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Article ; Online: Extra and intra cellular HSP70 levels in adults with and without metabolic disorders: a systematic review and meta-analysis.

de Lemos Muller, Carlos Henrique / Schroeder, Helena Trevisan / Rodrigues-Krause, Josianne / Krause, Maurício

2023 Volume 28, Issue 6, Page(s) 761–771

Abstract: Metabolic disorders, such as obesity, type 2 diabetes mellitus (T2DM), and metabolic syndrome (MS) are related to chronic pro-inflammatory conditions. Evidence suggests that heat shock proteins are linked to metabolic disorders. Intracellular HSP70 ( ... ...

Abstract	Metabolic disorders, such as obesity, type 2 diabetes mellitus (T2DM), and metabolic syndrome (MS) are related to chronic pro-inflammatory conditions. Evidence suggests that heat shock proteins are linked to metabolic disorders. Intracellular HSP70 (iHSP70) is mandatory for normal insulin signalling, and proteostasis, and exerts a powerful anti-inflammatory role. On the other hand, the extracellular (eHSP72) is linked with a pro-inflammatory state and induces insulin resistance in humans. Then, we conducted a systematic review with meta-analysis to summarize the data of HSP70 in people with and without metabolic disorders. PubMed, Embase, Scopus, and Web of Science databases were used. Eligibility criteria included observational and baseline data of experimental studies that assessed iHSP70 and/or eHSP72 in adults with metabolic disorders and healthy people. The risk of bias was assessed by the Newcastle-Ottawa scale. Meta-analysis was performed using a random-effect model and the mean difference was estimated for eHSP72 and the standardized mean difference for iHSP70. A total of 11,255 articles were retrieved, 31 articles were assessed for eligibility and 15 were included for data extraction. There was no difference in eHSP72 between metabolic disorders and healthy controls (mean difference (MD) = 0.11; 95% confidence interval (CIs) = -0.05 to 0.27; I
MeSH term(s)	Adult ; Humans ; Diabetes Mellitus, Type 2/metabolism ; HSP70 Heat-Shock Proteins/metabolism ; Insulin Resistance ; Obesity/metabolism ; Insulin
Chemical Substances	HSP70 Heat-Shock Proteins ; Insulin
Language	English
Publishing date	2023-07-26
Publishing country	Netherlands
Document type	Meta-Analysis ; Systematic Review ; Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1362749-1
ISSN	1466-1268 ; 1355-8145
ISSN (online)	1466-1268
ISSN	1355-8145
DOI	10.1007/s12192-023-01368-3
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Article ; Online: Resolution of inflammation in chronic disease via restoration of the heat shock response (HSR).

Schroeder, Helena Trevisan / De Lemos Muller, Carlos Henrique / Heck, Thiago Gomes / Krause, Mauricio / Homem de Bittencourt, Paulo Ivo

Cell stress & chaperones

2024 Volume 29, Issue 1, Page(s) 66–87

Abstract: Effective resolution of inflammation via the heat shock response (HSR) is pivotal in averting the transition to chronic inflammatory states. This transition characterizes a spectrum of debilitating conditions, including insulin resistance, obesity, type ... ...

Abstract	Effective resolution of inflammation via the heat shock response (HSR) is pivotal in averting the transition to chronic inflammatory states. This transition characterizes a spectrum of debilitating conditions, including insulin resistance, obesity, type 2 diabetes, nonalcoholic fatty liver disease, and cardiovascular ailments. This manuscript explores a range of physiological, pharmacological, and nutraceutical interventions aimed at reinstating the HSR in the context of chronic low-grade inflammation, as well as protocols to assess the HSR. Monitoring the progression or suppression of the HSR in patients and laboratory animals offers predictive insights into the organism's capacity to combat chronic inflammation, as well as the impact of exercise and hyperthermic treatments (e.g., sauna or hot tub baths) on the HSR. Interestingly, a reciprocal correlation exists between the expression of HSR components in peripheral blood leukocytes (PBL) and the extent of local tissue proinflammatory activity in individuals afflicted by chronic inflammatory disorders. Therefore, the Heck index, contrasting extracellular 70 kDa family of heat shock proteins (HSP70) (proinflammatory) and intracellular HSP70 (anti-inflammatory) in PBL, serves as a valuable metric for HSR assessment. Our laboratory has also developed straightforward protocols for evaluating HSR by subjecting whole blood samples from both rodents and human volunteers to ex vivo heat challenges. Collectively, this discussion underscores the critical role of HSR disruption in the pathogenesis of chronic inflammatory states and emphasizes the significance of simple, cost-effective tools for clinical HSR assessment. This understanding is instrumental in the development of innovative strategies for preventing and managing chronic inflammatory diseases, which continue to exert a substantial global burden on morbidity and mortality.
MeSH term(s)	Animals ; Humans ; Diabetes Mellitus, Type 2 ; Heat-Shock Response ; Heat-Shock Proteins/metabolism ; HSP70 Heat-Shock Proteins/metabolism ; Inflammation ; Chronic Disease
Chemical Substances	Heat-Shock Proteins ; HSP70 Heat-Shock Proteins
Language	English
Publishing date	2024-02-01
Publishing country	Netherlands
Document type	Journal Article ; Review
ZDB-ID	1362749-1
ISSN	1466-1268 ; 1355-8145
ISSN (online)	1466-1268
ISSN	1355-8145
DOI	10.1016/j.cstres.2024.01.005
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Article ; Online: The dance of proteostasis and metabolism: Unveiling the caloristatic controlling switch.

