Chronic sciatic nerve compression induces fibrosis in dorsal root ganglia

Li, Qinwen; Chen, Jianghai; Chen, Yanhua; Cong, Xiaobin; Chen, Zhenbing

doi:10.3892/mmr.2016.4810

Cited by 15 publications

(10 citation statements)

References 45 publications

(46 reference statements)

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“…Moreover, compression of the sciatic nerve in rats induced fibrosis near the lesions and the ipsilateral dorsal root ganglion. This occurred 3 weeks after the compression using the Silastic tube [25].…”

Section: Genetics and Vitamin Dmentioning

confidence: 99%

“…They found the cicatrix formed after the injury may sensitize the dominant nerve in the dorsal root ganglia [24]. Li et al [25] in 2016 studied the effects of compression of the sciatic nerve in rats to investigate the pathological alterations in the neurons of the dorsal root ganglia [25]. They reported at 3 weeks after the compression, collagen fibers accumulated around the compressed sciatic nerve, and at 8 weeks, excessive collagen formation with muscle atrophy was observed [25].…”

Section: The Role Of Vitamin D In the Etiopathogenesis Of Adolescent mentioning

confidence: 99%

“…Li et al [25] in 2016 studied the effects of compression of the sciatic nerve in rats to investigate the pathological alterations in the neurons of the dorsal root ganglia [25]. They reported at 3 weeks after the compression, collagen fibers accumulated around the compressed sciatic nerve, and at 8 weeks, excessive collagen formation with muscle atrophy was observed [25]. The volume of collagen gradually and significantly increased following sciatic nerve compression.…”

Section: The Role Of Vitamin D In the Etiopathogenesis Of Adolescent mentioning

confidence: 99%

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The Role of Vitamin D in the Pathogenesis of Adolescent Idiopathic Scoliosis

Ng¹,

Bettany‐Saltikov

Cheung³

et al. 2018

Asian Spine J

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Several theories have been proposed to explain the etiology of adolescent idiopathic scoliosis (AIS) until present. However, limited data are available regarding the impact of vitamin D insufficiency or deficiency on scoliosis. Previous studies have shown that vitamin D deficiency and insufficiency are prevalent in adolescents, including AIS patients. A series of studies conducted in Hong Kong have shown that as many as 30% of these patients have osteopenia. The 25-hydroxyvitamin D3 level has been found to positively correlate with bone mineral density (BMD) in healthy adolescents and negatively with Cobb angle in AIS patients; therefore, vitamin D deficiency is believed to play a role in AIS pathogenesis. This study attempts to review the relevant literature on AIS etiology to examine the association of vitamin D and various current theories. Our review suggested that vitamin D deficiency is associated with several current etiological theories of AIS. We postulate that vitamin D deficiency and/or insufficiency affects AIS development by its effect on the regulation of fibrosis, postural control, and BMD. Subclinical deficiency of vitamin K2, a fat-soluble vitamin, is also prevalent in adolescents; therefore, it is possible that the high prevalence of vitamin D deficiency is related to decreased fat intake. Further studies are required to elucidate the possible role of vitamin D in the pathogenesis and clinical management of AIS.

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Section: Genetics and Vitamin Dmentioning

confidence: 99%

Section: The Role Of Vitamin D In the Etiopathogenesis Of Adolescent mentioning

confidence: 99%

Section: The Role Of Vitamin D In the Etiopathogenesis Of Adolescent mentioning

confidence: 99%

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The Role of Vitamin D in the Pathogenesis of Adolescent Idiopathic Scoliosis

Ng¹,

Bettany‐Saltikov

Cheung³

et al. 2018

Asian Spine J

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“…Studies (Lv et al., ; Wang, Hurwitz, et al., ) have shown that Tau is more sensitive in neuronal ischemic injury after molecular markers. In the vascular dementia rat model, Tau expression was significantly increased, and neuronal apoptosis occurred simultaneously, suggesting the function of Tau phosphorylation in initiating cellular apoptosis (Li, Chen, Chen, Cong, & Chen, ). In our study, we found that vGlut3, a glutamate transporter that is closely related to PSD‐95, was significantly decreased in the rat DRG after sustained compression of DRG.…”

Section: Discussionmentioning

confidence: 99%

Tau protein function: The mechanical exploration of axonal transport disorder caused by persistent pressure in dorsal root ganglia

