Shiroh Kishioka

ORCID: 0009-0005-9067-7553
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About
Contact & Profiles
Research Areas
  • Pain Mechanisms and Treatments
  • Neuropeptides and Animal Physiology
  • Neurotransmitter Receptor Influence on Behavior
  • Receptor Mechanisms and Signaling
  • Nerve injury and regeneration
  • Neuroscience and Neuropharmacology Research
  • Pharmacological Effects of Natural Compounds
  • Nicotinic Acetylcholine Receptors Study
  • Acupuncture Treatment Research Studies
  • Pharmacological Receptor Mechanisms and Effects
  • Stress Responses and Cortisol
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Dermatology and Skin Diseases
  • Healthcare and Venom Research
  • Botulinum Toxin and Related Neurological Disorders
  • Ion channel regulation and function
  • Urticaria and Related Conditions
  • Adipose Tissue and Metabolism
  • Exercise and Physiological Responses
  • Pharmacological Effects and Toxicity Studies
  • Drug Transport and Resistance Mechanisms
  • Epilepsy research and treatment
  • Cancer Treatment and Pharmacology
  • Peroxisome Proliferator-Activated Receptors
  • Pain Management and Placebo Effect

Takarazuka University of Medical and Health Care
2020-2024

Wakayama Medical University
2011-2020

Pharmac
2020

Wakayama University
2009-2020

Saitama Prefectural University
2015

Wake Forest University
2015

Japan Society for the Promotion of Science
2009

Osaka Sangyo University
2009

University of Michigan
1996-2000

National College of Technology, Wakayama College
1999

In the present study, we investigated role of macrophage inflammatory protein-1α (MIP-1α) in pathogenesis neuropathic pain following partial sciatic nerve ligation (PSL) mice. MIP-1α mRNA and its protein were dramatically up-regulated after PSL, was localized on macrophages Schwann cells injured (SCN). PSL-induced long-lasting tactile allodynia thermal hyperalgesia prevented by perineural injection anti-MIP-1α (2 ng). Intraneural (20 ng) (100 recombinant elicited sham-operated limb....

10.1016/j.pain.2010.02.025 article EN Pain 2010-03-15

The small-molecule AT-121 is an agonist of nociceptin and mu opioid peptide receptors mediates analgesia without opioid-associated side effects in nonhuman primates.

10.1126/scitranslmed.aar3483 article EN Science Translational Medicine 2018-08-29

There is increasing evidence that inflammatory (M1-polarized) macrophages drive the nonresolving neuroinflammation causes neuropathic pain after nerve injury. As interleukin-4 (IL-4) promotes suppressive (M2-polarized) state in macrophages, we examined whether exploiting an IL-4-mediated pathway could ameliorate M1 macrophage-dependent pain. The mRNA and protein expression of IL-4 receptor α chain (IL-4Rα) were upregulated accumulating F4/80 injured sciatic (SCN). In mouse macrophage cell...

10.1097/j.pain.0000000000000097 article EN Pain 2015-01-28

Nerve injury may result in neuropathic pain, characterized by allodynia and hyperalgesia. Accumulating evidence suggests the existence of a molecular substrate for pain produced neurons, glia, immune cells. Here, we show that leptin, an adipokine exclusively adipocytes, is critical development tactile through macrophage activation mice with partial sciatic nerve ligation (PSL). PSL increased leptin expression adipocytes distributed at epineurium injured (SCN). Leptin-deficient animals, ob/ob...

10.1073/pnas.0903524106 article EN Proceedings of the National Academy of Sciences 2009-07-22

Although there is growing evidence showing that the involvement of chemokines in pathogenesis neuropathic pain associated with neuroinflammation, details are unclear. We investigated C-X-C chemokine ligand type 2 [macrophage inflammatory protein (MIP-2)]/C-X-C receptor (CXCR2) axis and epigenetic regulation these molecules after peripheral nerve injury. Expression MIP-2 CXCR2 were up-regulated localized on accumulated neutrophils macrophages injured sciatic (SCN) partial ligation (PSL)....

10.1124/jpet.111.187724 article EN Journal of Pharmacology and Experimental Therapeutics 2011-12-01

Peripheral neuroinflammation caused by activated immune cells can provoke neuropathic pain. Herein, we investigate the actions of macrophages and T through glucocorticoid-induced tumor neurosis factor receptor ligand (GITRL) its (GITR) in After partial sciatic nerve ligation (PSL) enhanced green fluorescent protein (eGFP) chimeric mice generated transplantation eGFP(+) bone marrow cells, macrophages, markedly migrated to injured site after PSL. Administration agents deplete...

