Up-regulation of CX3CL1 <i>via</i> Nuclear Factor-κB–dependent Histone Acetylation Is Involved in Paclitaxel-induced Peripheral Neuropathy

Li, Dai; Huang, Zhenzhen; Ling, Yunzhi; Wei, Jia-You; Chen, Yu; Zhang, Xiangzhong; Zhu, He-Quan; Xin, Wenjun

doi:10.1097/aln.0000000000000560

Cited by 70 publications

(59 citation statements)

References 49 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Studies have shown that GAD67 was responsible for Ͼ90% of basal GABA synthesis (Asada et al, 1997) and knock-down of Gad1, but not Gad2, resulted in cell-autonomous deficits in axon branching, perisomatic synapse formation, and complexity of the innervation fields (Chattopadhyaya et al, 2007), suggesting a specific role of GAD67 in maintining proper neural function. Furthermore, depletion of Gad1 markedly reduced the amplitude and frequency of miniature IPSCs (mIPSCs) in central neurons (Lau and Murthy, 2012) and chronic constriction of the sciatic nerve significantly decreased the expression of GAD67 (Vaysse et al, 2011). These results implied the potential involvement of GAD67 downregulation in the adaptation of spinal nociceptive circuits in the setting of neuropathic pain.…”

Section: Introductionmentioning

confidence: 63%

“…Intrathecal injection of mir-500 antagomir (0.5 nmol/d) was performed according to previously described methods (Li et al, 2015). In brief, a polyethylene-10 catheter was inserted into the rat's subarachnoid space through L5 to L6 spinal cord segmental intervertebral space and the tip of the catheter was located at the L5 spinal segmental level.…”

Section: Methodsmentioning

confidence: 99%

“…Western blot analyses were performed as described previously Li et al, 2015). Briefly, lysates of spinal dorsal horn tissues or cells were prepared and separated by gel electrophoresis (SDS-PAGE) and transferred onto a polyvinylidene fluoride membrane.…”

Section: Methodsmentioning

confidence: 99%

“…GAD67 is a critical enzyme for the synthesis of cytoplasmic GABA and control GABA vesicular filling and synaptic homeostasis (Lau and Murthy, 2012). Impaired synthesis and release of GABA may cause the loss of GABAergic inhibition, leading to the hyperexcitation of neurons.…”

Section: Role Of Gad67 In the Spinal Dorsal Horn In Neuropathic Painmentioning

confidence: 99%

See 3 more Smart Citations

mir-500-Mediated GAD67 Downregulation Contributes to Neuropathic Pain

et al. 2016

Self Cite

View full text Add to dashboard Cite

Neuropathic pain is a common neurobiological disease involving multifaceted maladaptations ranging from gene modulation to synaptic dysfunction, but the interactions between synaptic dysfunction and the genes that are involved in persistent pain remain elusive. In the present study, we found that neuropathic pain induced by the chemotherapeutic drug paclitaxel or L5 ventral root transection significantly impaired the function of GABAergic synapses of spinal dorsal horn neurons via the reduction of the GAD67 expression. We also found that mir-500 expression was significantly increased and involved in the modulation of GAD67 expression via targeting the specific site of Gad1 gene in the dorsal horn. In addition, knock-out of mir-500 or using mir-500 antagomir rescued the GABAergic synapses in the spinal dorsal horn neurons and attenuated the sensitized pain behavior in the rats with neuropathic pain. To our knowledge, this is the first study to investigate the function significance and the underlying molecular mechanisms of mir-500 in the process of neuropathic pain, which sheds light on the development of novel therapeutic options for neuropathic pain.

show abstract

Section: Introductionmentioning

confidence: 63%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Role Of Gad67 In the Spinal Dorsal Horn In Neuropathic Painmentioning

confidence: 99%

See 2 more Smart Citations

mir-500-Mediated GAD67 Downregulation Contributes to Neuropathic Pain

et al. 2016

Self Cite

View full text Add to dashboard Cite

show abstract

“…Recently, a growing body of preclinical studies has suggested that chemokine axis functions as an important modulator in chronic pain processing. Chemokine C-X3-C motif ligand 1/chemokine C-X3-C motif receptor 1 (CX3CL1/CX3CR1) and chemokine C-C motif ligand 2/chemokine C-C motif receptor 2 (CCL2/CCR2) are two well-studied chemokine axes in pain research, and they modulate the peripheral and central processing of pathological pain via multiple mechanisms (White et al, 2007;Thacker et al, 2009;Li et al, 2015).…”

