Engagement of MicroRNA-155 in Exaggerated Oxidative Stress Signal and TRPA1 in the Dorsal Horn of the Spinal Cord and Neuropathic Pain During Chemotherapeutic Oxaliplatin

Feng-hua, Miao; Wang, Rong; Cui, Guozhen; Li, Xiaoguang; Wang, Ting; Li, Xue

doi:10.1007/s12640-019-00039-5

Cited by 32 publications

(31 citation statements)

References 65 publications

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“…In general, cytotoxic drugs used for chemotherapy activate oxidative stress signals and thereby induce peripheral neuropathy (35,54,55). The previous study has demonstrated that TRPA1 is activated in the process of BTZ-induced pain and oxidative stress is involved in activation of the signal pathways (55).…”

Section: Discussionmentioning

confidence: 99%

“…After the end of BTZ administration, the following intrathecal injection was performed each day for three consecutive days: miR-155 inhibitor (sequence: 5 ′ AAU UAC GAU UAG CAC UAU CCC CA-3 ′ ; 3 µg, Biomics Biotech, Nantong, China), miR-155 mimics (sequence: 5 ′ -UUA AUG CUA AUC GUG AUA GGG GU-3 ′ ; 3 µg, Biomics Biotech, Nantong, China) and their corresponding scramble for negative controls (3 µg, Biomics Biotech, Nantong, China). MiR-155 inhibitor, miR-155 mimics and their respective scramble were dissolved in artificial cerebrospinal fluid (aCSF) before they were used; and their dosages used in this study were based on the published work (35). TNF-α synthesis inhibitor pentoxifylline (PTX, 10 µg), TRPA1 antagonist HC030031 (5 µg), p38-MAPK inhibitor SB203580 (5 µg), and JNK inhibitor SP600125 (5 µg) were also given by individual intrathecal injection each day for three consecutive days.…”

Section: Development Of Neuropathic Pain and Intrathecal Administrationmentioning

confidence: 99%

“…As described in our previous publication (35), "the tissues of the L5-L6 spinal cord dorsal horn were processed for the extraction of total RNA (RNeasy Mini Kit; Qiagen). RT-PCR was performed using the TaqmanW Universal PCR Master Mix and 18 s rRNA (TaqmanW PDAR) was used as an endogenous control to correct for variations in the samples.…”

Section: Real-time Pcrmentioning

confidence: 99%

“…As described previously in our publications (34,35), "we examined mechanical paw withdrawal threshold (PWT) of rat hindpaw in response to the stimulation of von Frey filaments. In brief, the filaments were bent for 5-10 s in our protocols.…”

Section: Behavioral Testmentioning

confidence: 99%

“…We used Thermal Place Preference System to execute the thermal place preference test to assess a cold avoidance behavior as described in our previous study (34,35). "We kept the first plate at neutral temperature (25 • C) and the second plate at cold temperature (12 • C).…”

Section: Behavioral Testmentioning

confidence: 99%

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Inhibition of microRNA-155 Reduces Neuropathic Pain During Chemotherapeutic Bortezomib via Engagement of Neuroinflammation

Duan

Zhang

et al. 2020

Front. Oncol.

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As a chemotherapeutic agent, bortezomib (BTZ) is used for the treatment of multiple myeloma with adverse effect of painful peripheral neuropathy. Our current study was to determine the inhibitory effects of blocking microRNA-155 (miR-155) signal on BTZ-induced neuropathic pain and the underlying mechanisms. We employed real time RT-PCR and western blot analysis to examine the miR-155 and expression of pro − inflammatory tumor necrosis factor-α receptor (TNFR1) in the dorsal horn of the spinal cord. Its downstream signals p38-MAPK and JNK and transient receptor potential ankyrin 1 (TRPA1) were also determined. Mechanical pain and cold sensitivity were assessed by behavioral test. In result, inhibition of miR-155 significantly attenuated mechanical allodynia and thermal hyperalgesia in BTZ rats, which was accompanied with decreasing expression of TNFR1, p38-MAPK, JNK, and TRPA1. In contrast, miRNA-155 mimics amplified TNFR1-TRPA1 pathway and augmented mechanical pain and cold sensitivity. In addition, mechanical and thermal hypersensitivity induced by miRNA-155 mimics were attenuated after blocking TNFR1, p38-MAPK, JNK, and TRPA1. Overall, we show the key role of miR-155 in modifying BTZ-induced neuropathic pain through TNFR1-TRPA1 pathway, suggesting that miR-155 is a potential target in preventing neuropathic pain development during intervention of BTZ.

