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24 results on '"Ding, Yanning"'

3. Sodium Channels in Primary Sensory Neurons: Relationship to Pain States

Author

Wood, John N., primary, Akopian, Armen N., additional, Baker, Mark, additional, Ding, Yanning, additional, Geoghegan, Fleur, additional, Nassar, Mohammed, additional, Malik-Hall, Misbah, additional, Okuse, Kenji, additional, Poon, Louisa, additional, Ravenall, Samantha, additional, Sukumaran, Madhu, additional, and Souslova, Veronika, additional

Published
2008
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6. Amniotic membrane extract and eye drops: a review of literature and clinical application

Author

Murri,Michael S, Moshirfar,Majid, Birdsong,Orry C, Ronquillo,Yasmyne, Ding,Yanning, and Hoopes,Phillip C

Subjects
genetic structures, Clinical Ophthalmology, sense organs, eye diseases
Abstract

Michael S Murri,1 Majid Moshirfar,1,2 Orry C Birdsong,2 Yasmyne C Ronquillo,2 Yanning Ding,2 Phillip C Hoopes2 1John A Moran Eye Center, Department of Ophthalmology and Visual Sciences, University of Utah School of Medicine, Salt Lake City, UT, USA; 2HDR Research Center, Hoopes Vision, Draper, UT, USA Abstract: The amniotic membrane (AM) has a long history of use in the treatment of various diseases of the ocular surface. It contains pluripotent cells, highly organized collagen, anti-fibrotic and anti-inflammatory cytokines, immune-modulators, growth factors, and matrix proteins. It is used to promote corneal healing in severely damaged eyes. Recently, AM extract and AM extract eye drops have been successfully used in clinical applications, including dry eye and chemical burns. We provide an overview on the recent progress in the preparation, mechanisms of action, and use of AM extract/AM extract eye drops for corneal and external eye diseases. Keywords: amniotic membrane, amniotic membrane extract, amniotic membrane extract eye drops, AME, AMEED, AMT, umbilical cord, amnion, Regenesol, Genesis, Regener-Eyes, corneal wound healing, amniotic membrane transplant

Published
2018

8. Warm-coding deficits and aberrant inflammatory pain in mice lacking P2X 3 receptors

Author

Souslova, Veronika, Cesare, Paolo, Ding, Yanning, Akopian, Armen N., Stanfa, Louise, Suzuki, Rie, Carpenter, Katherine, Dickenson, Anthony, Boyce, Susan, Hill, Ray, Nebenius-Oosthuizen, Daniela, Smith, Andrew J.H., Kidd, Emma J., and Wood, John N.

Abstract

Author(s): Veronika Souslova [1]; Paolo Cesare [1]; Yanning Ding [1]; Armen N. Akopian [1]; Louise Stanfa [2]; Rie Suzuki [2]; Katherine Carpenter [2]; Anthony Dickenson [2]; Susan Boyce [3]; Ray [...]

Published
2000
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12. GTP-induced tetrodotoxin-resistant Na+ current regulates excitability in mouse and rat small diameter sensory neurones

Author

Baker, Mark D, Chandra, Sonia Y, Ding, Yanning, Waxman, Stephen G, and Wood, John N

Subjects
Patch-Clamp Techniques, Physiology, Neuropeptides, Action Potentials, Excitatory Postsynaptic Potentials, Original Articles, Tetrodotoxin, Sodium Channel Agonists, Sodium Channels, Rats, Up-Regulation, Electrophysiology, Rats, Sprague-Dawley, Mice, GTP-Binding Proteins, Guanosine 5'-O-(3-Thiotriphosphate), Animals, Guanosine Triphosphate, Neurons, Afferent, NAV1.9 Voltage-Gated Sodium Channel, Protein Kinase Inhibitors, Algorithms, Sodium Channel Blockers
Abstract

