Therapeutic benefits of maintaining mitochondrial integrity and calcium homeostasis by forced expression of Hsp27 in chemotherapy-induced peripheral neuropathy

Chine, Virendra Bhagawan; Au, Ngan Pan Bennett; Eddie, Chi Him

doi:10.1016/j.nbd.2019.104492

Cited by 26 publications

(34 citation statements)

References 104 publications

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“…An enhanced expression of HSP27 is reported to correlate with axonal regeneration in mature retinal ganglion cells, indicating a growth-associated role of HSP27 in neurons from the central nervous system [43]. Indirect and direct support for promotion of nerve regeneration has also been presented in other nerve injury models and in chemotherapy-induced neuropathy models in vitro and in vivo [17,28,31,[44][45][46].…”

Section: Discussionmentioning

confidence: 92%

Injury-Induced HSP27 Expression in Peripheral Nervous Tissue Is Not Associated with Any Alteration in Axonal Outgrowth after Immediate or Delayed Nerve Repair

Stenberg

Hazer

Kohyama

et al. 2021

IJMS

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We investigated injury-induced heat shock protein 27 (HSP27) expression and its association to axonal outgrowth after injury and different nerve repair models in healthy Wistar and diabetic Goto-Kakizaki rats. By immunohistochemistry, expression of HSP27 in sciatic nerves and DRG and axonal outgrowth (neurofilaments) in sciatic nerves were analyzed after no, immediate, and delayed (7-day delay) nerve repairs (7- or 14-day follow-up). An increased HSP27 expression in nerves and in DRG at the uninjured side was associated with diabetes. HSP27 expression in nerves and in DRG increased substantially after the nerve injuries, being higher at the site where axons and Schwann cells interacted. Regression analysis indicated a positive influence of immediate nerve repair compared to an unrepaired injury, but a shortly delayed nerve repair had no impact on axonal outgrowth. Diabetes was associated with a decreased axonal outgrowth. The increased expression of HSP27 in sciatic nerve and DRG did not influence axonal outgrowth. Injured sciatic nerves should appropriately be repaired in healthy and diabetic rats, but a short delay does not influence axonal outgrowth. HSP27 expression in sciatic nerve or DRG, despite an increase after nerve injury with or without a repair, is not associated with any alteration in axonal outgrowth.

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Section: Discussionmentioning

confidence: 92%

Injury-Induced HSP27 Expression in Peripheral Nervous Tissue Is Not Associated with Any Alteration in Axonal Outgrowth after Immediate or Delayed Nerve Repair

Stenberg

Hazer

Kohyama

et al. 2021

IJMS

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“…1e ). Motor function recovery was further validated by electromyography (EMG) recording 6 , 7 , 37 showing decreased compound muscle action potential amplitude (CMAP) in proximal (gastrocnemius) and distal (interosseous) plantar muscles of ataxia mice at weeks 2, 3 and 4 after injury. The EMG activities of ataxia mice dropped to 77.7% (gastrocnemius) and 69.5% (interosseous) of the baseline values, and the controls were fully recovered in both proximal (Fig.…”

Section: Resultsmentioning

confidence: 99%

“…Adult male mice were anesthetized with 2.5% isoflurane, and the left sciatic nerve was crushed once with 5/45 smooth forceps (Fine Science Tools) for 15 s at the level of the external rotator muscles distal to the sciatic notch 1 , 2 , 6 , 7 , 37 . To delay muscle reinnervation for a specific period of time (16, 22, and 25 days), we crushed the sciatic nerves four times at 2-, 4-, and 5-day intervals for 16, 22, and 25 days of muscle denervation, respectively 1 , 7 .…”