Schroeder, Helena Trevisan / De Lemos Muller, Carlos Henrique / Heck, Thiago Gomes / Krause, Mauricio / Homem de Bittencourt, Paulo Ivo

Cell stress & chaperones

2024 Volume 29, Issue 1, Page(s) 175–200

Abstract: The heat shock response (HSR) is an ancient and evolutionarily conserved mechanism designed to restore cellular homeostasis following proteotoxic challenges. However, it has become increasingly evident that disruptions in energy metabolism also trigger ... ...

Abstract	The heat shock response (HSR) is an ancient and evolutionarily conserved mechanism designed to restore cellular homeostasis following proteotoxic challenges. However, it has become increasingly evident that disruptions in energy metabolism also trigger the HSR. This interplay between proteostasis and energy regulation is rooted in the fundamental need for ATP to fuel protein synthesis and repair, making the HSR an essential component of cellular energy management. Recent findings suggest that the origins of proteostasis-defending systems can be traced back over 3.6 billion years, aligning with the emergence of sugar kinases that optimized glycolysis around 3.594 billion years ago. This evolutionary connection is underscored by the spatial similarities between the nucleotide-binding domain of HSP70, the key player in protein chaperone machinery, and hexokinases. The HSR serves as a hub that integrates energy metabolism and resolution of inflammation, further highlighting its role in maintaining cellular homeostasis. Notably, 5'-adenosine monophosphate-activated protein kinase emerges as a central regulator, promoting the HSR during predominantly proteotoxic stress while suppressing it in response to predominantly metabolic stress. The complex relationship between 5'-adenosine monophosphate-activated protein kinase and the HSR is finely tuned, with paradoxical effects observed under different stress conditions. This delicate equilibrium, known as caloristasis, ensures that cellular homeostasis is maintained despite shifting environmental and intracellular conditions. Understanding the caloristatic controlling switch at the heart of this interplay is crucial. It offers insights into a wide range of conditions, including glycemic control, obesity, type 2 diabetes, cardiovascular and neurodegenerative diseases, reproductive abnormalities, and the optimization of exercise routines. These findings highlight the profound interconnectedness of proteostasis and energy metabolism in cellular function and adaptation.
MeSH term(s)	Humans ; Proteostasis ; Diabetes Mellitus, Type 2 ; HSP70 Heat-Shock Proteins/metabolism ; Heat-Shock Response ; Adenosine Monophosphate/metabolism ; Protein Kinases/metabolism
Chemical Substances	HSP70 Heat-Shock Proteins ; Adenosine Monophosphate (415SHH325A) ; Protein Kinases (EC 2.7.-)
Language	English
Publishing date	2024-02-06
Publishing country	Netherlands
Document type	Journal Article ; Review
ZDB-ID	1362749-1
ISSN	1466-1268 ; 1355-8145
ISSN (online)	1466-1268
ISSN	1355-8145
DOI	10.1016/j.cstres.2024.02.002
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Article ; Online: Heat shock response during the resolution of inflammation and its progressive suppression in chronic-degenerative inflammatory diseases.

Schroeder, Helena Trevisan / De Lemos Muller, Carlos Henrique / Heck, Thiago Gomes / Krause, Mauricio / Homem de Bittencourt, Paulo Ivo

Cell stress & chaperones

2024 Volume 29, Issue 1, Page(s) 116–142

Abstract: The heat shock response (HSR) is a crucial biochemical pathway that orchestrates the resolution of inflammation, primarily under proteotoxic stress conditions. This process hinges on the upregulation of heat shock proteins (HSPs) and other chaperones, ... ...

