Molecular Mechanisms of Anti-Aging Hormetic Effects of Mild Heat Stress on Human Cells

Rattan, Suresh; Eskildsen‐Helmond, Yvonne E. G.; Beedholm, Rasmus

doi:10.1080/15401420490464376

Cited by 21 publications

(21 citation statements)

References 52 publications

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“…The stress response is one of the body's most important cellular defense mechanisms (Rattan et al 2004). Heat stress is one of the inducers of the stress response pathway and is used in this study to activate the HSR.…”

Section: Discussionmentioning

confidence: 99%

“…Heat is a form of stress which activates the heat stress response (Gabai et al 1997) and involves the signaling of heat shock factors which translocate to the nucleus and bind to heat shock elements to induce the transcription and translation of heat shock proteins (HSP) (Morimoto 1998;Rattan et al 2004). The main role of the heat stress response is to protect the cell during stressful conditions by promoting its cell survival.…”

Section: Introductionmentioning

confidence: 99%

“…The heat stress response is one of the body's most important cellular defense mechanisms and is important for cellular function (Rattan et al 2004). Heat is a form of stress which activates the heat stress response (Gabai et al 1997) and involves the signaling of heat shock factors which translocate to the nucleus and bind to heat shock elements to induce the transcription and translation of heat shock proteins (HSP) (Morimoto 1998;Rattan et al 2004).…”

Section: Introductionmentioning

confidence: 99%

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The regulation of TNFα production after heat and endotoxin stimulation is dependent on Annexin-A1 and HSP70

Nair

Arora

Lim

et al. 2015

Cell Stress and Chaperones

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Febrile temperatures can induce stress responses which protect cells from damage and can reduce inflammation during infections and sepsis. However, the mechanisms behind the protective functions of heat in response to the bacterial endotoxin LPS are unclear. We have recently shown that Annexin-1 (ANXA1)-deficient macrophages exhibited higher TNFα levels after LPS stimulation. Moreover, we have previously reported that ANXA1 can function as a stress protein.Therefore in this study, we determined if ANXA1 is involved in the protective effects of heat on cytokine levels in macrophages after heat and LPS. Exposure of macrophages to 42°C for 1 h prior to LPS results in an inhibition of TNFα production, which was not evident in ANXA1 −/− macrophages. We show that this regulation involves primarily MYD88-independent pathways. ANXA1 regulates TNFα mRNA stability after heat and LPS, and this is dependent on endogenous ANXA1 expression and not exogenously secreted factors. Further mechanistic studies revealed the possible involvement of the heat shock protein HSP70 and JNK in the heat and inflammatory stress response regulated by ANXA1. This study shows that ANXA1, an immunomodulatory protein, is critical in the heat stress response induced after heat and endotoxin stimulation.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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The regulation of TNFα production after heat and endotoxin stimulation is dependent on Annexin-A1 and HSP70

Nair

Arora

Lim

et al. 2015

Cell Stress and Chaperones

View full text Add to dashboard Cite

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“…in its redox status, protein metabolism and stability, DNA synthesis, etc. (Rattan et al 2004). Moreover, these stresses affect cellular longevity.…”

Section: Discussionmentioning

confidence: 98%

“…In a series of studies, Rattan and collaborators have shown that repeated mild heat stress (exposure to 41 0 C for 1h twice a week) has anti-ageing effects. In particular, this treatment reduces the accumulation of oxidatively and glycoxidatively damaged proteins, stimulates the proteasomal activities for the degradation of abnormal proteins, enhances the cellular antioxidant ability and its resistance to other stresses (Rattan et al 2004). Calorie restriction represents another type of mild stress.…”

Section: Discussionmentioning

confidence: 99%

The Unexpected Anabolic Phenotype and Extended Longevity of Skin Fibroblasts after Chronic Glucocorticoid Excess

et al. 2006

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Intense stress can challenge tissue homeostasis and accelerate the ageing process. However, several lines of evidence indicate that repeated mild stresses can have beneficial and even life-prolonging effects. Hypersecretion of glucocorticoids (GC) represents the major hormonal response to stress. Besides its life-sustaining role, GC excess, usually due to several side-effects that promote a "catabolic" phenotype, can be detrimental for several tissues. Cushing's syndrome patients are characterized by chronic endogenous GC excess and consequently at the time of diagnosis they have an atrophic elderly-like skin. Interestingly, when Cushing's syndrome fibroblasts were removed from the high-GC milieu in vivo and cultured in vitro under standard conditions they express an "anabolic" phenotype, i.e. they restore their ability for collagen synthesis, they secrete reduced levels of metalloproteases (MMP-1 and MMP-2) and have an increased proliferative capacity and contractility. Furthermore, these cells exhibit a significant extension of their proliferative lifespan, while they respond better to exogenous stress by producing significantly higher levels of heat-shock protein-70 (HSP70). These results imply that long-term hypercortisolism in vivo can have beneficial consequences on fibroblast physiology in vitro.

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Hormesis, cellular stress response and neuroinflammation in schizophrenia: Early onset versus late onset state

Calabrese

Giordano

Crupi

et al. 2016

J of Neuroscience Research

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Abnormal redox homeostasis and oxidative stress have been proposed to play a role in the etiology of several neuropsychiatric spectrum disorders. Emerging interest has recently focused on markers of oxidative stress and neuroinflammation in schizophrenic spectrum disorders, at least in particular subgroups of patients. Altered expression of genes related to oxidative stress, oxidative damage to DNA, protein and lipids, as well as reduced glutathione levels in central and peripheral tissues could act synergistically, and contribute to the course of the disease. Herein, we discuss cellular mechanisms that may be operative in neuroinflammation and contributory to schizophrenia. We address modulation of endogenous cellular defense mechanisms as a potentially innovative approach to therapeutics for schizophrenia, and other neuropsychiatric conditions that are associated with neuroinflammation. Specifically, we discuss the emerging role of heme oxygenase as prominent member of neuroprotective network in redox stress responsive mechanisms, as well as the importance of glutathione relevant in schizophrenia pathophysiology. Finally we introduce the hormetic dose response concept as relevant and important to neuroprotection, and review hormetic mechanisms as possible approaches to manipulation of neuroinflammatory targets that may be viable for treating schizophrenia spectrum disorders. © 2016 Wiley Periodicals, Inc.

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Molecular Mechanisms of Anti-Aging Hormetic Effects of Mild Heat Stress on Human Cells

Cited by 21 publications

References 52 publications

The regulation of TNFα production after heat and endotoxin stimulation is dependent on Annexin-A1 and HSP70

The regulation of TNFα production after heat and endotoxin stimulation is dependent on Annexin-A1 and HSP70

The Unexpected Anabolic Phenotype and Extended Longevity of Skin Fibroblasts after Chronic Glucocorticoid Excess

Hormesis, cellular stress response and neuroinflammation in schizophrenia: Early onset versus late onset state

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