Peripheral pain thresholds are regulated by the actions of inflammatory mediators. Some act through G-protein-coupled receptors on voltage-gated sodium channels. We have found that a low-threshold, persistent tetrodotoxin-resistant Na+ current, attributed to NaV1.9, is upregulated by GTP and its non-hydrolysable analogue GTP-gamma-S, but not by GDP. Inclusion of GTP-gamma-S (500 microM) in the internal solution led to an increase in maximal current amplitude of300 % within 5 min. In current clamp, upregulation of persistent current was associated with a more negative threshold for action potential induction (by 15-16 mV) assessed from a holding potential of -90 mV. This was not seen in neurones without the low-threshold current or with internal GDP (P0.001). In addition, persistent current upregulation depolarized neurones. At -60 mV, internal GTP-gamma-S led to the generation of spontaneous activity in initially silent neurones only when persistent current was upregulated. These findings suggest that regulation of the persistent current has important consequences for nociceptor excitability.

Published
2003
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13. Epidermal growth factor upregulates motility of Mat-LyLu rat prostate cancer cells partially via voltage-gated Na+ channel activity

Author

Ding, Yanning, Brackenbury, William J., Onganer, Pinar U., Montano, Ximena, Porter, Louise M., Bates, Lucy F., and Djamgoz, Mustafa B. A.

Subjects
hormones, hormone substitutes, and hormone antagonists
Abstract

The main aim of this investigation was to determine whether a functional relationship existed between epidermal growth factor (EGF) and voltage-gated sodium channel (VGSC) upregulation, both associated with strongly metastatic prostate cancer cells. Incubation with EGF for 24 h more than doubled VGSC current density. Similar treatment with EGF significantly and dose-dependently enhanced the cells' migration through Transwell filters. Both the patch clamp recordings and the migration assay suggested that endogenous EGF played a similar role. Importantly, co-application of EGF and tetrodotoxin, a highly selective VGSC blocker, abolished 65% of the potentiating effect of EGF. It is suggested that a significant portion of the EGF-induced enhancement of migration occurred via VGSC activity.

Published
2008

17. correction: Warm-coding deficits and aberrant inflammatory pain in mice lacking P2X3

Author

Souslova, Veronika, Cesare, Paolo, Ding, Yanning, Akoplan, Armen N., Stanfa, Louise, Suzuki, Rie, Carpenter, Katherine, Nebenius-Oosthuizen, Daniela, Smith, Andrew J. H., Kidd, Emma J., and Wood, John N.

Abstract

Author(s): Veronika Souslova; Paolo Cesare; Yanning Ding; Armen N. Akoplan; Louise Stanfa; Rie Suzuki; Katherine Carpenter; Daniela Nebenius-Oosthuizen; Andrew J. H. Smith; Emma J. Kidd; John N. Wood Nature 407 [...]

Published
2001
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21. GTP‐induced tetrodotoxin‐resistant Na+current regulates excitability in mouse and rat small diameter sensory neurones

Author

Baker, Mark D., Chandra, Sonia Y., Ding, Yanning, Waxman, Stephen G., and Wood, John N.

Abstract

Peripheral pain thresholds are regulated by the actions of inflammatory mediators. Some act through G‐protein‐coupled receptors on voltage‐gated sodium channels. We have found that a low‐threshold, persistent tetrodotoxin‐resistant Na+current, attributed to NaV1.9, is upregulated by GTP and its non‐hydrolysable analogue GTP‐γ‐S, but not by GDP. Inclusion of GTP‐γ‐S (500 μm) in the internal solution led to an increase in maximal current amplitude of > 300 % within 5 min. In current clamp, upregulation of persistent current was associated with a more negative threshold for action potential induction (by 15–16 mV) assessed from a holding potential of −90 mV. This was not seen in neurones without the low‐threshold current or with internal GDP (P< 0.001). In addition, persistent current upregulation depolarized neurones. At −60 mV, internal GTP‐γ‐S led to the generation of spontaneous activity in initially silent neurones only when persistent current was upregulated. These findings suggest that regulation of the persistent current has important consequences for nociceptor excitability.