Abstract	The heat shock response (HSR) is a crucial biochemical pathway that orchestrates the resolution of inflammation, primarily under proteotoxic stress conditions. This process hinges on the upregulation of heat shock proteins (HSPs) and other chaperones, notably the 70 kDa family of heat shock proteins, under the command of the heat shock transcription factor-1. However, in the context of chronic degenerative disorders characterized by persistent low-grade inflammation (such as insulin resistance, obesity, type 2 diabetes, nonalcoholic fatty liver disease, and cardiovascular diseases) a gradual suppression of the HSR does occur. This work delves into the mechanisms behind this phenomenon. It explores how the Western diet and sedentary lifestyle, culminating in the endoplasmic reticulum stress within adipose tissue cells, trigger a cascade of events. This cascade includes the unfolded protein response and activation of the NOD-like receptor pyrin domain-containing protein-3 inflammasome, leading to the emergence of the senescence-associated secretory phenotype and the propagation of inflammation throughout the body. Notably, the activation of the NOD-like receptor pyrin domain-containing protein-3 inflammasome not only fuels inflammation but also sabotages the HSR by degrading human antigen R, a crucial mRNA-binding protein responsible for maintaining heat shock transcription factor-1 mRNA expression and stability on heat shock gene promoters. This paper underscores the imperative need to comprehend how chronic inflammation stifles the HSR and the clinical significance of evaluating the HSR using cost-effective and accessible tools. Such understanding is pivotal in the development of innovative strategies aimed at the prevention and treatment of these chronic inflammatory ailments, which continue to take a heavy toll on global health and well-being.
MeSH term(s)	Humans ; Heat Shock Transcription Factors ; Diabetes Mellitus, Type 2 ; Inflammasomes/metabolism ; Inflammasomes/pharmacology ; Heat-Shock Response ; Heat-Shock Proteins/metabolism ; Inflammation ; RNA, Messenger ; NLR Proteins/metabolism ; HSP70 Heat-Shock Proteins/metabolism
Chemical Substances	Heat Shock Transcription Factors ; Inflammasomes ; Heat-Shock Proteins ; RNA, Messenger ; NLR Proteins ; HSP70 Heat-Shock Proteins
Language	English
Publishing date	2024-01-19
Publishing country	Netherlands
Document type	Journal Article ; Review
ZDB-ID	1362749-1
ISSN	1466-1268 ; 1355-8145
ISSN (online)	1466-1268
ISSN	1355-8145
DOI	10.1016/j.cstres.2024.01.002
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Article ; Online: Cross-sectional evaluation of socioeconomic and clinical factors and the impact of fibromyalgia on the quality of life of patients during the COVID-19 pandemic.

Schroeder, Helena Trevisan / Cavalheiro, Joana Caline Alves / Martins, Edna Thaís Jeremias / Bock, Patricia Martins

Sao Paulo medical journal = Revista paulista de medicina

2022 Volume 141, Issue 2, Page(s) 138–145

Abstract: Background: The fibromyalgia impact questionnaire (FIQ) relates to the functional capacity, professional situation, psychological disorders, and physical symptoms, and can identify the factors that determine the impact of the syndrome and ... ...

Abstract	Background: The fibromyalgia impact questionnaire (FIQ) relates to the functional capacity, professional situation, psychological disorders, and physical symptoms, and can identify the factors that determine the impact of the syndrome and characteristics of its carriers; the higher the score, the greater the impact of fibromyalgia on the quality of life. Objective: To evaluate the impact of fibromyalgia on the quality of life of individuals with fibromyalgia, who were categorized according to the FIQ during the coronavirus disease pandemic. Design and setting: A cross-sectional study was conducted at an institution of higher education in Taquara, RS, Brazil. Methods: A quantitative study was carried out, with the application of a sociodemographic and clinical questionnaire, and the FIQ in 163 Brazilian individuals with a medical diagnosis of fibromyalgia. Data were collected using SurveyMonkey software. Results: Of the female carriers, 98.2% were living in urban areas, working, and under pharmacological and complementary treatment. The FIQ results showed that seven of the 10 items had the maximum score. The items "physical function" and "feel good" had intermediate scores, and the item "missed work" had a low score. The average total score was 79.9 points, indicating that fibromyalgia had a severe impact on the participants' lives. A severe impact of fibromyalgia was observed in 61.3% of the participants, a moderate impact in 30.7%, and a low impact in 8%. Conclusion: The survey findings suggest a severe impact in the majority of the Brazilian fibromyalgic population.
MeSH term(s)	Humans ; Female ; Quality of Life ; Fibromyalgia/epidemiology ; Cross-Sectional Studies ; Pandemics ; COVID-19 ; Surveys and Questionnaires ; Socioeconomic Factors
Language	English
Publishing date	2022-09-12
Publishing country	Brazil
Document type	Journal Article
ZDB-ID	1203171-9
ISSN	1806-9460 ; 1516-3180 ; 0035-0362
ISSN (online)	1806-9460
ISSN	1516-3180 ; 0035-0362
DOI	10.1590/1516-3180.2022.0051.R2119052022
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Article ; Online: Effects of resistance training on heat shock response (HSR), HSP70 expression, oxidative stress, inflammation, and metabolism in middle-aged people.