Section: Introductionmentioning

confidence: 99%

CXCL12/CXCR4 axis: an emerging neuromodulator in pathological pain

Luo¹,

Wang²,

Xia³

et al. 2016

Reviews in the Neurosciences

View full text Add to dashboard Cite

AbstractThe roles of chemokine C-X-C motif ligand 12 (CXCL12) and its receptor chemokine C-X-C motif receptor 4 (CXCR4) reveal this chemokine axis as an emerging neuromodulator in the nervous system. In the peripheral and central nervous systems, both CXCL12 and CXCR4 are expressed in various kinds of nociceptive structures, and CXCL12/CXCR4 axis possesses pronociceptive property. Recent studies have demonstrated its critical roles in the development and maintenance of pathological pain, and both neuronal and glial mechanisms are involved in this CXCL12/CXCR4 axis-mediated pain processing. In this review, we summarize the recent development of the roles and mechanisms of CXCL12/CXCR4 axis in the pathogenesis of chronic pain by sciatic nerve injury, human immunodeficiency virus-associated sensory neuropathy, diabetic neuropathy, spinal cord injury, bone cancer, opioid tolerance, or opioid-induced hyperalgesia. The potential targeting of CXCL12/CXCR4 axis as an effective and broad-spectrum pharmacological approach for chronic pain therapy was also discussed.

show abstract

Ac4C Enhances the Translation Efficiency of Vegfa mRNA and Mediates Central Sensitization in Spinal Dorsal Horn in Neuropathic Pain

Xu,

Wang,

et al. 2023

Advanced Science

View full text Add to dashboard Cite

N4‐Acetylcytidine (ac4C), a highly conserved post‐transcriptional machinery with extensive existence for RNA modification, plays versatile roles in various cellular processes and functions. However, the molecular mechanism by which ac4C modification mediates neuropathic pain remains elusive. Here, it is found that the enhanced ac4C modification promotes the recruitment of polysome in Vegfa mRNA and strengthens the translation efficiency following SNI. Nerve injury increases the expression of NAT10 and the interaction between NAT10 and Vegfa mRNA in the dorsal horn neurons, and the gain and loss of NAT10 function further confirm that NAT10 is involved in the ac4C modification in Vegfa mRNA and pain behavior. Moreover, the ac4C‐mediated VEGFA upregulation contributes to the central sensitivity and neuropathic pain induced by SNI or AAV‐hSyn‐NAT10. Finally, SNI promotes the binding of HNRNPK in Vegfa mRNA and subsequently recruits the NAT10. The enhanced interaction between HNRNPK and NAT10 contributes to the ac4C modification of Vegfa mRNA and neuropathic pain. These findings suggest that the enhanced interaction between HNRNPK and Vegfa mRNA upregulates the ac4C level by recruiting NAT10 and contributes to the central sensitivity and neuropathic pain following SNI. Blocking this cascade may be a novel therapeutic approach in patients with neuropathic pain.

show abstract

Up-regulation of CX3CL1 via Nuclear Factor-κB–dependent Histone Acetylation Is Involved in Paclitaxel-induced Peripheral Neuropathy

Abstract: These findings suggest that up-regulation of CX3CL1 via NF-κB-dependent H4 acetylation might be critical for paclitaxel-induced mechanical allodynia.

Cited by 70 publications

References 49 publications

mir-500-Mediated GAD67 Downregulation Contributes to Neuropathic Pain

mir-500-Mediated GAD67 Downregulation Contributes to Neuropathic Pain

CXCL12/CXCR4 axis: an emerging neuromodulator in pathological pain

Ac4C Enhances the Translation Efficiency of Vegfa mRNA and Mediates Central Sensitization in Spinal Dorsal Horn in Neuropathic Pain

Contact Info

Product

Resources

About