Expression of human HSP27 in yeast extends replicative lifespan and uncovers a hormetic response

Camandona, Vittoria de Lima; Rios-Anjos, Rafaela Maria; Alegria, Thiago Gerônimo Pires; Pereira, Fábio Renato; Bicev, Renata N.; Cunha, Fernanda Marques da; Digiampietri, Luciano Antônio; Barros, Mário H.; Netto, Luís Eduardo Soares; Ferreira-Junior, Jose Ribamar

doi:10.1007/s10522-020-09869-9

Cited by 10 publications

(9 citation statements)

References 79 publications

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“…Further evidence for a hormetic response by the NDV infection of tumor cells was obtained in 2002 with a paper entitled: "Dendritic cells pulsed with viral oncolysate potently stimulate autologous T cells from cancer patients" [108]. The paper reports that primary operated breast cancer patients contain in their BM cancer-reactive memory T cells (MTCs).…”

Section: Hormetic Aspects Of Oncolytic Viruses and Cancer Vaccinesmentioning

confidence: 99%

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Less Can Be More: The Hormesis Theory of Stress Adaptation in the Global Biosphere and Its Implications

Schirrmacher¹

2021

Biomedicines

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A dose-response relationship to stressors, according to the hormesis theory, is characterized by low-dose stimulation and high-dose inhibition. It is non-linear with a low-dose optimum. Stress responses by cells lead to adapted vitality and fitness. Physical stress can be exerted through heat, radiation, or physical exercise. Chemical stressors include reactive species from oxygen (ROS), nitrogen (RNS), and carbon (RCS), carcinogens, elements, such as lithium (Li) and silicon (Si), and metals, such as silver (Ag), cadmium (Cd), and lead (Pb). Anthropogenic chemicals are agrochemicals (phytotoxins, herbicides), industrial chemicals, and pharmaceuticals. Biochemical stress can be exerted through toxins, medical drugs (e.g., cytostatics, psychopharmaceuticals, non-steroidal inhibitors of inflammation), and through fasting (dietary restriction). Key-lock interactions between enzymes and substrates, antigens and antibodies, antigen-presenting cells, and cognate T cells are the basics of biology, biochemistry, and immunology. Their rules do not obey linear dose-response relationships. The review provides examples of biologic stressors: oncolytic viruses (e.g., immuno-virotherapy of cancer) and hormones (e.g., melatonin, stress hormones). Molecular mechanisms of cellular stress adaptation involve the protein quality control system (PQS) and homeostasis of proteasome, endoplasmic reticulum, and mitochondria. Important components are transcription factors (e.g., Nrf2), micro-RNAs, heat shock proteins, ionic calcium, and enzymes (e.g., glutathion redox enzymes, DNA methyltransferases, and DNA repair enzymes). Cellular growth control, intercellular communication, and resistance to stress from microbial infections involve growth factors, cytokines, chemokines, interferons, and their respective receptors. The effects of hormesis during evolution are multifarious: cell protection and survival, evolutionary flexibility, and epigenetic memory. According to the hormesis theory, this is true for the entire biosphere, e.g., archaia, bacteria, fungi, plants, and the animal kingdoms.

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Section: Hormetic Aspects Of Oncolytic Viruses and Cancer Vaccinesmentioning

confidence: 99%

“…NDV infection of MCF-7 cells resulted in a number of differences in protein expression by Western blots. MALDI mass spectrometry of prominent proteins revealed a heat-shock protein (HSP), which, upon NDV infection, became phosphorylated: HSP27 [108].…”

Section: Hormetic Aspects Of Oncolytic Viruses and Cancer Vaccinesmentioning

confidence: 99%

Less Can Be More: The Hormesis Theory of Stress Adaptation in the Global Biosphere and Its Implications

Schirrmacher¹

2021

Biomedicines

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“…Hsp27 is a member of a small HSP family and is constitutively expressed in cells. Its main functions include modulating the ability of cells to respond to several types of injury, such as heat shock and oxidative stress [ 40 ]. It can be rapidly activated at elevated temperatures.…”

Section: Discussionmentioning

confidence: 99%

Effect of Heat Shock Preconditioning on Pressure Injury Prevention via Hsp27 Upregulation in Rat Models

