Angiotensin (1–7) Attenuates the Nociceptive Behavior Induced by Substance P and NMDA &lt;i&gt;via&lt;/i&gt; Spinal MAS1

Yamagata, Ryota; Nemoto, Wataru; Fujita, Maho; Nakagawasai, Osamu; Tanno, Koichi

doi:10.1248/bpb.b20-01004

Cited by 7 publications

(6 citation statements)

References 20 publications

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“…There were 13 genes involved in neuroactive ligand‒receptor interactions: Glra1,Grpr,Tbxa2r,Edn1,Lhb,P2rx1,Mas1,Galr3,Chrne,Ucn,Fpr1,Fpr2,Ghrl. Previous studies have shown that the gastrin-releasing peptide receptor ( Grpr ), 39 Spinal Mas1, 40 Galr3 , 41 Nos2 , 42 Arg 1 43 , Ccl11 and S100a8 44 were closely involved with neuropathic pain or inflammatory pain. KEGG enrichment pathway analysis and previous study results suggested that the mechanism of neuropathic pain in IRF4 knockout mice may be related to Grpr, Mas1, Galr3, Nos2, Arg1, Ccl11, Ptgs2, and S100a8.…”

Section: Discussionmentioning

confidence: 99%

RNA-seq analysis revealed genes associated with neuropathic pain induced by chronic compressive injury in interferon regulatory factors 4 knockout mice

Peng,

Wu,

et al. 2023

Hum Exp Toxicol

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Objective To explore the differential expression of genes between wild-type chronic compressive injury (CCI) mice (WT-CCI) and interferon regulatory factors 4 (IRF4) knockout CCI mice (KO-CCI) by RNA-seq analysis of the mouse spinal cord. Methods RNA-seq analysis of the spinal cord tissue of the chronic sciatic nerve ligation mice and Gene Ontology and Kyoto Encyclopedia of Genes and Genomes analyses were used. Results A total of 104 genes were up-regulated and 116 genes were down-regulated in spinal cord of the mice in IRF4 knockout (KO-CCI) group compared with that in the wild-type CCI (WT-CCI) group. There were 1472 differentially expressed genes in the biological process group, 62 differentially expressed genes in the cellular component group, and 163 differentially expressed genes in the molecular function group in KO-CCI mice. A total of 14 genes related to inflammatory reactions were differentially expressed. Real-time PCR results confirmed that Pparg and Grpr mRNA expression was up-regulated and Arg 1 and Ccl11 mRNA expression was down-regulated in the KO-CCI group. Conclusion IRF4 is involved in neuropathic pain in CCI mice, IRF4 may participate in neuropathic pain by regulating Grpr, Mas1, Galr3, Nos2, Arg1, Ccl11, Ptgs2, S100a8, Pparg, Cd40, Has2, Gpr151, Il123a, Capns2, Ankrd1, Ccnb1, and Nppb genes.

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Section: Discussionmentioning

confidence: 99%

RNA-seq analysis revealed genes associated with neuropathic pain induced by chronic compressive injury in interferon regulatory factors 4 knockout mice

Peng,

Wu,

et al. 2023

Hum Exp Toxicol

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“…The activity linked to AT2Rs is similar in general; however, with respect to pain transmission, this is not the case. The possible analgesic effect of Ang (1-7) was investigated following mostly local (intraplantar [21,23] or intrathecal [34,[89][90][91][92][93]) administration. Studies using intraplantar administration reported that Ang (1-7) attenuated PGE2 [21,23,90,91] or carrageenan [23] induced inflammatory mechanical hyperalgesia.…”

Section: Mas Receptor Agonistsmentioning

confidence: 99%

“…Intrathecal administration of Ang (1-7) resulted in a decrease in spontaneous nociceptive behavior induced by intrathecal AngII [91], AngIII [92], substance P or NMDA [34]. Furthermore, intrathecal Ang (1-7) showed an antiallodynic and antihyperalgesic effect in neuropathic pain induced by CCI [89], STZ [90], or genetic model of diabetes (ob/ob mice) [93].…”

Section: Mas Receptor Agonistsmentioning

confidence: 99%

“…Accumulating evidence has proven that drugs affecting the renin-angiotensin system can modulate pain transmission [17][18][19][20][21][22][23][24][25][26][27][28][29][30][31][32][33][34]. Recent studies have also shown that drugs mimic or antagonize angiotensin type 1 and 2 (AT1R and AT2R) receptor-mediated actions do produce a beneficial analgesic effect in rodent models of chronic pain types [17,20,22,28,29,[35][36][37][38].…”

