Intramuscular nerve damage in lacerated skeletal muscles may direct the inflammatory cytokine response during recovery

Pereira, Barry P.; Tan, Bernard; Han, Hui; Yu, Zhen; Aung, Khin Zarchi; Leong, David Tai

doi:10.1002/jcb.24105

Cited by 8 publications

(5 citation statements)

References 46 publications

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“…The Ki67 staining for proliferative cells serves as an indicator of the changing microenvironment. Figure b presents muscles absent of injected ASCs showed little presence of Ki67, potentially representative of stasis in the non‐operated muscle, and perhaps of the slow regeneration and scar formation consistent with injury to the gastrocnemius in laceration models . Presence of Ki67 was observed has having increased prevalence in the Autograft & 1 Injection cohort relative to the others, which may be a corollary to an increased inflammatory response as suggested by the iNOS/IL‐10 staining, and consistent with an advanced stage of healing per the normalized muscle mass results.…”

Section: Discussionsupporting

confidence: 55%

Adipose‐derived stem cells delay muscle atrophy after peripheral nerve injury in the rodent model

et al. 2019

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Introduction: Injuries to peripheral nerves cause distal muscle atrophy. The effects of adipose‐derived stem cell (ASC) injections into a muscle after injury were examined. Methods: A 1.5 cm defect in the rat sciatic nerve was created, resulting in gastrocnemius muscle atrophy. The nerve defect was repaired with autograft; DiR‐labeled ASCs were injected into the gastrocnemius immediately postoperatively. Quantitation of gross musculature and muscle fiber area, cell survival, fibrosis, lipid deposition, inflammation, and reconstructive responses were investigated. Results: ASCs were identified in the muscle at 6 weeks, where injections showed increased muscle mass percentage retained, larger average fiber area, and less overall lipid content accumulated throughout the musculature. Muscles having received ASCs showed increased presence of interlukin‐10 and Ki67, and decreased inducible nitric oxide synthase (iNOS). Discussion: This investigation is suggestive that an ASC injection into denervated muscle post‐operatively is able to delay the onset of atrophy. Muscle Nerve 59:603–603, 2019

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Section: Discussionsupporting

confidence: 55%

Adipose‐derived stem cells delay muscle atrophy after peripheral nerve injury in the rodent model

et al. 2019

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“…Moreover, sham rats showed a steep and significant increase in T cells and CD4 + T cells between 2 and 10 weeks, whereas in the SCI rats we did not observe significant differences for the same course of the study. While the increase in circulating T cells in sham rats may have resulted from the sham injury itself (characterized by extensive hemorrhage, severe skeletal muscle injury and resection of the bone of the spinal column) [61][62][63], the SCI rats seem to have lost the ability to mount a similar immunological response to the muscle and bone injury they incurred. Taken together, the changes in blood T-and B-lymphocytes observed here are largely in line with observations in SCI patients, suggesting that our rat C7/ T1 SCI model has important clinical relevance for studying the effects of SCI on systemic lymphocytes.…”

Section: Plos Onementioning

confidence: 99%

Effects of experimental cervical spinal cord injury on peripheral adaptive immunity

et al. 2020

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Adaptive immunity is critical for controlling infections, which are a leading cause of morbidity and mortality in patients with spinal cord injury (SCI). In rats and mice, compromised peripheral adaptive immune responses, as shown by splenic atrophy and lowered frequencies of peripheral lymphocytes, were shown to result from high-level thoracic SCI. However, whether cervical SCI, which is the most common level of SCI in humans, impairs adaptive immunity remains largely unknown. In the present study, we induced cervical SCI in rats at the C7/T1 level by clip compression and looked at changes in peripheral adaptive immunity at 2-, 10- and 20-weeks post-injury. Specifically, we quantified changes in the frequencies of T- and B- lymphocytes in the blood and the mandibular and deep cervical lymph nodes, which drain the cervical spinal cord. We also assessed changes in serum IgG and IgM immunoglobulin levels, as well as spleen size. We found a significant decline in circulating T- and B- cell frequencies at 10 weeks post-SCI, which returned to normal at 20 weeks after injury. We found no effect of cervical SCI on T- and B- cell frequencies in the draining lymph nodes. Moreover, cervical SCI had no effect on net spleen size, although injured rats had a higher spleen/body weight ratio than sham controls at all time points of the study. Lastly, IgG and IgM immunoglobulin declined at 2 weeks, followed by a significant increase in IgM levels at 10 weeks of injury. These data indicate that cervical SCI causes a significant imbalance in circulating lymphocytes and immunoglobulin levels at 2 and 10 weeks. As we discuss in this article, these findings are largely in line with clinical observations, and we anticipate that this study will fuel more research on the effect of adaptive immunity on SCI recovery.

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“…The search for solutions to these obstacles starts with understanding the pathophysiological processes of peripheral nerve regeneration. Neural repair is a complex biological process, including the clearance of myelin debris ( Rotshenker, 2011 ), the formation of bands of Büngner that provide physical guidance for regrowing axons ( Min et al, 2021 ), and the synthesis of neurotrophic factors, extracellular matrix (ECM) and cell-adhesion molecules ( Luo et al, 2012 ; Pereira et al, 2012 ; Carvalho et al, 2020 ). In addition, the activation of the neuronal intrinsic growth capacity ( Chandran et al, 2016 ), blood nerve barrier (BNB) permeability ( Mizisin and Weerasuriya, 2011 ) and the inflammation level of wound microenvironment ( Molnár et al, 2022 ; Yu et al, 2022 ) also affect the outcome of neural regeneration.…”

Section: Introductionmentioning

confidence: 99%

Role of Transforming Growth Factor Beta in Peripheral Nerve Regeneration: Cellular and Molecular Mechanisms

Wei

Zhan

et al. 2022

Front. Neurosci.

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Peripheral nerve injury (PNI) is one of the most common concerns in trauma patients. Despite significant advances in repair surgeries, the outcome can still be unsatisfactory, resulting in morbidities such as loss of sensory or motor function and reduced quality of life. This highlights the need for more supportive strategies for nerve regrowth and adequate recovery. Multifunctional cytokine transforming growth factor-β (TGF-β) is essential for the development of the nervous system and is known for its neuroprotective functions. Accumulating evidence indicates its involvement in multiple cellular and molecular responses that are critical to peripheral nerve repair. Following PNI, TGF-β is released at the site of injury where it can initiate a series of phenotypic changes in Schwann cells (SCs), modulate immune cells, activate neuronal intrinsic growth capacity, and regulate blood nerve barrier (BNB) permeability, thus enhancing the regeneration of the nerves. Notably, TGF-β has already been applied experimentally in the treatment of PNI. These treatments with encouraging outcomes further demonstrate its regeneration-promoting capacity. Herein, we review the possible roles of TGF-β in peripheral nerve regeneration and discuss the underlying mechanisms, thus providing new cues for better treatment of PNI.

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Intramuscular nerve damage in lacerated skeletal muscles may direct the inflammatory cytokine response during recovery

Cited by 8 publications

References 46 publications

Adipose‐derived stem cells delay muscle atrophy after peripheral nerve injury in the rodent model

Adipose‐derived stem cells delay muscle atrophy after peripheral nerve injury in the rodent model

Effects of experimental cervical spinal cord injury on peripheral adaptive immunity

Role of Transforming Growth Factor Beta in Peripheral Nerve Regeneration: Cellular and Molecular Mechanisms

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