The potential role of heat shock proteins in acute spinal cord injury

Zhou, Yijun; Xu, Leilei; Song, Xinghua; Ding, Liwen; Chen, Jiangtao; Wang, Chong; Gan, Yuling; Zhu, Xiaomeng; Yu, Yipin; Liang, Qiuzhen

doi:10.1007/s00586-014-3214-1

Cited by 17 publications

(12 citation statements)

References 48 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This raises the question of direct effect of HSP 72 vs. downstream signaling involving NFκB or entirely different neuroprotective effect by different mechanism such as upregulation of micro RNAs from exercise. A recent study demonstrated down regulation of HSP 90 ab1, HSP a4 and HSP e1 in acute SCI [34]. These findings suggest the involvement of other HSPs in SCI besides HSP 72.…”

Section: Discussionmentioning

confidence: 78%

Exercise Preconditioning Protects against Spinal Cord Injury in Rats by Upregulating Neuronal and Astroglial Heat Shock Protein 72

Chang

Chou

Lin

et al. 2014

IJMS

View full text Add to dashboard Cite

The heat shock protein 72 (HSP 72) is a universal marker of stress protein whose expression can be induced by physical exercise. Here we report that, in a localized model of spinal cord injury (SCI), exercised rats (given pre-SCI exercise) had significantly higher levels of neuronal and astroglial HSP 72, a lower functional deficit, fewer spinal cord contusions, and fewer apoptotic cells than did non-exercised rats. pSUPER plasmid expressing HSP 72 small interfering RNA (SiRNA-HSP 72) was injected into the injured spinal cords. In addition to reducing neuronal and astroglial HSP 72, the (SiRNA-HSP 72) significantly attenuated the beneficial effects of exercise preconditioning in reducing functional deficits as well as spinal cord contusion and apoptosis. Because exercise preconditioning induces increased neuronal and astroglial levels of HSP 72 in the gray matter of normal spinal cord tissue, exercise preconditioning promoted functional recovery in rats after SCI by upregulating neuronal and astroglial HSP 72 in the gray matter of the injured spinal cord. We reveal an important function of neuronal and astroglial HSP 72 in protecting neuronal and astroglial apoptosis in the injured spinal cord. We conclude that HSP 72-mediated exercise preconditioning is a promising strategy for facilitating functional recovery from SCI.

show abstract

Section: Discussionmentioning

confidence: 78%

Exercise Preconditioning Protects against Spinal Cord Injury in Rats by Upregulating Neuronal and Astroglial Heat Shock Protein 72

Chang

Chou

Lin

et al. 2014

IJMS

View full text Add to dashboard Cite

show abstract

“…), protein folding (Hspa4, Uggt1; Zhou et al . ; Wang et al . ), transcription [Atf6, Ern2 (IRE1β); Rutkowski & Kaufman, ; Oikawa et al .…”

Section: Resultsmentioning

confidence: 99%

Nicotinic receptor activation contrasts pathophysiological bursting and neurodegeneration evoked by glutamate uptake block on rat hypoglossal motoneurons

Corsini

Tortora

Nistri

2016

The Journal of Physiology

View full text Add to dashboard Cite

Excitotoxicity is thought to be one of the early processes in the onset of amyotrophic lateral sclerosis (ALS) because high levels of glutamate have been detected in the cerebrospinal fluid of such patients due to dysfunctional uptake of this transmitter that gradually damages brainstem and spinal motoneurons. To explore potential mechanisms to arrest ALS onset, we used an established in vitro model of rat brainstem slice preparation in which excitotoxicity is induced by the glutamate uptake blocker dl-threo-β-benzyloxyaspartate (TBOA). Because certain brain neurons may be neuroprotected via activation of nicotinic acetylcholine receptors (nAChRs) by nicotine, we investigated if nicotine could arrest excitotoxic damage to highly ALS-vulnerable hypoglossal motoneurons (HMs). On 50% of patch-clamped HMs, TBOA induced intense network bursts that were inhibited by 1-10 μm nicotine, whereas nAChR antagonists facilitated burst emergence in non-burster cells. Furthermore, nicotine inhibited excitatory transmission and enhanced synaptic inhibition. Strong neuroprotection by nicotine prevented the HM loss observed after 4 h of TBOA exposure. This neuroprotective action was due to suppression of downstream effectors of neurotoxicity such as increased intracellular levels of reactive oxygen species, impaired energy metabolism and upregulated genes involved in endoplasmic reticulum (ER) stress. In addition, HMs surviving TBOA toxicity often expressed UDP-glucose glycoprotein glucosyltransferase, a key element in repair of misfolded proteins: this phenomenon was absent after nicotine application, indicative of ER stress prevention. Our results suggest nAChRs to be potential targets for inhibiting excitotoxic damage of motoneurons at an early stage of the neurodegenerative process.

show abstract

“…The fragment intensity multiplier was set to 30. The maximum accumulation time was 0.1 s and the dynamic exclusion for the selected precursor ions was set at 25 s .…”

Section: Methodsmentioning

confidence: 99%

iTRAQ proteomic analysis of N‐acetylmuramic acid mediated anti‐inflammatory capacity in LPS‐induced RAW 264.7 cells

Pan

Guo

et al. 2015

Proteomics

View full text Add to dashboard Cite

Lactobacillus acidophilus probiotic bacteria have lasting beneficial health effects in the gastrointestinal tract, including protecting against pathogens, improving immunomodulation, and producing beneficial bacteria-derived molecules. In lipopolysaccharide (LPS) induced RAW 264.7 cells treated with peptidoglycan or N-acetylmuramic acid (NAM) from L. acidophilus, 390 differentially expressed proteins (8.76%) were identified by iTRAQ analysis, 257 (5.77%) of which were upregulated and 133 (2.99%) were downregulated under LPS-induced conditions. Most of these proteins were grouped into the following inflammation-related cellular signaling: lysosome pathway, calcium signaling pathway, and Toll-like receptor (TLR) signaling pathway. Among them, clathrin, SERCA, and interleukin 1 receptor antagonist were differentially expressed to a significant degree in peptidoglycan or NAM pretreated RAW 264.7 cells. Bioinformatics analysis indicated that NAM may mediate an anti-inflammatory process via a Ca(2+) -dependent NF-κB pathway. These observations reveal new insights into the molecular mechanisms involved in the suppression of LPS-induced macrophage inflammation by L. acidophilus.

show abstract

The potential role of heat shock proteins in acute spinal cord injury

Abstract: The differentially expressed proteins of spinal cord tissues after ASCI will provide scientific foundation for further study to explore the secondary injury mechanism of ASCI.

Cited by 17 publications

References 48 publications

Exercise Preconditioning Protects against Spinal Cord Injury in Rats by Upregulating Neuronal and Astroglial Heat Shock Protein 72

Exercise Preconditioning Protects against Spinal Cord Injury in Rats by Upregulating Neuronal and Astroglial Heat Shock Protein 72

Nicotinic receptor activation contrasts pathophysiological bursting and neurodegeneration evoked by glutamate uptake block on rat hypoglossal motoneurons

iTRAQ proteomic analysis of N‐acetylmuramic acid mediated anti‐inflammatory capacity in LPS‐induced RAW 264.7 cells

Contact Info

Product

Resources

About