Nuclear stress granules

Sandqvist, Anton; Sistonen, Lea

doi:10.1083/jcb.200311102

Cited by 20 publications

(7 citation statements)

References 19 publications

(25 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Curiously, after 6 h in culture, we could not observed this perinuclear labelling in any of the test groups or controls. Although we have at present no experimental evidence, we speculate that this change of location pattern could be related to workload-dependent reorganisation of iHSP70 location within lymphocytes in nuclear stress granules (Sandqvist and Sistonen 2004), as observed in fluorescent images of Fig. 5.…”

Section: Discussionmentioning

confidence: 79%

Acute exercise boosts cell proliferation and the heat shock response in lymphocytes: correlation with cytokine production and extracellular-to-intracellular HSP70 ratio

Heck

Scomazzon

Nunes

et al. 2017

Cell Stress and Chaperones

View full text Add to dashboard Cite

Exercise stimulates immune responses, but the appropriate "doses" for such achievements are unsettled. Conversely, in metabolic tissues, exercise improves the heat shock (HS) response, a universal cytoprotective response to proteostasis challenges that are centred on the expression of the 70-kDa family of intracellular heat shock proteins (iHSP70), which are anti-inflammatory. Concurrently, exercise triggers the export of HSP70 towards the extracellular milieu (eHSP70), where they work as pro-inflammatory cytokines. As the HS response is severely compromised in chronic degenerative diseases of inflammatory nature, we wondered whether acute exercise bouts of different intensities could alter the HS response of lymphocytes from secondary lymphoid organs and whether this would be related to immunoinflammatory responses. Adult male Wistar rats swam for 20 min at low, moderate, high or strenuous intensities as per an overload in tail base. Controls remained at rest under the same conditions. Afterwards, mesenteric lymph node lymphocytes were assessed for the potency of the HS response (42 °C for 2 h), NF-κB binding activity, mitogen-stimulated proliferation and cytokine production. Exercise stimulated cell proliferation in an "inverted-U" fashion peaking at moderate load, which was paralleled by suppression of NF-κB activation and nuclear location, and followed by enhanced HS response in relation to non-exercised animals. Comparative levels of eHSP70 to iHSP70 (H-index) matched IL-2/IL-10 ratios. We conclude that exercise, in a workload-dependent way, stimulates immunoinflammatory performance of lymphocytes of tissues far from the circulation and this is associated with H-index of stress response, which is useful to assess training status and immunosurveillance balance.

show abstract

Section: Discussionmentioning

confidence: 79%

Acute exercise boosts cell proliferation and the heat shock response in lymphocytes: correlation with cytokine production and extracellular-to-intracellular HSP70 ratio

Heck

Scomazzon

Nunes

et al. 2017

Cell Stress and Chaperones

View full text Add to dashboard Cite

show abstract

“…In this strain, HSF1 is present diffusely throughout nuclei at ambient temperatures of 20°C–22°C and upon heat shock relocalizes rapidly to stress-induced nuclear puncta (Figures 1B, 1C, S1A, and S1B). These HSF1 nuclear stress granules are a well-accepted readout for HSF1 activation in multiple model systems [19–21], and many have been shown to correspond to transcriptionally active sites in C. elegans [22]. Light activation of ChR2 requires the small molecule all- trans retinal (ATR), which in C. elegans is supplied through food [18].…”

Section: Resultsmentioning

confidence: 99%

“…Although HSF1 nuclear stress granules form concomitant with the induction of heat shock gene transcription, HSF1 stress granules do not typically localize to hsp70 promoters [19–21]. We therefore tested whether, along with the activation of HSF1 evidenced by nuclear stress granule formation, optogenetic stimulation of the ADF and NSM neurons also increased hsp70 mRNA levels.…”

Section: Resultsmentioning

confidence: 99%

Neuronal Serotonin Release Triggers the Heat Shock Response in C. elegans in the Absence of Temperature Increase

et al. 2015

View full text Add to dashboard Cite

Summary Background Cellular mechanisms aimed at repairing protein damage and maintaining homeostasis, widely understood to be triggered by the damage itself, have recently been shown to be under cell nonautonomous control in the metazoan C. elegans. The heat shock response (HSR) is one such conserved mechanism, activated by cells upon exposure to proteotoxic conditions such as heat. Previously, we had shown that this conserved cytoprotective response is regulated by the thermosensory neuronal circuitry of C. elegans. Here, we investigate the mechanisms and physiological relevance of neuronal control. Results By combining optogenetic methods with live visualization of the dynamics of the heat shock transcription factor (HSF1), we show that excitation of the AFD thermosensory neurons is sufficient to activate HSF1 in another cell, even in the absence of temperature increase. Excitation of the AFD thermosensory neurons enhances serotonin release. Serotonin release elicited by direct optogenetic stimulation of serotonergic neurons activates HSF1 and upregulates molecular chaperones through the metabotropic serotonin receptor SER-1. Consequently, excitation of serotonergic neurons alone can suppress protein misfolding in C. elegans peripheral tissue. Conclusions These studies imply that thermosensory activity coupled to serotonergic signaling is sufficient to activate the protective HSR prior to frank proteotoxic damage. The ability of neurosensory release of serotonin to control cellular stress responses and activate HSF1 has powerful implications for the treatment of protein conformation diseases.

show abstract

“…Environmental stress can trigger the formation of SGs, including nuclear SGs, which contain heat-shock transcription factor 1/2 (HSF1/2) and pre-mRNA processing factors [ 1 , 2 ] and also cytoplasmic SGs, which are composed of proteins and mRNAs [ 3 ]. This article focuses on cytoplasmic SGs, and the term SG refers to cytoplasmic stress granules hereafter.…”

Section: Introductionmentioning

confidence: 99%

Relationships between Stress Granules, Oxidative Stress, and Neurodegenerative Diseases

Chen

Liu

2017

Oxidative Medicine and Cellular Longevity

109

View full text Add to dashboard Cite

Cytoplasmic stress granules (SGs) are critical for facilitating stress responses and for preventing the accumulation of misfolded proteins. SGs, however, have been linked to the pathogenesis of neurodegenerative diseases, in part because SGs share many components with neuronal granules. Oxidative stress is one of the conditions that induce SG formation. SGs regulate redox levels, and SG formation in turn is differently regulated by various types of oxidative stress. These associations and other evidences suggest that SG formation contributes to the development of neurodegenerative diseases. In this paper, we review the regulation of SG formation/assembly and discuss the interactions between oxidative stress and SG formation. We then discuss the links between SGs and neurodegenerative diseases and the current therapeutic approaches for neurodegenerative diseases that target SGs.

show abstract

Nuclear stress granules

Cited by 20 publications

References 19 publications

Acute exercise boosts cell proliferation and the heat shock response in lymphocytes: correlation with cytokine production and extracellular-to-intracellular HSP70 ratio

Acute exercise boosts cell proliferation and the heat shock response in lymphocytes: correlation with cytokine production and extracellular-to-intracellular HSP70 ratio

Neuronal Serotonin Release Triggers the Heat Shock Response in C. elegans in the Absence of Temperature Increase

Relationships between Stress Granules, Oxidative Stress, and Neurodegenerative Diseases

Contact Info

Product

Resources

About