Section: Introductionmentioning

confidence: 99%

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Shedding Light on the Pharmacological Interactions between μ-Opioid Analgesics and Angiotensin Receptor Modulators: A New Option for Treating Chronic Pain

et al. 2021

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The current protocols for neuropathic pain management include µ-opioid receptor (MOR) analgesics alongside other drugs; however, there is debate on the effectiveness of opioids. Nevertheless, dose escalation is required to maintain their analgesia, which, in turn, contributes to a further increase in opioid side effects. Finding novel approaches to effectively control chronic pain, particularly neuropathic pain, is a great challenge clinically. Literature data related to pain transmission reveal that angiotensin and its receptors (the AT1R, AT2R, and MAS receptors) could affect the nociception both in the periphery and CNS. The MOR and angiotensin receptors or drugs interacting with these receptors have been independently investigated in relation to analgesia. However, the interaction between the MOR and angiotensin receptors has not been excessively studied in chronic pain, particularly neuropathy. This review aims to shed light on existing literature information in relation to the analgesic action of AT1R and AT2R or MASR ligands in neuropathic pain conditions. Finally, based on literature data, we can hypothesize that combining MOR agonists with AT1R or AT2R antagonists might improve analgesia.

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“…The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) virus enters the human body through angiotensin converting enzyme-2 (ACE-2) receptors on the surface of human cells and causes disease [2,3]. ACE2 receptors are also expressed on the surface of spinal cord cells; whether spinal cord neurons are concerned in COVID-19 is still unknown [4,5]. A spectrum of neuroimaging abnormalities has been described in patients with COVID-19, the most common of which are acute ischemic stroke, cortical FLAIR signal abnormality, cerebral microbleeds, leptomeningeal enhancement, cytotoxic lesions in the splenium of the corpus callosum and other manifestations of encephalitis [6].…”

Section: Introductionmentioning

confidence: 99%

COVID-19-Associated Acute Transverse Myelitis: A Case Series of a Rare Neurologic Condition

Ali¹,

Mohammed²,

Zada³

et al. 2021

Cureus

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Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) viral infection is not confined to the respiratory system, but has also shown extra-pulmonary invasion including the nervous system. About 36.4% of hospitalized patients in China with confirmed coronavirus disease 2019 (COVID-19) infection had neurological manifestations. SARS-CoV-2 virus enters the human body through angiotensin converting enzyme-2 (ACE-2) receptors on the surface of human cells and causes disease. ACE2 receptors are also expressed on the surface of spinal cord cells. More rare neurologic conditions have been reported in the literature to be associated with COVID-19 such as acute transverse myelitis (ATM), Guillain Barre syndrome, acute flaccid myelitis, etc. We report two cases of confirmed COVID-19 who presented four to five days of their COVID-19 symptoms and progressive bilateral lower limb weakness and urinary retention.ATM is an acquired spinal cord disorder. ATM is a relatively common neurological complication of COVID-19, accounting for 1.2% of all neurological complications associated with COVID-19. The mechanism by which COVID-19 causes ATM is not completely understood but has been assumed to be due to the structural resemblance of RNA viruses. Entrance of SARS-CoV-2 to the nervous system can take place through two pathways, either directly or indirectly. The direct pathway is through trans-synaptic transmission from the peripheral nervous system or by hematogenous spread into the blood-brain barrier through ACE-2, while the indirect pathway is through a systemic immune response.

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Angiotensin (1–7) Attenuates the Nociceptive Behavior Induced by Substance P and NMDA <i>via</i> Spinal MAS1

Cited by 7 publications

References 20 publications

RNA-seq analysis revealed genes associated with neuropathic pain induced by chronic compressive injury in interferon regulatory factors 4 knockout mice

RNA-seq analysis revealed genes associated with neuropathic pain induced by chronic compressive injury in interferon regulatory factors 4 knockout mice

Shedding Light on the Pharmacological Interactions between μ-Opioid Analgesics and Angiotensin Receptor Modulators: A New Option for Treating Chronic Pain

COVID-19-Associated Acute Transverse Myelitis: A Case Series of a Rare Neurologic Condition

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