Heat shock proteins, endothelin, and peripheral neuronal injury

Klass, Markus; Gavrikov, Vitaliy; Krishnamoorthy, Malini; Csete, Marie

doi:10.1016/j.neulet.2008.01.005

Cited by 5 publications

(3 citation statements)

References 38 publications

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“…Work by Willis et al ( 2005 ) expanded the list of HSPs found to be enhanced in the injured PNS to include HSP60, glucose-regulated protein (GRP)75 and αBC which they discovered were capable of being synthesized within damaged PNS axons. In the CNS, increases in the levels of HSP32, HSP72 and HSP90 were evident following transection of the spinal cord and even after constriction and transection of peripheral nerves (Klass et al, 2008 ; Sharma et al, 2015 ). The latter observation showed that PNS nerve damage could alter expression of hsps in the CNS.…”

Section: Expression Of Chaperones After Pns and Cns Nerve Injurymentioning

confidence: 99%

Chaperone Proteins in the Central Nervous System and Peripheral Nervous System after Nerve Injury

2017

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Injury to axons of the central nervous system (CNS) and the peripheral nervous system (PNS) is accompanied by the upregulation and downregulation of numerous molecules that are involved in mediating nerve repair, or in augmentation of the original damage. Promoting the functions of beneficial factors while reducing the properties of injurious agents determines whether regeneration and functional recovery ensues. A number of chaperone proteins display reduced or increased expression following CNS and PNS damage (crush, transection, contusion) where their roles have generally been found to be protective. For example, chaperones are involved in mediating survival of damaged neurons, promoting axon regeneration and remyelination and, improving behavioral outcomes. We review here the various chaperone proteins that are involved after nervous system axonal damage, the functions that they impact in the CNS and PNS, and the possible mechanisms by which they act.

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Section: Expression Of Chaperones After Pns and Cns Nerve Injurymentioning

confidence: 99%

Chaperone Proteins in the Central Nervous System and Peripheral Nervous System after Nerve Injury

2017

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“…HSP 4 and grp75 are heat shock proteins that have increased expression and show a nerve-protective action in inflammation and various disorders (8,15,19). Increased expression of these proteins has been found in the dorsal root ganglion (DRG) after nerve injury (17,18,46,48). Expression of HSP 4 and grp75 in the brainstem has not been reported previously, but in the present study their expression decreased in the brainstem after CCI (HSP 4 , 0.75 ± 0.07 compared to the control group; grp75, 0.65 ± 0.05 compared to the control group).…”

Section: Discussionmentioning

confidence: 99%

Proteomic analysis of rat brains in a model of neuropathic pain following exposure to electroconvulsive stimulation

et al. 2011

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Some reports have shown that electroconvulsive shock therapy is effective for treating refractory neuropathic pain. However, its mechanism of action remains unknown. This study analyzes changes in protein expression in the brainstems of neuropathic pain model rats with or without electroconvulsive stimulation (ECS). A neuropathic pain model rat is produced by chronic constrictive injury (CCI) of the sciatic nerve. An ECS was administered to rodents once daily for 6 days after the CCI operation. After ECS, the latency to withdrawal from thermal stimulation was significantly increased. The expression of several proteins was changed after CCI. Ten proteins that increased after CCI then had decreased expression levels (close to control) after ECS, and 8 proteins that decreased after CCI then had increased expression levels (close to control) after ECS. In conclusion, ECS improved thermal hypersensitivity in a rat CCI model. Proteomic analysis showed that altered expression levels of proteins in the brainstem of CCI model rats returned to close to control levels after ECS, including many proteins associated with pain. This trend suggests an association of ECS with improved hypersensitivity, and these results may help elucidate the mechanism of this effect.Electroconvulsive shock therapy (ECT) has been used widely as an effective and established treatment for refractory depression and schizophrenia, although the mechanism of action of this treatment has not been clarified precisely. Many recent studies in the psychiatric field have suggested that the expression levels of the genes for various cerebral neurotransmitters would change after ECT. This change in gene expression might be a possible mechanism of action of ECT (2,24,35,40). Also, some reports have shown that ECT is effective for treating refractory neuropathic pain (5,16,22,36,37). However, ECT has not been performed as a general treatment for neuropathic pain because the evidence for its therapeutic effect is insufficient, owing to a lack of data from large-scale controlled trials. Side effects, such as amnesia and injury from ECT, make this option rather unpopular (1). The mechanism of action of ECT in treating neuropathic pain has not been examined sufficiently, and thus remains unclear. We have previously shown that electroconvulsive stimulation (ECS) improves symptoms in rats with neuropathic pain. In the same study we also demonstrated that neuropeptide Y (NPY) expression in the brain was altered (28). Brainstem tissue was selected for our studies because it contains important nuclei involved in descending inhibition and facilitation of nociceptive or pain transmission, as well as ascending pain transmission and integration with higher structures such as the limbic system. The brainstem nuclei involved in descending control or ascending integration include the rostral ventromedial medulla (RVM), the parabrachial nuclei, the dorsal reticular nuclei and the solitary tract nucleus (25). We undertook a comprehensive study to clarify

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“…Up-regulation of HSPs also has been suggested to occur in the endogenous response to spinal cord injury ( Kang et al, 2006 ; Mautes and Noble, 2000 ; Song et al, 2001 ) and peripheral nerve injury ( Kim et al, 2001 ; Klass et al, 2008 ) among other responses such as the activation of endoplasmic reticulum stress response ( Penas et al, 2007 ), and upregulation of c-fos, nitric oxide synthase, heme oxygenase, chemokines and their receptors ( Hayashi et al, 2000 ; Kajander et al, 1996 ; Knerlich-Lukoschus and Held-Feindt, 2015 ; Mautes and Noble, 2000 ; Naik et al, 2006 ; Sharma et al, 1996 ). In the present study, we examined whether the new HSE-RFP reporter system can be used to identify cells that respond to the cellular damage in such traumatic insults, namely spinal cord and sciatic nerve injury, using mouse models.…”

Section: Introductionmentioning

confidence: 99%

Detection of local and remote cellular damage caused by spinal cord and peripheral nerve injury using a heat shock signaling reporter system

et al. 2018

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Heat shock proteins, endothelin, and peripheral neuronal injury

Cited by 5 publications

References 38 publications

Chaperone Proteins in the Central Nervous System and Peripheral Nervous System after Nerve Injury

Chaperone Proteins in the Central Nervous System and Peripheral Nervous System after Nerve Injury

Proteomic analysis of rat brains in a model of neuropathic pain following exposure to electroconvulsive stimulation

Detection of local and remote cellular damage caused by spinal cord and peripheral nerve injury using a heat shock signaling reporter system

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