Third Special Issue on Mechanisms of Pain and Itch

Ji, Ru-Rong

doi:10.1007/s12264-022-00851-8

Cited by 4 publications

(2 citation statements)

References 27 publications

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“…12 Inflammatory pain is a type of chronic pathologic pain that decreases a patient's quality of life and causes considerable economic losses to society. [13][14][15][16][17][18] In our present study, we used the classic CFA-induced model, involving a subcutaneous injection of CFA into the left hind paw of rats, to study the mechanisms of chronic inflammatory pain. Successfully induced rats in the CFA group showed significantly reduced activity and obvious redness and swelling in their left hind paw compared with the contralateral right hind paw.…”

Section: Discussionmentioning

confidence: 99%

LncRNA MEG3-TRPV1 signaling regulates chronic inflammatory pain in rats

Zhang

Peng

et al. 2022

Mol Pain

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Osteoarthritis (OA) is a common osteoarthropathy with chronic inflammatory pain as the core symptom in middle-aged and elderly people. LncRNA MEG3 (Maternally expressed gene 3) is involved in the development of OA via regulation of angiogenesis, which causes the activation and overexpression of transient receptor potential vanilloid type-1 (TRPV1). In this study, we investigated the mechanism of MEG3-TRPV1 signaling in chronic inflammatory pain (CIP) of rat model. Chronic inflammatory pain was modeled using subcutaneous microinjection of complete Freund’s adjuvant (CFA) into the left hind paw of rats. We showed that TRPV1 mRNA and protein were significantly increased, while MEG3 mRNA was significantly decreased, in the DRG and SDH of CFA-induced rats. In addition, intrathecal injection of MEG3-overexpressing lentivirus significantly downregulated TRPV1 expression and alleviated chronic inflammatory pain in CFA-induced rats. Treatment with a TRPV1 antagonist also significantly relieved chronic inflammatory pain in CFA-induced rats. In general, our results reveal that MEG3 alleviates chronic inflammatory pain by downregulating TRPV1 expression. These findings may provide new therapeutic targets in the treatment of patients with OA.

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Section: Discussionmentioning

confidence: 99%

LncRNA MEG3-TRPV1 signaling regulates chronic inflammatory pain in rats

Zhang

Peng

et al. 2022

Mol Pain

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“…Interestingly, the timing and type of contribution among these cells are found to be different [6]. Experimental results also show that glial modulation can potentially be a novel target for itch modulation [7]. This focused review aims to present what is known about the contribution of astrocytes, microglia, satellite glial cells (SGCs), and Schwann cells (SCs) in the development or persistence of itch and how glial modulation could be a potential future target in the therapeutic options for CI.…”

Section: Introductionmentioning

confidence: 86%

Contribution of Central and Peripheral Glial Cells in the Development and Persistence of Itch: Therapeutic Implication of Glial Modulation

Gazerani

2023

Neuroglia

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Chronic itch (CI) is an unpleasant skin sensation accompanied by an intense scratching desire that lasts 6 weeks or longer. Despite the high prevalence and negative impact on affected individuals and a huge healthcare burden, CI mechanisms are only partially understood, and consequently, treatment of CI remains sub-optimal. The complexity of CI treatment also stems from the comorbid existence of persistent itch with other somatic and psychological disorders. Etiologies of CI are multiple and diverse, although CI is often a result of dermatologically related conditions such as atopic dermatitis and psoriasis. Unfolding the pathophysiology of CI can provide possibilities for better therapy. Itch signaling is complex and neurons and non-neuronal cells play a role. This review focuses on recent findings on the role of glial cells in itch. Central glia (astrocytes and microglia) and peripheral glia (satellite glial cells and Schwann cells) are found to contribute to the development or persistence of itch. Hence, glial modulation has been proposed as a potential option in CI treatment. In experimental models of itch, the blockade of signal transducer and the activator of transcription (STAT) 3-mediated reactive astrogliosis have been shown to suppress chronic itch. Administration of a microglial inhibitor, minocycline, has also been demonstrated to suppress itch-related microglial activation and itch. In sensory ganglia, gap-junction blockers have successfully blocked itch, and hence, gap-junction-mediated coupling, with a potential role of satellite glial cells have been proposed. This review presents examples of glial involvement in itch and opportunities and challenges of glial modulation for targeting itch.

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