ArticleInternational journal of molecular sciences2014
Exercise preconditioning protects against spinal cord injury in rats by upregulating neuronal and astroglial heat shock protein 72.
Article in International journal of molecular sciences, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 25 citations in OpenAlex.
- Certolizumab enhances spinal cord injury recovery in rats through inhibition of the TNF-α signaling pathway and neuronal apoptosis.Inflammopharmacology · 2025Article
- CircSmox knockdown alleviates PC12 cell apoptosis and inflammation in spinal cord injury by miR-340-5p/Smurf1 axis.Immunity, inflammation and disease · 2023Article
- The Proteostasis Network: A Global Therapeutic Target for Neuroprotection after Spinal Cord Injury.Cells · 2022Review
- Heat Shock Protein 70 in Penile Neurovascular Regeneration Requires Cystathionine Gamma-Lyase.The world journal of men's health · 2022Article
- Histological and Top-Down Proteomic Analyses of the Visual Pathway in the Cuprizone Demyelination Model.Journal of molecular neuroscience : MN · 2022Article
- Exercise Rehabilitation and/or Astragaloside Attenuate Amyloid-beta Pathology by Reversing BDNF/TrkB Signaling Deficits and Mitochondrial Dysfunction.Molecular neurobiology · 2022Article
- Exosomes Derived from lncRNA TCTN2-Modified Mesenchymal Stem Cells Improve Spinal Cord Injury by miR-329-3p/IGF1R Axis.Journal of molecular neuroscience : MN · 2022Article
- Mechanism Underlying Acupuncture Therapy in Spinal Cord Injury: A Narrative Overview of Preclinical Studies.Frontiers in pharmacology · 2022Review
- Overexpression of lncRNA TCTN2 protects neurons from apoptosis by enhancing cell autophagy in spinal cord injury.FEBS open bio · 2019Article
- Exercise Preconditioning Attenuates Neurological Injury by Preserving Old and Newly Formed HSP72-Containing Neurons in Focal Brain Ischemia Rats.International journal of medical sciences · 2019Article
- D-β-hydroxybutyrate promotes functional recovery and relieves pain hypersensitivity in mice with spinal cord injury.British journal of pharmacology · 2017Article
- Exercise attenuates neurological deficits by stimulating a critical HSP70/NF-κB/IL-6/synapsin I axis in traumatic brain injury rats.Journal of neuroinflammation · 2017Article
- Chaperone Proteins in the Central Nervous System and Peripheral Nervous System after Nerve Injury.Frontiers in neuroscience · 2017Review
- Effects of voluntary exercise on apoptosis and cortisol after chronic restraint stress in mice.Journal of exercise nutrition & biochemistry · 2016Article
- Exercise promotes motor functional recovery in rats with corticospinal tract injury: anti-apoptosis mechanism.Neural regeneration research · 2015Article
- Decreasing or increasing heat shock protein 72 exacerbates or attenuates heat-induced cell death, respectively, in rat hypothalamic cells.FEBS open bio · 2015Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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.
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