Zhang

Cheng

et al. 2019

Molec Gen & Gen Med

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Objective We analyzed the function of Tau protein to explore the underlying mechanism of axonal transport disorder caused by persistent pressure in the dorsal root ganglia (DRG). Methods Wistar rats were divided into the sham operated group, the control group and the experimental group. The Wistar rat model of continuous compression of DRG was used for further investigation. DRG neurons were extracted and cultured, and the protein content was detected using bicinchoninic acid method. Western blotting and immunofluorescence assays were performed to detect the protein content. Intraperitoneal injection of lithium chloride was performed for interaction with Tau. The results were then analyzed statistically. Results After 2 weeks of sustained pressure, the expression level of Tau396 increased by 33%, while Tau404 increased by 25% in the DRG of the experimental group (p < 0.05). The expression level of PSD‐95 in the DRG decreased by 15% (p < 0.05), while the expression of vGluT1, vGluT3 and vAchT decreased significantly in the DRG of the experimental group (p < 0.05). There was no significant difference in the expression of vGluT2 and vGAT among the three groups (p > 0.05). After intervention with lithium chloride, the expression of phosphorylated Tau at the above sites decreased in varying degrees compared with the model group. The expression level of Tau404 was reduced by 55%, and that of Tau199 by 60% in the DRG of the experimental group. Conclusion Chronic compression of DRG and hypoxia caused phosphorylation of Tau in axons and inhibition of PSD‐95, and the function of the synaptic glutamic acid vesicle is defective in the synapse. This process is crucial in the development and progression of axonal transport dysfunction induced by chronic DRG compression, and phosphorylation of Tau plays a substantial role in this process.

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“…Three SD rats were used for retrograde tracing of Fluor-Gold (FG; Fluorochrome; 80014; Sigma-Aldrich, St. Louis, MO) as previously described (Li et al, 2016). The modified procedure was as follows: A glass micropipette (tip diameter 40–60 μm) connected to a microsyringe (1 μl, Hamilton, Reno, NV, United States) was inserted into the epineurium 2 mm from the distal point of the injured site of the sciatic nerve.…”

Section: Methodsmentioning

confidence: 99%

The ATP-P2X7 Signaling Pathway Participates in the Regulation of Slit1 Expression in Satellite Glial Cells

Zhang

Zhao

Shen

et al. 2019

Front. Cell. Neurosci.

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Slit1 is one of the known signaling factors of the slit family and can promote neurite growth by binding to its receptor, Robo2. Upregulation of Slit1 expression in dorsal root ganglia (DRG) after peripheral nerve injury plays an important role in nerve regeneration. Each sensory neuronal soma in the DRG is encapsulated by several surrounding satellite glial cells (SGCs) to form a neural structural unit. However, the temporal and spatial patterns of Slit1 upregulation in SGCs in DRG and its molecular mechanisms are not well understood. This study examined the spatial and temporal patterns of Slit1 expression in DRG after sciatic nerve crush by immunohistochemistry and western blotting. The effect of neuronal damage signaling on the expression of Slit1 in SGCs was studied in vivo by fluorescent gold retrograde tracing and double immunofluorescence staining. The relationship between the expression of Slit1 in SGCs and neuronal somas was also observed by culturing DRG cells and double immunofluorescence labeling. The molecular mechanism of Slit1 was further explored by immunohistochemistry and western blotting after intraperitoneal injection of Bright Blue G (BBG, P2X7R inhibitor). The results showed that after peripheral nerve injury, the expression of Slit1 in the neurons and SGCs of DRG increased. The expression of Slit1 was presented with a time lag in SGCs than in neurons. The expression of Slit1 in SGCs was induced by contact with surrounding neuronal somas. Through injured cell localization, it was found that the expression of Slit1 was stronger in SGCs surrounding injured neurons than in SGCs surrounding non-injured neurons. The expression of vesicular nucleotide transporter (VNUT) in DRG neurons was increased by injury signaling. After the inhibition of P2X7R, the expression of Slit1 in SGCs was downregulated, and the expression of VNUT in DRG neurons was upregulated. These results indicate that the ATP-P2X7R pathway is involved in signal transduction from peripheral nerve injury to SGCs, leading to the upregulation of Slit1 expression.

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Chronic sciatic nerve compression induces fibrosis in dorsal root ganglia

Cited by 15 publications

References 45 publications

The Role of Vitamin D in the Pathogenesis of Adolescent Idiopathic Scoliosis

The Role of Vitamin D in the Pathogenesis of Adolescent Idiopathic Scoliosis

Tau protein function: The mechanical exploration of axonal transport disorder caused by persistent pressure in dorsal root ganglia

The ATP-P2X7 Signaling Pathway Participates in the Regulation of Slit1 Expression in Satellite Glial Cells

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