Exchange proteins directly activated by cyclic adenosine monophosphate inhibitor reverses mechanical allodynia via the modification of astrocytes activity in the spinal cord

Qing, She; Chen, Junjie; Zhong, Chaochao; Huang, Saisai; Lu, Cui’e; Qin, Yibin

doi:10.21037/atm-21-5384

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Epac1 Is Involved In Chronic Pain1

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2023

2024

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Cited by 3 publications

(1 citation statement)

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“…Therefore, it can be inferred that EPAC1-Cav1 is a possible mechanism of CPSP. Inhibition of EPAC1 has also been shown to alleviate CPSP by inhibiting astrocyte activation [ 87 ].…”

Section: Epac1 Is Involved In Chronic Painmentioning

confidence: 99%

Role of EPAC1 in chronic pain

Jiang,

Zhao,

Zhang

et al. 2024

Biochemistry and Biophysics Reports

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“…Therefore, it can be inferred that EPAC1-Cav1 is a possible mechanism of CPSP. Inhibition of EPAC1 has also been shown to alleviate CPSP by inhibiting astrocyte activation [ 87 ].…”

Section: Epac1 Is Involved In Chronic Painmentioning

confidence: 99%

Role of EPAC1 in chronic pain

Jiang,

Zhao,

Zhang

et al. 2024

Biochemistry and Biophysics Reports

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Epac as a tractable therapeutic target

Slika

Mansour

Nasser

et al. 2023

European Journal of Pharmacology

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Inhibition of CXCR2 as a therapeutic target for chronic post-surgical pain: Insights from animal and cell models

Zhao,

Jian,

Chen

et al. 2024

Cytojournal

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Objective: Studies have shown that chemokines can stimulate the migration and activation of microglia to cause chronic post-surgical pain (CPSP). However, the involvement of C-X-C motif chemokine receptor 2 (CXCR2) as a new chemotactic factor in regulating CPSP and its underlying mechanism remains unclear. This study is to investigate the role of CXCR2 in the development of CPSP and reveal the underlying mechanism. Material and Methods: A rat model of skin/muscle incision and retraction was established, and treated with or without SB225002 (a selective inhibitor of CXCR2). In addition, the primary microglia cells induced by lipopolysaccharide were applied as an in vitro model for CPSP and treated individually with si-negative control (NC), si-CXCR2, si-CXCR2+Interleukin (IL)-6 (an agonist of the janus kinase (JAK)/signal transducers and activators of transcription (STAT)3 signaling pathway), si-CXCR2+IL-6+si-NC, or si-CXCR2+IL-6+si-exchange protein 1 directly activated by cAMP (EPAC1). Results: Results from the database analysis showed that CXCR2 and JAK/STAT3 signaling pathway-related genes, including JAK1, STAT3, and EPAC1, were mainly involved in the development of CPSP. Inhibition of CXCR2 expression not only inhibited the reduction of foot pain threshold in CPSP models but also led to a decreased expression of CXCR2 and the phosphorylation levels of JAK and STAT3 in both animal and cell models. Furthermore, inhibition of EPAC1 expression can hinder the regulatory function of CXCR2. Conclusion: This study indicated that the high expression of CXCR2 activates the JAK1/STAT3 signaling pathway, enhances EPAC1 activation in microglial cells, and exacerbates CPSP.

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Exchange proteins directly activated by cyclic adenosine monophosphate inhibitor reverses mechanical allodynia via the modification of astrocytes activity in the spinal cord

Cited by 3 publications

References 45 publications

Role of EPAC1 in chronic pain

Role of EPAC1 in chronic pain

Epac as a tractable therapeutic target

Inhibition of CXCR2 as a therapeutic target for chronic post-surgical pain: Insights from animal and cell models

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