10.1074/jbc.m115.636506 article EN cc-by Journal of Biological Chemistry 2015-03-19

Abstract Background Neuropathic pain is caused by neural damage or dysfunction and neuropathic pain‐related symptoms are resistant to conventional analgesics. Neuroinflammation due the cytokine‐chemokine network may play a pivotal role in pain. We demonstrate that macrophage inflammatory protein‐1β ( MIP ‐1β) participates Methods Mice received partial sciatic nerve ligation PSL ), tactile allodynia thermal hyperalgesia were assessed von F rey test H argreaves test, respectively. Agents...

10.1002/j.1532-2149.2012.00146.x article EN European Journal of Pain 2012-04-24

Despite growing evidence suggesting that spinal microglia play an important role in the molecular mechanism underlying experimental neuropathic pain (NP) male rodents, regarding sex-dependent of these NP is insufficient. In this study, we evaluated effects microglial regulation on using Gi-designer receptors exclusively activated by designer drugs (Gi-DREADD) driven microglia-specific Cx3cr1 promoter. For Cre-dependent expression human Gi-coupled M4 muscarinic (hM4Di) CX3C chemokine receptor...

10.3389/fphar.2020.00925 article EN cc-by Frontiers in Pharmacology 2020-06-19

Pruritus (itch sensation) is the most common side effect associated with spinal administration of morphine given to humans for analgesia. A variety agents have been proposed as antipruritics poorly understood mechanisms and they are effective variable success. κ-Opioid agonists possess several actions that opposite μ-opioid agonists. We investigate role κ-opioid receptors (KORs) in morphine-induced scratching antinociception monkeys. Scratching responses were counted by observers blinded...

10.1124/jpet.102.044909 article EN Journal of Pharmacology and Experimental Therapeutics 2003-01-21

Chronic neuroinflammation may be a critical component of intractable inflammatory diseases, including neuropathic pain. Because angiogenesis as result vascular endothelial growth factor (VEGF) signaling plays pivotal role in inflammation, we focused on the mechanisms VEGF-regulated pain mice. The mRNA and protein expression VEGFA were up-regulated injured sciatic nerve after partial ligation (PSL). was localized to accumulated macrophages neutrophils derived from bone marrow. Up-regulation...

10.1111/jnc.12614 article EN Journal of Neurochemistry 2013-11-21

Neuro-immune interaction underlies chronic neuroinflammation and aberrant sensory processing resulting in neuropathic pain. Despite the pathological significance of both neuroinflammation-driven peripheral sensitization spinal sensitization, functional relationship between these two distinct events has not been understood.In this study, we determined whether inhibition inflammatory macrophages by administration α4β2 nicotinic acetylcholine receptor (nAChR) agonists improves pain affects...

10.1186/s12974-018-1133-5 article EN cc-by Journal of Neuroinflammation 2018-03-27

This study characterized the antinociceptive, respiratory and heart rate effects of cannabinoid receptor agonists Δ-9-tetrahydrocannabinol (Δ-9-THC) WIN 55212 {( R )-(+)-2,3-dihydro-5-methyl-3-[(4-morpholinyl)methyl]pyrol-[1,2,3-de]-1,4-benzoxazin-6-yl)(1-naphtalenyl)methanone monomethanesulfonate}, N-arachidonyl ethanolamide (anandamide) mu kappa opioid heroin U69593, alone in conjunction with a antagonist, SR 141716A [N-(piperidin-1–1-yl)-5-(4-chlorophenyl)-1(2,4-dichlorophenyl)-4-methyl-1...

10.1016/s0022-3565(24)37642-6 article EN Journal of Pharmacology and Experimental Therapeutics 1998-08-01

Inflammatory macrophages play a fundamental role in neuropathic pain. In this study, we demonstrate the effects of peripheral interleukin-13 (IL-13) on pain after partial sciatic nerve (SCN) ligation (PSL) mice. IL-13 receptor α1 was upregulated accumulating injured SCN PSL. Treatment with reduced inflammatory macrophage-dominant molecules and increased suppressive cultured lipopolysaccharide-stimulated peritoneal ex vivo subjected to Moreover, perineural administration relieved tactile...

10.1016/j.jphs.2016.11.005 article EN cc-by-nc-nd Journal of Pharmacological Sciences 2016-12-23
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