstract:We report a novel in vivo mouse model system to study regeneration of injured motor nerve and spatiotemporal pattern of denervation in experimental nerve diseases. The lateral thoracic nerve (LTN), as a pure motor nerve, innervates the cutaneous maximus muscle (CMM) by some of the shortest and the longest motor nerve fibers in the mouse body. Its branches and nerve terminals can be imaged in whole mount preparations. Here we describe the branching pattern of the LTN and its innervation of the CMM, and characterize Degeneration and regeneration over time after a LTN crush by morphological and electrophysiological analyses. We demonstrate the utility of this model in a well-established neurotoxicity paradigm and in a genetic disease model of the peripheral neuropathy. Furthermore, this system enables punch biopsies that allow repeated and multi-location examinations for LTN regeneration and CMM reinnervation over time. The presence of the LTN and the CMM in a variety of species and its easy accessibility suggests that this in vivo model system offers considerable promise for future nerve Degeneration and regeneration research.
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The lateral thoracic nerve and the cutaneous maximus muscle—A novel in vivo model system for nerve Degeneration and regeneration studies
Experimental neurology, 2012Co-Authors: Bao Han Pan, Thien Nguyen, Benedikt Grunewald, Mohamed H Farah, Michael Polydefkis, John W Mcdonald, Lawrence P Schramm, Klaus V Toyka, Ahmet Hoke, John W. GriffinAbstract:We report a novel in vivo mouse model system to study regeneration of injured motor nerve and spatiotemporal pattern of denervation in experimental nerve diseases. The lateral thoracic nerve (LTN), as a pure motor nerve, innervates the cutaneous maximus muscle (CMM) by some of the shortest and the longest motor nerve fibers in the mouse body. Its branches and nerve terminals can be imaged in whole mount preparations. Here we describe the branching pattern of the LTN and its innervation of the CMM, and characterize Degeneration and regeneration over time after a LTN crush by morphological and electrophysiological analyses. We demonstrate the utility of this model in a well-established neurotoxicity paradigm and in a genetic disease model of the peripheral neuropathy. Furthermore, this system enables punch biopsies that allow repeated and multi-location examinations for LTN regeneration and CMM reinnervation over time. The presence of the LTN and the CMM in a variety of species and its easy accessibility suggests that this in vivo model system offers considerable promise for future nerve Degeneration and regeneration research.
John W Mcdonald - One of the best experts on this subject based on the ideXlab platform.
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the lateral thoracic nerve and the cutaneous maximus muscle a novel in vivo model system for nerve Degeneration and regeneration studies
Experimental Neurology, 2012Co-Authors: Thien Nguyen, Bao Han Pan, Benedikt Grunewald, Mohamed H Farah, Michael Polydefkis, John W Mcdonald, Lawrence P Schramm, Klaus V ToykaAbstract:We report a novel in vivo mouse model system to study regeneration of injured motor nerve and spatiotemporal pattern of denervation in experimental nerve diseases. The lateral thoracic nerve (LTN), as a pure motor nerve, innervates the cutaneous maximus muscle (CMM) by some of the shortest and the longest motor nerve fibers in the mouse body. Its branches and nerve terminals can be imaged in whole mount preparations. Here we describe the branching pattern of the LTN and its innervation of the CMM, and characterize Degeneration and regeneration over time after a LTN crush by morphological and electrophysiological analyses. We demonstrate the utility of this model in a well-established neurotoxicity paradigm and in a genetic disease model of the peripheral neuropathy. Furthermore, this system enables punch biopsies that allow repeated and multi-location examinations for LTN regeneration and CMM reinnervation over time. The presence of the LTN and the CMM in a variety of species and its easy accessibility suggests that this in vivo model system offers considerable promise for future nerve Degeneration and regeneration research.