Published
2003
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22. A new member of the acidsensing ion channel family

Author

Akopian, Armen N., Chen, Chih-Cheng, Ding, Yanning, Cesare, Paolo, and Wood, John N.

Abstract

Acid-sensing ion channels (ASICs) are members of the epithelial sodium channel (ENaC)-degenerin family of two-pass transmembrane segment protein subunits which form multi-meric cation channels. Members of the ENaC-degenerin family are gated by stimuli as diverse as protons, peptides and mechanical distension. Here we describe a new member of the family, SPASIC or ASIC 4 (spinal cord ASIC) which is expressed throughout the central nervous system in an overlapping population of neurons that also express the ASIC subunit MDEG2. ASIC-4 which shows 44 identify with ASIC is developmentally regulated and expressed in a subset of sensory neurons as well as in the CNS. However, despite the strong homology with ASIC, the ASIC-4 transcript does not encode a proton gated cation channel.

Published
2000

23. Epidermal growth factor upregulates motility of Mat-LyLu rat prostate cancer cells partially via voltage-gated Na+ channel activity.

Author

Ding Y, Brackenbury WJ, Onganer PU, Montano X, Porter LM, Bates LF, and Djamgoz MB

Subjects
Animals, Male, Quinazolines, Rats, Tetrodotoxin pharmacology, Tyrphostins pharmacology, Cell Movement drug effects, Epidermal Growth Factor pharmacology, Ion Channel Gating drug effects, Prostatic Neoplasms pathology, Sodium Channels metabolism, Up-Regulation drug effects
Abstract

The main aim of this investigation was to determine whether a functional relationship existed between epidermal growth factor (EGF) and voltage-gated sodium channel (VGSC) upregulation, both associated with strongly metastatic prostate cancer cells. Incubation with EGF for 24 h more than doubled VGSC current density. Similar treatment with EGF significantly and dose-dependently enhanced the cells' migration through Transwell filters. Both the patch clamp recordings and the migration assay suggested that endogenous EGF played a similar role. Importantly, co-application of EGF and tetrodotoxin, a highly selective VGSC blocker, abolished 65% of the potentiating effect of EGF. It is suggested that a significant portion of the EGF-induced enhancement of migration occurred via VGSC activity., ((c) 2007 Wiley-Liss, Inc.)

Published
2008
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24. Sodium channels in primary sensory neurons: relationship to pain states.

Author

Wood JN, Akopian AN, Baker M, Ding Y, Geoghegan F, Nassar M, Malik-Hall M, Okuse K, Poon L, Ravenall S, Sukumaran M, and Souslova V

Subjects
Animals, Chromosome Mapping, Gene Expression Regulation, Humans, Pain genetics, Sodium Channels drug effects, Sodium Channels genetics, Tetrodotoxin pharmacology, Ganglia, Spinal physiopathology, Neurons, Afferent physiology, Pain physiopathology, Sodium Channels physiology
Abstract

Electrophysiological studies of dorsal root ganglion (DRG) neurons, and the results of PCR, Northern blot and in situ hybridization analyses have demonstrated the molecular diversity of Na+ channels that operate in sensory neurons. Several subtypes of alpha-subunit have been detected in DRG neurons and transcripts encoding all three beta-subunits are also present. Interestingly, one alpha subunit, Na(v)1.8, is selectively expressed in C-fibre and Adelta fibre associated sensory neurons that are predominantly involved in damage sensing. Another channel, Na(v).3, is selectively up regulated in a variety of models of neuropathic pain. In this review we focus on Na+ channels that are selectively expressed in DRG neurons as potential analgesic drug targets. In the absence of subtype specific inhibitors, the production of null mutant mice provides useful information on the specialized functions of particular Na+ channels. A refinement of this approach is to delete Na+ channel genes flanked by lox-P sites in the sensory ganglia of adult animals, using viruses to deliver the bacteriophage Cre recombinase enzyme.

Published
2002

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