Significance of alpha smooth muscle actin expression in traumatic painful neuromas: a pilot study in rats

Weng, Weidong; Zhao, Bin; Lin, Dingshen; Gao, Weiyang; Li, Zhijie; Yan, Hede

doi:10.1038/srep23828

Cited by 34 publications

(36 citation statements)

References 37 publications

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“…Although αSMA plays a role in the mechanism generating neuroma‐associated pain, our study indicates that this protein is not a reliable marker of areas of neural fibrosis (Weng et al., ). In contrast, the accelerated expression of HSP47 and αβP4H in fibroblastic cells and Schwann cells clearly suggests their pro‐fibrotic activity in response to nerve injury and defines areas of collagen deposition.…”

Section: Discussionmentioning

confidence: 69%

Patterns of production of collagen‐rich deposits in peripheral nerves in response to injury: A pilot study in a rabbit model

et al. 2017

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IntroductionAlthough collagen‐rich deposits are the main component of neural scars, the patterns of their formation are ill defined. Essential to the biosynthesis of collagen fibrils are enzymes catalyzing posttranslational modifications and chaperones that control the formation of the collagen triple helix. Prolyl‐4‐hydroxylase (P4H) and heat shock protein‐47 (HSP47) play a key role, and their production is upregulated during scar formation in human tissues. Alpha smooth muscle actin (αSMA) is also produced during fibrotic processes in myofibroblasts that participate in fibrotic response. In injured peripheral nerves, however, the distribution of cells that produce these markers is poorly understood.MethodsThe goal of this study was to determine the distribution of the αSMA‐positive, HSP47‐positive, and the P4H‐positive cells to better understand the formation of collagen‐rich fibrotic tissue (FT) in response to peripheral nerve injury. To reach this goal, we employed a rabbit model of crush‐injury and partial‐transection injury of the sciatic nerves.ResultsOur study demonstrated that αSMA is expressed in a relatively small number of cells seen in neural FT. In contrast, cells producing P4H and HSP47 are ubiquitously present in sites of injury of the sciatic nerves.ConclusionWe contemplate that these proteins may serve as valuable markers that define fibrotic activities in the injured peripheral nerves.

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Section: Discussionmentioning

confidence: 69%

Patterns of production of collagen‐rich deposits in peripheral nerves in response to injury: A pilot study in a rabbit model

et al. 2017

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“…To further evaluate the pain state at the molecular level, we examined the expression of c‐Fos in the dorsal horn of the L5 spinal cord, which was reported as a pain‐related protein . The results of immunohistological analysis of c‐Fos showed only very few neuron cells which had positive c‐Fos staining in the sham group.…”

Section: Resultsmentioning

confidence: 99%

Metformin relieves neuropathic pain after spinal nerve ligation via autophagy flux stimulation

Weng

Yao

Poonit

et al. 2018

J Cellular Molecular Medi

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Neuropathic pain is a well‐known type of chronic pain caused by damage to the nervous system. Autophagy is involved in the development and/or progression of many diseases, including neuropathic pain. Emerging evidence suggests that metformin relieves neuropathic pain in several neuropathic pain models; however, metformin's cellular and molecular mechanism for pain relief remains unknown. In this study, we investigated the therapeutic effects of metformin on pain relief after spinal nerve ligation (SNL) and its underlying mechanism of autophagy regulation. Behavioural analysis, histological assessment, expression of c‐Fos and molecular biological changes, as well as ultrastructural features, were investigated. Our findings showed that the number of autophagosomes and expression of autophagy markers, such as LC3 and beclin1, were increased, while the autophagy substrate protein p62, as well as the ubiquitinated proteins, were accumulated in the ipsilateral spinal cord. However, metformin enhanced the expression of autophagy markers, while it abrogated the abundance of p62 and ubiquitinated proteins. Blockage of autophagy flux by chloroquine partially abolished the apoptosis inhibition and analgesic effects of metformin on SNL. Taken together, these results illustrated that metformin relieved neuropathic pain through autophagy flux stimulation and provided a new direction for metformin drug development to treat neuropathic pain.

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“…NT, NGF, and BDNF regulate neuronal survival, neuronal growth, and neuroma formation ( 5 ). After getting these striking behavioral and histological results, we investigated how NT expression changed in TNT rats and whether swimming exercise could influence NT expression.…”

Section: Resultsmentioning

confidence: 99%

“…Neuroma consists of an unorganized network of connective tissue intermingled with spouting fibers, Schwann cells, macrophages, and fibroblasts. Several mechanisms may be involved in the process of neuroma-induced pain, including ectopic discharge of axons, altered sodium iron channels, transient receptor potential cation channel subfamily A1, and nerve growth factor (NGF) ( 4 , 5 ). However, the exact mechanisms are not fully elucidated.…”

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confidence: 99%

Swimming Training Reduces Neuroma Pain by Regulating Neurotrophins

Tian

et al. 2018

Medicine &Amp; Science in Sports &Amp; Exercise

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IntroductionNeuroma formation after peripheral nerve transection leads to severe neuropathic pain in amputees. Previous studies suggested that physical exercise could bring beneficial effect on alleviating neuropathic pain. However, the effect of exercise on neuroma pain still remained unclear. In addition, long-term exercise can affect the expression of neurotrophins (NT), such as nerve growth factor (NGF) and brain-derived neurotrophic factor (BDNF), which play key roles in nociceptor sensitization and nerve sprouting after nerve injury. Here, we investigated whether long-term swimming exercise could relieve neuroma pain by modulating NT expression.MethodsWe used a tibial neuroma transposition (TNT) rat model to mimic neuroma pain. After TNT surgery, rats performed swimming exercise for 5 wk. Neuroma pain and tactile sensitivities were detected using von Frey filaments. Immunofluorescence was applied to analyze neuroma formation. NGF and BDNF expressions in peripheral neuroma, dorsal root ganglion, and the spinal cord were measured using enzyme-linked immunosorbent assay and Western blotting.ResultsTNT led to neuroma formation, induced neuroma pain, and mechanical allodynia in hind paw. Five-week swimming exercise inhibited neuroma formation and relieved mechanical allodynia in the hind paw and neuroma pain in the lateral ankle. The analgesic effect lasted for at least 1 wk, even when the exercise ceased. TNT elevated the expressions of BDNF and NGF in peripheral neuroma, dorsal root ganglion, and the spinal cord to different extents. Swimming also decreased the elevation of NT expression.ConclusionsSwimming exercise not only inhibits neuroma formation induced by nerve transection but also relieves pain behavior. These effects might be associated with the modulation of NT.

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Significance of alpha smooth muscle actin expression in traumatic painful neuromas: a pilot study in rats

Cited by 34 publications

References 37 publications

Patterns of production of collagen‐rich deposits in peripheral nerves in response to injury: A pilot study in a rabbit model

Patterns of production of collagen‐rich deposits in peripheral nerves in response to injury: A pilot study in a rabbit model

Metformin relieves neuropathic pain after spinal nerve ligation via autophagy flux stimulation

Swimming Training Reduces Neuroma Pain by Regulating Neurotrophins

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