Compounds > 1-1--((4-4-7-7-tetramethyl)-4-7-diazaundecamethylene)bis-4-(3-methyl-2-3-dihydro(benzo-1-3-oxazole)-2-methylidine)quinolinium--tetraiodide

1-1--((4-4-7-7-tetramethyl)-4-7-diazaundecamethylene)bis-4-(3-methyl-2-3-dihydro(benzo-1-3-oxazole)-2-methylidine)quinolinium--tetraiodide and Inflammation

1-1--((4-4-7-7-tetramethyl)-4-7-diazaundecamethylene)bis-4-(3-methyl-2-3-dihydro(benzo-1-3-oxazole)-2-methylidine)quinolinium--tetraiodide has been researched along with Inflammation* in 1 studies

Other Studies

1 other study(ies) available for 1-1--((4-4-7-7-tetramethyl)-4-7-diazaundecamethylene)bis-4-(3-methyl-2-3-dihydro(benzo-1-3-oxazole)-2-methylidine)quinolinium--tetraiodide and Inflammation

Article	Year
Proteomic analysis uncovers novel actions of the neurosecretory protein VGF in nociceptive processing. The Journal of neuroscience : the official journal of the Society for Neuroscience, 2009, Oct-21, Volume: 29, Issue:42 Peripheral tissue injury is associated with changes in protein expression in sensory neurons that may contribute to abnormal nociceptive processing. We used cultured dorsal root ganglion (DRG) neurons as a model of axotomized neurons to investigate early changes in protein expression after nerve injury. Comparing protein levels immediately after DRG dissociation and 24 h later by proteomic differential expression analysis, we found a substantial increase in the levels of the neurotrophin-inducible protein VGF (nonacronymic), a putative neuropeptide precursor. In a rodent model of nerve injury, VGF levels were increased within 24 h in both injured and uninjured DRG neurons, and the increase persisted for at least 7 d. VGF was also upregulated 24 h after hindpaw inflammation. To determine whether peptides derived from proteolytic processing of VGF participate in nociceptive signaling, we examined the spinal effects of AQEE-30 and LQEQ-19, potential proteolytic products shown previously to be bioactive. Each peptide evoked dose-dependent thermal hyperalgesia that required activation of the mitogen-activated protein kinase p38. In addition, LQEQ-19 induced p38 phosphorylation in spinal microglia when injected intrathecally and in the BV-2 microglial cell line when applied in vitro. In summary, our results demonstrate rapid upregulation of VGF in sensory neurons after nerve injury and inflammation and activation of microglial p38 by VGF peptides. Therefore, VGF peptides released from sensory neurons may participate in activation of spinal microglia after peripheral tissue injury. Topics: Animals; Benzoxazoles; Cells, Cultured; Disease Models, Animal; Dose-Response Relationship, Drug; Enzyme Inhibitors; Freund's Adjuvant; Ganglia, Spinal; Hyperalgesia; Imidazoles; Inflammation; Male; Microglia; Neurons, Afferent; Neuropeptides; Nociceptors; Organ Culture Techniques; Pain Measurement; Peptides; Peripheral Nervous System Diseases; Proteomics; Pyridines; Quinolinium Compounds; Rats; Rats, Sprague-Dawley; Reaction Time; Receptor, trkA; Receptors, Purinergic P2; Receptors, Purinergic P2X3; Signal Transduction; Spinal Cord Injuries; Time Factors; Up-Regulation	2009

Article

Year

Proteomic analysis uncovers novel actions of the neurosecretory protein VGF in nociceptive processing.

The Journal of neuroscience : the official journal of the Society for Neuroscience, 2009, Oct-21, Volume: 29, Issue:42

Peripheral tissue injury is associated with changes in protein expression in sensory neurons that may contribute to abnormal nociceptive processing. We used cultured dorsal root ganglion (DRG) neurons as a model of axotomized neurons to investigate early changes in protein expression after nerve injury. Comparing protein levels immediately after DRG dissociation and 24 h later by proteomic differential expression analysis, we found a substantial increase in the levels of the neurotrophin-inducible protein VGF (nonacronymic), a putative neuropeptide precursor. In a rodent model of nerve injury, VGF levels were increased within 24 h in both injured and uninjured DRG neurons, and the increase persisted for at least 7 d. VGF was also upregulated 24 h after hindpaw inflammation. To determine whether peptides derived from proteolytic processing of VGF participate in nociceptive signaling, we examined the spinal effects of AQEE-30 and LQEQ-19, potential proteolytic products shown previously to be bioactive. Each peptide evoked dose-dependent thermal hyperalgesia that required activation of the mitogen-activated protein kinase p38. In addition, LQEQ-19 induced p38 phosphorylation in spinal microglia when injected intrathecally and in the BV-2 microglial cell line when applied in vitro. In summary, our results demonstrate rapid upregulation of VGF in sensory neurons after nerve injury and inflammation and activation of microglial p38 by VGF peptides. Therefore, VGF peptides released from sensory neurons may participate in activation of spinal microglia after peripheral tissue injury.

Topics: Animals; Benzoxazoles; Cells, Cultured; Disease Models, Animal; Dose-Response Relationship, Drug; Enzyme Inhibitors; Freund's Adjuvant; Ganglia, Spinal; Hyperalgesia; Imidazoles; Inflammation; Male; Microglia; Neurons, Afferent; Neuropeptides; Nociceptors; Organ Culture Techniques; Pain Measurement; Peptides; Peripheral Nervous System Diseases; Proteomics; Pyridines; Quinolinium Compounds; Rats; Rats, Sprague-Dawley; Reaction Time; Receptor, trkA; Receptors, Purinergic P2; Receptors, Purinergic P2X3; Signal Transduction; Spinal Cord Injuries; Time Factors; Up-Regulation

2009