Takashi

Liang

et al. 2022

IJMS

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Pressure injury (PI) prevention is a huge industry and involves various interventions. Temperature and moisture are important factors for wound healing; however, the active mechanism by which “moist heat” affects PI prevention has not yet been clarified. Thus, we explored the protective and therapeutic effects of hydrotherapy on PI based on the preconditioning (PC) principle, which might be useful for clinical practice. This study aimed to investigate the preventive mechanisms of heat shock preconditioning on PIs in rat models. The experiment was performed in the basic medical laboratory of Nagano College of Nursing in Japan. Ten rats were divided into two groups, with five rats in each group. Rats in the control group were not bathed. Rats in the preconditioning group (PC group) were bathed with hot tap-water. Bathing was conducted thrice a week. After bathing for 4 weeks, the PI model was constructed on the rats’ dorsal skin. The skin temperature, skin moisture, and area of ulcers were compared between the two groups. In vitro, we investigated the expression of heat shock protein 27 (Hsp27) in 6, 12, and 24 h after the PI model was constructed through Western blot analysis. Ulcers occurred in the control group 24 h after the PI model constructed, wheras the PC group exhibited ulcers after 36 h. The ulcer area was larger in the control group than that in the PC group after 24 h (all p < 0.05). The temperatures of PI wounds in the control group decreased and were lower than those in the PC group after 1, 6, 12, 36, and 48 h (all p < 0.05). However, the skin moisture levels of PI wounds increased in the control group and were higher than those in the PC group at the same time (all p < 0.05). Using Western blot analysis, hydrotherapy preconditioning showed the potential to increase Hsp27 expression after pressure was released (p < 0.05). We determine that heat shock preconditioning had a preventive effect on PIs in rat models, a result that may be associated with their actions in the upregulation of Hsp27.

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“…HSP27 is present in both cytoplasm and nucleus, although it is located predominantly in the cytosol [48]. In response to different stress conditions, it can also be found in the perinuclear region and within the nucleus [49]. HSP27 is capable of oligomerization and phosphorylation.…”

Section: Figurementioning

confidence: 99%

“…The main function of HSP27 is to modulate the ability of cells to respond to various types of injury, including heat shock and oxidative stress. In these cases, the phosphorylated form of HSP27 interacts with denatured and aggregated nuclear proteins, protecting cells from severe damage due to stress [49]. HSP27 also acts as a chaperone independent of ATP, mediating a wide range of cytoprotective functions by ensuring proper protein folding and stabilization and translocation of proteins in response to oxidative stress, ischemia, and viral infections, including coronavirus infection [55][56][57].…”

Section: Figurementioning

confidence: 99%

Could Small Heat Shock Protein HSP27 Be a First-Line Target for Preventing Protein Aggregation in Parkinson’s Disease?

Navarro‐Zaragoza

Cuenca‐Bermejo

Almela

et al. 2021

IJMS

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Small heat shock proteins (HSPs), such as HSP27, are ubiquitously expressed molecular chaperones and are essential for cellular homeostasis. The major functions of HSP27 include chaperoning misfolded or unfolded polypeptides and protecting cells from toxic stress. Dysregulation of stress proteins is associated with many human diseases including neurodegenerative diseases, such as Parkinson’s disease (PD). PD is characterized by the presence of aggregates of α-synuclein in the central and peripheral nervous system, which induces the degeneration of dopaminergic neurons in the substantia nigra pars compacta (SNpc) and in the autonomic nervous system. Autonomic dysfunction is an important non-motor phenotype of PD, which includes cardiovascular dysregulation, among others. Nowadays, the therapies for PD focus on dopamine (DA) replacement. However, certain non-motor symptoms with a great impact on quality of life do not respond to dopaminergic drugs; therefore, the development and testing of new treatments for non-motor symptoms of PD remain a priority. Since small HSP27 was shown to prevent α-synuclein aggregation and cytotoxicity, this protein might constitute a suitable target to prevent or delay the motor and non-motor symptoms of PD. In the first part of our review, we focus on the cardiovascular dysregulation observed in PD patients. In the second part, we present data on the possible role of HSP27 in preventing the accumulation of amyloid fibrils and aggregated forms of α-synuclein. We also include our own studies, highlighting the possible protective cardiac effects induced by L-DOPA treatment through the enhancement of HSP27 levels and activity.

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Expression of human HSP27 in yeast extends replicative lifespan and uncovers a hormetic response

Cited by 10 publications

References 79 publications

Less Can Be More: The Hormesis Theory of Stress Adaptation in the Global Biosphere and Its Implications

Less Can Be More: The Hormesis Theory of Stress Adaptation in the Global Biosphere and Its Implications

Effect of Heat Shock Preconditioning on Pressure Injury Prevention via Hsp27 Upregulation in Rat Models

Could Small Heat Shock Protein HSP27 Be a First-Line Target for Preventing Protein Aggregation in Parkinson’s Disease?

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