ArticlePLoS computational biology2014
Overexpression of heat shock protein 72 attenuates NF-κB activation using a combination of regulatory mechanisms in microglia.
Article in PLoS computational biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 40 citations in OpenAlex.
- Activation of heat shock response to treat obese subjects with type 2 diabetes: a prospective, frequency-escalating, randomized, open-label, triple-arm trial.Scientific reports · 2016Trial
- Acupuncture-induced HSP70 upregulation in neuroprotection: mitochondrial and anti-apoptotic mechanisms.American journal of translational research · 2026Review
- Article
- HSPA2 influences the differentiation and production of immunomodulatory mediators in human immortalized epidermal keratinocyte lines.Cell death & disease · 2025Article
- Modulation of Abundance and Location of High-Mobility Group Box 1 in Human Microglia and Macrophages under Oxygen-Glucose Deprivation.ACS pharmacology & translational science · 2024Article
- HSP70 Family in Cancer: Signaling Mechanisms and Therapeutic Advances.Biomolecules · 2023Review
- Increased supply of methionine during a heat-stress challenge in lactating holstein cows alters mammary tissue mTOR signaling and its response to lipopolysaccharide.Journal of animal science · 2022Article
- Hsc70-4 aggravates PolyQ-mediated neurodegeneration by modulating NF-κB mediated immune response inFrontiers in molecular neuroscience · 2022Article
- Advances in the study of HSP70 inhibitors to enhance the sensitivity of tumor cells to radiotherapy.Frontiers in cell and developmental biology · 2022Review
- Baicalin alleviates chronic obstructive pulmonary disease through regulation of HSP72-mediated JNK pathway.Molecular medicine (Cambridge, Mass.) · 2021Article
- Systemic Response of Antioxidants, Heat Shock Proteins, and Inflammatory Biomarkers to Short-Lasting Exercise Training in Healthy Male Subjects.Oxidative medicine and cellular longevity · 2021Article
- Hsp70 and NF-kB Mediated Control of Innate Inflammatory Responses in a Canine Macrophage Cell Line.International journal of molecular sciences · 2020Article
- Heat shock response regulates stimulus-specificity and sensitivity of the pro-inflammatory NF-κB signalling.Cell communication and signaling : CCS · 2020Article
- Expression of NaV-1.7, TNF-α and HSP-70 in experimental flare-up post-extirpated dental pulp tissue through a neuroimmunological approach.The Saudi dental journal · 2020Article
- Preventive Effects of Dulaglutide on Disuse Muscle Atrophy Through Inhibition of Inflammation and Apoptosis by Induction of Hsp72 Expression.Frontiers in pharmacology · 2020Article
- The effect of exposure time and concentration of airborne PMRedox biology · 2019Article
- Heat-Shock Proteins in Neuroinflammation.Frontiers in pharmacology · 2019Review
- Quantitative analysis reveals crosstalk mechanisms of heat shock-induced attenuation of NF-κB signaling at the single cell level.PLoS computational biology · 2018Article
- Danger signals in stroke and their role on microglia activation after ischemia.Therapeutic advances in neurological disorders · 2018Review
- Twelve hours of heat stress induces inflammatory signaling in porcine skeletal muscle.American journal of physiology. Regulatory, integrative and comparative physiology · 2016Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
Overexpression of the inducible heat shock protein 70, Hsp72, has broadly cytoprotective effects and improves outcome following stroke. A full understanding of how Hsp72 protects cells against injury is elusive, though several distinct mechanisms are implicated. One mechanism is its anti-inflammatory effects. We study the effects of Hsp72 overexpression on activation of the transcription factor NF-κB in microglia combining experimentation and mathematical modeling, using TNFα to stimulate a microglial cell line stably overexpressing Hsp72. We find that Hsp72 overexpression reduces the amount of NF-κB DNA binding activity, activity of the upstream kinase IKK, and amount of IκBα inhibitor phosphorylated following TNFα application. Simulations evaluating several proposed mechanisms suggest that inhibition of IKK activation is an essential component of its regulatory activities. Unexpectedly we find that Hsp72 overexpression reduces the initial amount of the RelA/p65 NF-κB subunit in cells, contributing to the attenuated response. Neither mechanism in isolation, however, is sufficient to attenuate the response, providing evidence that Hsp72 relies upon multiple mechanisms to attenuate NF-κB activation. An additional observation from our study is that the induced expression of IκBα is altered significantly in Hsp72 expressing cells. While the mechanism responsible for this observation is not known, it points to yet another means by which Hsp72 may alter the NF-κB response. This study illustrates the multi-faceted nature of Hsp72 regulation of NF-κB activation in microglia and offers further clues to a novel mechanism by which Hsp72 may protect cells against injury.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.