Involvement of LPA1 receptor signaling in cerebral ischemia-induced neuropathic pain

Halder, Sebok Kumar; Yano, Ryo; Chun, Jerold; Ueda, Hiroshi

doi:10.1016/j.neuroscience.2013.01.005

Cited by 35 publications

(27 citation statements)

References 45 publications

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“…Neuropathic pain is related to changes in the current thresholds of sensory fibers. In previous studies, neuropathic pain model mice has been found be to be decreased in the 2000-Hz (Aβ fibers) and 250-Hz (Aδ fibers) current thresholds and increased or unchanged in 5-Hz (C fibers) current thresholds compared with those of control mice 28,29 . In the present study, TNX deficiency significantly decreased the current thresholds for responses to transcutaneous sine wave stimuli at frequencies of 250 Hz and 2000 Hz (Fig.…”

Section: Discussionmentioning

confidence: 85%

Mechanical allodynia in mice with tenascin-X deficiency associated with Ehlers-Danlos syndrome

Okuda‐Ashitaka

Kakuchi

Kakumoto

et al. 2020

Sci Rep

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tenascin-X (tnX) is a member of the extracellular matrix glycoprotein tenascin family, and tnX deficiency leads to Ehlers-Danlos syndrome, a heritable human disorder characterized mostly by skin hyperextensibility, joint hypermobility, and easy bruising. TNX-deficient patients complain of chronic joint pain, myalgia, paresthesia, and axonal polyneuropathy. However, the molecular mechanisms by which TNX deficiency complicates pain are unknown. Here, we examined the nociceptive behavioral responses of TNX-deficient mice. Compared with wild-type mice, TNX-deficient mice exhibited mechanical allodynia but not thermal hyperalgesia. TNX deficiency also increased pain sensitivity to chemical stimuli and aggravated early inflammatory pain elicited by formalin. TNX-deficient mice were significantly hypersensitive to transcutaneous sine wave stimuli at frequencies of 250 Hz (Aδ fiber responses) and 2000 Hz (Aβ fiber responses), but not to stimuli at frequency of 5 Hz (C fiber responses). in addition, the phosphorylation levels of extracellular signal-related kinase, an active neuronal marker, and the activity of nADpH-diaphorase, a neuronal nitric oxide activation marker, were enhanced in the spinal dorsal horns of TNX-deficient mice. These results suggest that TNX deficiency contributes to the development of mechanical allodynia and hypersensitivity to chemical stimuli, and it induces hypersensitization of myelinated A fibers and activation of the spinal dorsal horn.

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Section: Discussionmentioning

confidence: 85%

Mechanical allodynia in mice with tenascin-X deficiency associated with Ehlers-Danlos syndrome

Okuda‐Ashitaka

Kakuchi

Kakumoto

et al. 2020

Sci Rep

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“…Specifically, to illustrate the therapeutic mechanism of the combination group, we base on the published literatures to further explain the differentially expressed genes of the pathways in BJ group. Neuropathic pain signaling in dorsal horn neurons arises from an injury discharge originating at the site of nerve injury which may result from stroke and other causes . Molecules such as BDNF and CAMK1G in this pathway in our experimental data showed down‐regulated expressions, which can directly or indirectly activate N‐methyl‐D‐aspartate‐(NMDA) and α ‐amino‐3‐hydroxy‐5‐methyl‐4‐isoxazolepro‐pionic acid (AMPA) receptor, the dependent receptor of calcium ions, leading to calcium influx restrictedly.…”

Section: Discussionmentioning

confidence: 70%

Convergent and Divergent Pathways Decoding Hierarchical Additive Mechanisms in Treating Cerebral Ischemia–Reperfusion Injury

Zhang

Chen

et al. 2013

CNS Neurosci Ther

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“…It should be noted that, one of the potential markers for DWI positivity was a low level of LPA. These molecules, and their signaling through their cognate receptor LPA1, have been implicated in the generation of ischemia-related neuropathic pain (Halder et al, 2013). Moreover, some molecules from this family are also considered angiogenic factors (Ren et al, 2011, Binder et al, 2013).…”

Section: Discussionmentioning

confidence: 99%

Metabolomics Predicts Neuroimaging Characteristics of Transient Ischemic Attack Patients

et al. 2016

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BackgroundNeuroimaging is essential for the diagnosis and prognosis of transient ischemic attack (TIA). The discovery of a plasmatic biomarker related to neuroimaging findings is of enormous interest because, despite its relevance, magnetic resonance diffusion weighted imaging (DWI) is not always available in all hospitals that attend to TIA patients.MethodsMetabolomic analyses were performed by liquid chromatography coupled to mass spectrometry in order to establish the metabolomic patterns of positive DWI, DWI patterns and acute ischemic lesion volumes. We used these methods with an initial TIA cohort of 129 patients and validated them with a 2nd independent cohort of 152 patients.FindingsPositive DWI was observed in 115 (40.9%) subjects and scattered pearls in one arterial territory was the most frequent lesion pattern (35.7%). The median acute ischemic lesion volume was 0.33 (0.15–1.90) cm3. We detected a specific metabolomic profile common to both cohorts for positive DWI (11 molecules including creatinine, threoninyl-threonine, N-acetyl-glucosamine, lyso phosphatidic acid and cholesterol-related molecules) and ischemic lesion volume (10 molecules including lysophosphatidylcholine, hypoxanthine/threonate, and leucines). Moreover lysophospholipids and creatinine clearly differed the subcortical DWI pattern from other patterns.InterpretationThere are specific metabolomic profiles associated with representative neuroimaging features in TIA patients. Our findings could allow the development of serum biomarkers related to acute ischemic lesions and specific acute ischemic patterns.

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Involvement of LPA1 receptor signaling in cerebral ischemia-induced neuropathic pain

Cited by 35 publications

References 45 publications

Mechanical allodynia in mice with tenascin-X deficiency associated with Ehlers-Danlos syndrome

Mechanical allodynia in mice with tenascin-X deficiency associated with Ehlers-Danlos syndrome

Convergent and Divergent Pathways Decoding Hierarchical Additive Mechanisms in Treating Cerebral Ischemia–Reperfusion Injury

Metabolomics Predicts Neuroimaging Characteristics of Transient Ischemic Attack Patients

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