Effect of cGMP-activated aquaporin 1 on TRPV4 in rats with allodynia induced by chronic compression of the dorsal root ganglion

Wei, Hui; Gao, Wen-Shuang; Qi, Lei; Jia, Lei; Qu, Yu-Juan; Yue, Shouwei; Zhang, Yang

doi:10.1016/j.neulet.2019.134630

Cited by 10 publications

(6 citation statements)

References 18 publications

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“…Aquaporins, mainly responsible for water transport and clearance, play an important role in the development of CNS diseases. Studies have shown that AQP1, AQP2, AQP4, AQP5, and AQP9 are directly or indirectly related to neuropathic pain, and among them, AQP4 is closely related to neuropathic pain [13][14][15][16][17]. The CNS is sensitive to changes in the surrounding environment and lacks traditional lymphatic pathways.…”

Section: Discussionmentioning

confidence: 99%

“…In a clinical study on leprosy, Salgado et al [28] found that AQP1 may be involved in the loss of sensation or lep-rosy neuropathic pain. Moreover, animal experiments have shown that inhibition of AQP1 expression alleviated neuropathic pain caused by chronic dorsal root ganglion compression and melatonin decreased mechanical allodynia by regulating AQP1 [14,29]. In the treatment of a series of diseases targeting AQP1, many traditional Chinese medicines were found to play therapeutic effects by regulating AQP1, such as alpinetin, dachengqi, and shenmai injection [30][31][32].…”

Section: Aqp1mentioning

confidence: 99%

“…Studies have shown that several aquaporins are closely related to neuropathic pain, including aquaporin 1 (AQP1), aquaporin 2 (AQP2), aquaporin 4 (AQP4), aquaporin 5 (AQP5) and aquaporin 9 (AQP9) [13][14][15][16][17]. Since AQPs promote water and solute transport and are involved in the occurrence and development of many diseases, it is logical that AQPs are involved in the occurrence and development of neuropathic pain.…”

Section: Introductionmentioning

confidence: 99%

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Aquaporins and Neuropathic Pain

Wang¹,

Xu²,

Xu³

et al. 2023

Front. Biosci. (Landmark Ed)

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Neuropathic pain is a chronic secondary pain condition resulting from lesions or diseases of the peripheral or central nervous system (CNS). Neuropathic pain is closely related to edema, inflammation, increased neuronal excitability, and central sensitization caused by glutamate accumulation. Aquaporins (AQPs), mainly responsible for the transport and clearance of water and solute, play important roles in developing CNS diseases, especially neuropathic pain. This review focuses on the interaction of AQPs with neuropathic pain, and the potential of AQPs, especially aquaporins 4, as therapeutic targets.

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Section: Discussionmentioning

confidence: 99%

Section: Aqp1mentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Aquaporins and Neuropathic Pain

Wang¹,

Xu²,

Xu³

et al. 2023

Front. Biosci. (Landmark Ed)

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“…There are 13 known aquaporins in mammals, whose main function is to regulate intracellular and intercellular water flow [ 43 ]. Earlier research has established that AQP1, AQP4, AQP2 and AQP9 are associated with spinal cord injury- or nerve injury-induced nerve pain in rats [ 44–47 ]. AQP5, an AQP family member, is highly expressed in astrocytes and is related to the hypoxia of astrocytes [ 48 ].…”

Section: Discussionmentioning

confidence: 99%

Targeting Forkhead box O1-aquaporin 5 axis mitigates neuropathic pain in a CCI rat model through inhibiting astrocytic and microglial activation

Wang

et al. 2022

Bioengineered

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Forkhead box O1 (FoxO1) is a critical molecule in modulating cell growth, differentiation and metabolism, acting as a vital transcription factor. This study explored the role of FoxO1 in chronic constriction injury (CCI)-induced neuropathic pain (NP). Microglial and astrocyte activation was achieved with lipopolysaccharide (LPS, 100 ng/mL) to establish an in-vitro NP model. Morphological alterations in LPS-induced microglia and astrocytes were assayed by light microscopy. The levels of inflammatory cytokines and proteins in microglia and astrocytes were gauged by enzyme-linked immunosorbent assay (ELISA), and Western blot (WB). The CCI-induced NP rat model was constructed for investigating the FoxO1-AQP5 axis in NP. LPS markedly expanded the expression of inflammatory factors and boosted the expression of FoxO1 and AQP5 in microglia and astrocytes. Inhibition of FoxO1 or AQP5 dramatically decreased the LPS-induced inflammation in microglia and astrocytes. In vivo , CCI exacerbated the inflammatory response and NP symptoms and substantially raised the contents of FoxO1 and AQP5 in rats’ spinal cord tissues. Intrathecal administration of the Sirt1 agonist Resveratrol abated CCI-induced activation of FoxO1 and AQP5, abrogated CCI-induced mechanical hyperalgesia and thermal hyperalgesia, depressed microglial and astrocyte activation, and declined the generation of pro-inflammatory mediators in spinal cord tissues. Mechanistically, blocking the FoxO1-AQP5 pathway inactivated the ERK and p38 MAPK pathways. Suppressing the FoxO1-AQP5 axis alleviated CCI-induced NP and inflammatory responses by modulating the ERK and p38 MAPK signaling pathways.

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“…That is to say, AQP1 is not only involved in the conduction of pain, but may also be related to local inflammation caused by orthodontic tooth movement 116 . AQP1 co‐localises with SP and TRPV1 and may be involved in the regulation of pain 114,117,118 . The response of AQP1 −/− mice to capsaicin was significantly weakened, but the degree was lower than that of TRPV1 −/− mice.…”

Section: Mechanismmentioning

confidence: 99%

Molecular mechanism in trigeminal nerve and treatment methods related to orthodontic pain

Tang

Long

Gao

et al. 2021

J of Oral Rehabilitation

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Background Orthodontic treatment is the main treatment approach for malocclusion. Orthodontic pain is an inevitable undesirable adverse reaction during orthodontic treatment. It is reported orthodontic pain has become one of the most common reason that patients withdraw from orthodontic treatment. Therefore, understanding the underlying mechanism and finding treatment of orthodontic pain are in urgent need. Aims This article aims to sort out the mechanisms and treatments of orthodontic pain, hoping to provide some ideas for future orthodontic pain relief. Materials Tooth movement will cause local inflammation. Certain inflammatory factors and cytokines stimulating the trigeminal nerve and further generating pain perception, as well as drugs and molecular targeted therapy blocking nerve conduction pathways, will be reviewed in this article. Method We review and summaries current studies related to molecular mechanisms and treatment approaches in orthodontic pain control. Results Orthodontics pain related influencing factors and molecular mechanisms has been introduced. Commonly used clinical methods in orthodontic pain control has been evaluated. Discussion With the clarification of more molecular mechanisms, the direction of orthodontic pain treatment will shift to targeted drugs.

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Effect of cGMP-activated aquaporin 1 on TRPV4 in rats with allodynia induced by chronic compression of the dorsal root ganglion

Cited by 10 publications

References 18 publications

Aquaporins and Neuropathic Pain

Aquaporins and Neuropathic Pain

Targeting Forkhead box O1-aquaporin 5 axis mitigates neuropathic pain in a CCI rat model through inhibiting astrocytic and microglial activation

Molecular mechanism in trigeminal nerve and treatment methods related to orthodontic pain

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