de Lemos Muller, Carlos Henrique / Schroeder, Helena Trevisan / Farinha, Juliano Boufleur / Lopez, Pedro / Reischak-Oliveira, Álvaro / Pinto, Ronei Silveira / de Bittencourt Júnior, Paulo Ivo Homem / Krause, Mauricio

Journal of physiology and biochemistry

2023 Volume 80, Issue 1, Page(s) 161–173

Abstract: Resistance training (RT) can increase the heat shock response (HSR) in the elderly. As middle-aged subjects already suffer physiological declines related to aging, it is hypothesized that RT may increase the HSR in these people. To assess the effects of ... ...

Abstract	Resistance training (RT) can increase the heat shock response (HSR) in the elderly. As middle-aged subjects already suffer physiological declines related to aging, it is hypothesized that RT may increase the HSR in these people. To assess the effects of resistance training on heat shock response, intra and extracellular HSP70, oxidative stress, inflammation, body composition, and metabolism in middle-aged subjects. Sixteen volunteers (40 - 59 years) were allocated to two groups: the trained group (n = 7), which performed 12 weeks of RT; and the physically inactive-control group (n = 9), which did not perform any type of exercise. The RT program consisted of 9 whole-body exercises (using standard gym equipment) and functional exercises, carried out 3 times/week. Before and after the intervention, body composition, muscle mass, strength, functional capacity, and blood sample measurements (lipid profile, glucose, insulin, oxidative damage, TNF-α, the HSR, HSP70 expression in leukocytes, and HSP72 in plasma) were performed. The HSR analysis demonstrated that this response is maintained at normal levels in middle-aged people and that RT did not cause any improvement. Also, RT increases muscle mass, strength, and functional capacity. Despite no additional changes of RT on the antioxidant defenses (catalase, glutathione peroxidase, and reductase) or inflammation, lipid peroxidation was diminished by RT (group x time interaction, p = 0.009), indicating that other antioxidant defenses may be improved after RT. HSR is preserved in middle-aged subjects without metabolic complications. In addition, RT reduces lipid peroxidation and can retard muscle mass and strength loss related to the aging process.
MeSH term(s)	Aged ; Humans ; Middle Aged ; Antioxidants ; Heat-Shock Response/physiology ; Inflammation/metabolism ; Oxidative Stress/physiology ; Resistance Training ; HSP70 Heat-Shock Proteins/metabolism
Chemical Substances	Antioxidants ; HSP70 Heat-Shock Proteins
Language	English
Publishing date	2023-11-06
Publishing country	Spain
Document type	Journal Article
ZDB-ID	1325104-1
ISSN	1877-8755 ; 0034-9402 ; 1138-7548
ISSN (online)	1877-8755
ISSN	0034-9402 ; 1138-7548
DOI	10.1007/s13105-023-00994-w
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Article ; Online: Influence of body composition and cardiorespiratory fitness on plasma HSP72, norepinephrine, insulin, and glucose responses to an acute aerobic exercise bout performed in the fed state.

de Lemos Muller, Carlos Henrique / Moritz, Cesar Eduardo Jacintho / Schroeder, Helena Trevisan / Battastini, Ana Maria Oliveira / Reischak-Oliveira, Alvaro / de Bittencourt Júnior, Paulo Ivo Homem / De Vito, Giuseppe / Krause, Maurício

Cell stress & chaperones

2023 Volume 28, Issue 6, Page(s) 721–729

Abstract: Being overweight is already considered a metabolic risk factor, which can be overcome by increasing cardiorespiratory fitness (CRF). Acute exercise is known to induce changes in plasma hormones and heat shock proteins release. However, there is a lack of ...