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Section: Discussionmentioning

confidence: 99%

Section: Development Of Neuropathic Pain and Intrathecal Administrationmentioning

confidence: 99%

Section: Real-time Pcrmentioning

confidence: 99%

Section: Behavioral Testmentioning

confidence: 99%

Section: Behavioral Testmentioning

confidence: 99%

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Inhibition of microRNA-155 Reduces Neuropathic Pain During Chemotherapeutic Bortezomib via Engagement of Neuroinflammation

Duan

Zhang

et al. 2020

Front. Oncol.

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The etiological roles of miRNAs, lncRNAs, and circRNAs in neuropathic pain: A narrative review

Jiang

Wang

et al. 2022

Clinical Laboratory Analysis

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Background Non‐coding RNAs (ncRNAs) are involved in neuropathic pain development. Herein, we systematically searched for neuropathic pain‐related ncRNAs expression changes, including microRNAs (miRNAs), long non‐coding RNAs (lncRNAs), and circular non‐coding RNAs (circRNAs). Methods We searched two databases, PubMed and GeenMedical, for relevant studies. Results Peripheral nerve injury or noxious stimuli can induce extensive changes in the expression of ncRNAs. For example, higher serum miR‐132‐3p, ‐146b‐5p, and ‐384 was observed in neuropathic pain patients. Either sciatic nerve ligation, dorsal root ganglion (DRG) transaction, or ventral root transection (VRT) could upregulate miR‐21 and miR‐31 while downregulating miR‐668 and miR‐672 in the injured DRG. lncRNAs, such as early growth response 2‐antisense‐RNA (Egr2‐AS‐RNA) and Kcna2‐AS‐RNA, were upregulated in Schwann cells and inflicted DRG after nerve injury, respectively. Dysregulated circRNA homeodomain‐interacting protein kinase 3 (circHIPK3) in serum and the DRG, abnormally expressed lncRNAs X‐inactive specific transcript (XIST), nuclear enriched abundant transcript 1 (NEAT1), small nucleolar RNA host gene 1 (SNHG1), as well as ciRS‐7, zinc finger protein 609 (cirZNF609), circ_0005075, and circAnks1a in the spinal cord were suggested to participate in neuropathic pain development. Dysregulated miRNAs contribute to neuropathic pain via neuroinflammation, autophagy, abnormal ion channel expression, regulating pain‐related mediators, protein kinases, structural proteins, neurotransmission excitatory–inhibitory imbalances, or exosome miRNA‐mediated neuron–glia communication. In addition, lncRNAs and circRNAs are essential in neuropathic pain by acting as antisense RNA and miRNA sponges, epigenetically regulating pain‐related molecules expression, or modulating miRNA processing. Conclusions Numerous dysregulated ncRNAs have been suggested to participate in neuropathic pain development. However, there is much work to be done before ncRNA‐based analgesics can be clinically used for various reasons such as conservation among species, proper delivery, stability, and off‐target effects.

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MiR-672-5p-Mediated Upregulation of REEP6 in Spinal Dorsal Horn Participates in Bortezomib-Induced Neuropathic Pain in Rats

Sun

Chen

et al. 2022

Neurochem Res

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Engagement of MicroRNA-155 in Exaggerated Oxidative Stress Signal and TRPA1 in the Dorsal Horn of the Spinal Cord and Neuropathic Pain During Chemotherapeutic Oxaliplatin

Cited by 32 publications

References 65 publications

Inhibition of microRNA-155 Reduces Neuropathic Pain During Chemotherapeutic Bortezomib via Engagement of Neuroinflammation

Inhibition of microRNA-155 Reduces Neuropathic Pain During Chemotherapeutic Bortezomib via Engagement of Neuroinflammation

The etiological roles of miRNAs, lncRNAs, and circRNAs in neuropathic pain: A narrative review

MiR-672-5p-Mediated Upregulation of REEP6 in Spinal Dorsal Horn Participates in Bortezomib-Induced Neuropathic Pain in Rats

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