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The lateral thoracic nerve and the cutaneous maximus muscle—A novel in vivo model system for nerve Degeneration and regeneration studies
Experimental neurology, 2012Co-Authors: Bao Han Pan, Thien Nguyen, Benedikt Grunewald, Mohamed H Farah, Michael Polydefkis, John W Mcdonald, Lawrence P Schramm, Klaus V Toyka, Ahmet Hoke, John W. GriffinAbstract:We report a novel in vivo mouse model system to study regeneration of injured motor nerve and spatiotemporal pattern of denervation in experimental nerve diseases. The lateral thoracic nerve (LTN), as a pure motor nerve, innervates the cutaneous maximus muscle (CMM) by some of the shortest and the longest motor nerve fibers in the mouse body. Its branches and nerve terminals can be imaged in whole mount preparations. Here we describe the branching pattern of the LTN and its innervation of the CMM, and characterize Degeneration and regeneration over time after a LTN crush by morphological and electrophysiological analyses. We demonstrate the utility of this model in a well-established neurotoxicity paradigm and in a genetic disease model of the peripheral neuropathy. Furthermore, this system enables punch biopsies that allow repeated and multi-location examinations for LTN regeneration and CMM reinnervation over time. The presence of the LTN and the CMM in a variety of species and its easy accessibility suggests that this in vivo model system offers considerable promise for future nerve Degeneration and regeneration research.
Dengbing Yao - One of the best experts on this subject based on the ideXlab platform.
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Effect of Spp1 on nerve Degeneration and regeneration after rat sciatic nerve injury.
BMC neuroscience, 2017Co-Authors: Xingyu Liu, Yuhua Sun, Ying Yuan, Shusen Cui, Dengbing YaoAbstract:Abstract Background Wallerian Degeneration (WD) in injured peripheral nerves is associated with a large number of up- or down-regulated genes, but the effects of these changes are poorly understood. In our previous studies, we reported some key factors that are differentially expressed to activate nerve Degeneration and regeneration during WD. Here, we determined the effects of secreted phosphoprotein 1 (Spp1) on WD after rat sciatic nerve injury. Results Spp1 was upregulated from 6 h to 14 days after sciatic nerve injury. Altered expression of Spp1 in Schwann cells (SC) resulted in altered mRNA and protein expression levels for cytokines, c-Fos, PKCα and phospho-ERK/ERK and affected SC apoptosis in vitro. Silencing of Spp1 expression in SCs using siRNA technology reduced proliferation and promoted migration of SCs in vitro. By contrast, overexpression of Spp1 promoted proliferation and reduced migration in SCs in vitro. Differential expression of Spp1 after sciatic nerve injury in vivo altered the expression of cytokines, c-Fos, PKCα, and the p-ERK/ERK pathway. Conclusions Spp1 is a key regulatory factor that affects nerve Degeneration and regeneration through c-Fos, PKCα and p-ERK/ERK pathways after rat sciatic nerve injury. These results shed new light on the role of Spp1 in nerve Degeneration and regeneration during WD.
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TGF-β1 is critical for Wallerian Degeneration after rat sciatic nerve injury.
Neuroscience, 2014Co-Authors: Pingan Zhang, Shusen Cui, Y. Zhu, Dengbing YaoAbstract:Wallerian Degeneration (WD) is a process of axonal Degeneration distal to the injury site followed by a robust regenerative response. It involves Degeneration and regeneration which can be directly induced by nerve injury and activated by transcription factors. Although WD has been studied extensively, the precise mechanisms of transcription factors regulating WD are still elusive. In this study, we reported the effect of transforming growth factor-β1 (TGF-β1) on WD after rat sciatic nerve injury. The data showed that TGF-β1 may express in injured rat sciatic nerve and cultured Schwann cells (SCs). Knock down of TGF-β1 expressions resulted in the reduction of SC proliferation and apoptosis, up regulation of cytokines and Smad2, 4. Enhanced expression of TGF-β1 could promote SC proliferation and apoptosis, down regulation of cytokines and Smad2, 4. Altered expressions of TGF-β1 may affect Smad and AKT but not c-Jun and extracellular regulated protein kinase (ERK) pathways. Our results revealed the role of TGF-β1 on WD and provided the basis for the molecular mechanisms of TGF-β1-regulated nerve Degeneration and/or regeneration.