Section: Methodsmentioning

confidence: 99%

Cerebellar glutamatergic system impacts spontaneous motor recovery by regulating Gria1 expression

et al. 2022

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Peripheral nerve injury (PNI) often results in spontaneous motor recovery; however, how disrupted cerebellar circuitry affects PNI-associated motor recovery is unknown. Here, we demonstrated disrupted cerebellar circuitry and poor motor recovery in ataxia mice after PNI. This effect was mimicked by deep cerebellar nuclei (DCN) lesion, but not by damaging non-motor area hippocampus. By restoring cerebellar circuitry through DCN stimulation, and reversal of neurotransmitter imbalance using baclofen, ataxia mice achieve full motor recovery after PNI. Mechanistically, elevated glutamate-glutamine level was detected in DCN of ataxia mice by magnetic resonance spectroscopy. Transcriptomic study revealed that Gria1, an ionotropic glutamate receptor, was upregulated in DCN of control mice but failed to be upregulated in ataxia mice after sciatic nerve crush. AAV-mediated overexpression of Gria1 in DCN rescued motor deficits of ataxia mice after PNI. Finally, we found a correlative decrease in human GRIA1 mRNA expression in the cerebellum of patients with ataxia-telangiectasia and spinocerebellar ataxia type 6 patient iPSC-derived Purkinje cells, pointing to the clinical relevance of glutamatergic system. By conducting a large-scale analysis of 9,655,320 patients with ataxia, they failed to recover from carpal tunnel decompression surgery and tibial neuropathy, while aged-match non-ataxia patients fully recovered. Our results provide insight into cerebellar disorders and motor deficits after PNI.

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“…Vincristine injected in rats caused ER stress by an unfolded protein response (UPR), upregulation of PERK, IRE1, ATF-6, and chaperone glucose-regulating protein 78 (GRP78) that belong to Heat Shock Protein 70 family (Hsp70), followed by an increase in apoptotic proteins BCL-2 associated X (Bax), caspase 3 and a decrease in anti-apoptotic molecule B-cell lymphoma 2 (Bcl-2) [ 88 ]. In several preclinical studies in laboratory animals and cell lines, the modulation of chaperons Hsp29, Hsp90, and Hsp70 has shown significant therapeutic potential in treating CIPN [ 89 , 90 , 91 ]. Bortezomib-induced ER stress is known to cause peripheral neuropathy [ 15 ].…”

Section: Preclinical Evidence Of Er Stress In Cipnmentioning

confidence: 99%

Endoplasmic Reticulum Stress in Chemotherapy-Induced Peripheral Neuropathy: Emerging Role of Phytochemicals

2022

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Chemotherapy-induced peripheral neuropathy (CIPN) is a significant dose-limiting long-term sequela in cancer patients undergoing treatment, often leading to discontinuation of treatment. No established therapy exists to prevent and/or ameliorate CIPN. Reactive oxygen species (ROS) and mitochondrial dysregulation have been proposed to underlie the pathobiology of CIPN. However, interventions to prevent and treat CIPN are largely ineffective. Additional factors and mechanism-based targets need to be identified to develop novel strategies to target CIPN. The role of oxidative stress appears to be central, but the contribution of endoplasmic reticulum (ER) stress remains under-examined in the pathobiology of CIPN. This review describes the significance of ER stress and its contribution to CIPN, the protective role of herbal agents in countering ER stress in nervous system-associated disorders, and their possible repurposing for preventing CIPN.

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Therapeutic benefits of maintaining mitochondrial integrity and calcium homeostasis by forced expression of Hsp27 in chemotherapy-induced peripheral neuropathy

Cited by 26 publications

References 104 publications

Injury-Induced HSP27 Expression in Peripheral Nervous Tissue Is Not Associated with Any Alteration in Axonal Outgrowth after Immediate or Delayed Nerve Repair

Injury-Induced HSP27 Expression in Peripheral Nervous Tissue Is Not Associated with Any Alteration in Axonal Outgrowth after Immediate or Delayed Nerve Repair

Cerebellar glutamatergic system impacts spontaneous motor recovery by regulating Gria1 expression

Endoplasmic Reticulum Stress in Chemotherapy-Induced Peripheral Neuropathy: Emerging Role of Phytochemicals

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