Abstract	Being overweight is already considered a metabolic risk factor, which can be overcome by increasing cardiorespiratory fitness (CRF). Acute exercise is known to induce changes in plasma hormones and heat shock proteins release. However, there is a lack of studies investigating the impact of body composition and CRF on these variables following acute aerobic exercise. To assess the influence of body composition and cardiorespiratory fitness on plasma heat shock protein 72 kDa (HSP72), norepinephrine (NE), insulin, and glucose responses to an acute aerobic exercise bout in the fed state. Twenty-four healthy male adults were recruited and allocated into three groups: overweight sedentary (n = 8), normal weight sedentary (n = 8), and normal weight active (n = 8). The volunteers performed an acute moderate exercise session on a treadmill at 70% of VO
MeSH term(s)	Adult ; Humans ; Male ; Insulin ; Overweight ; Glucose ; HSP72 Heat-Shock Proteins ; Cardiorespiratory Fitness/physiology ; Norepinephrine ; Exercise/physiology ; Body Composition
Chemical Substances	Insulin ; Glucose (IY9XDZ35W2) ; HSP72 Heat-Shock Proteins ; Norepinephrine (X4W3ENH1CV)
Language	English
Publishing date	2023-07-18
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1362749-1
ISSN	1466-1268 ; 1355-8145
ISSN (online)	1466-1268
ISSN	1355-8145
DOI	10.1007/s12192-023-01364-7
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Article: A-family anti-inflammatory cyclopentenone prostaglandins: A novel class of non-statin inhibitors of HMG-CoA reductase

Gutierrez, Lucila Ludmila Paula / Marques, Claudia Vieira / Scomazzon, Sofia Pizzato / Schroeder, Helena Trevisan / Fernandes, João Roberto / da Silva Rossato, Juliane / Homem de Bittencourt, Paulo Ivo

Biochimie. 2021 Mar., v. 182

2021

Abstract: Disruption of the intracellular lipid balance leading to cholesterol accumulation is one of the features of cells that participate in the development of atherosclerotic lesions. Evidence form our laboratory indicates that anti-inflammatory cyclopentenone ...

Abstract	Disruption of the intracellular lipid balance leading to cholesterol accumulation is one of the features of cells that participate in the development of atherosclerotic lesions. Evidence form our laboratory indicates that anti-inflammatory cyclopentenone prostaglandins (cyPGs) of A- and J-family deviate lipid metabolism from the synthesis of cholesterol and cholesteryl esters to the synthesis of phospholipids in foam-cell macrophages. cyPGs possessing an α,β-unsaturated cyclopentane ring are highly electrophilic substances able to promptly react with reactive cysteines of intracellular molecules through Michael addition. On the other hand, HMG-CoA reductase (HMGCR), the enzyme responsible for the rate-limiting step in cholesterol biosynthesis, presents critically reactive cysteines at the entry of catalytic domain, particularly Cys561, that could be target of cyPG inhibition. In the present study, we showed that cyPGs (but not other non-α,β-unsaturated PGs) physically interact with HMGCR, in a dithiothreitol- and β-mercaptoethanol-sensitive way, and block the activity of the catalytic subunit of the enzyme (IC₅₀ for PGA₂ = 0.17 μM). PGA₂ inhibits HMGCR activity in cultured rat and human macrophages/macrophage-foam cells and leads to enhanced expression of HMGCR protein, as observed with statins. In cell culture models, PGA₂ effectively inhibits the reductase at non-toxic doses (e.g., 1 μM) that block cell proliferation thus suggesting that part of the well-known antiproliferative effect of PGA₂ may be due to its ability of blocking HMGCR activity, as cells cannot proliferate without a robust cholesterogenesis. Therefore, besides the powerfully anti-inflammatory and antiproliferative effects, the anticholesterogenic effects of PGA₂ should be exploited in atherosclerosis therapeutics.
Keywords	Lewis acids ; active sites ; atherosclerosis ; biosynthesis ; cell culture ; cell proliferation ; chemical reactions ; cholesterol ; humans ; lipid metabolism ; phospholipids ; prostaglandins ; protein subunits ; rats ; reaction kinetics ; therapeutics
Language	English
Dates of publication	2021-03
Size	p. 37-50.
Publishing place	Elsevier B.V.
Document type	Article
Note	NAL-AP-2-clean
ZDB-ID	120345-9
ISSN	0300-9084
ISSN	0300-9084
DOI	10.1016/j.biochi.2020.12.019
Database	NAL-Catalogue (AGRICOLA)

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Article: Heat shock response to exercise in pancreatic islets of obese mice

Bittencourt, Aline / de Lemos Muller, Carlos Henrique / Homem de Bittencourt, Paulo Ivo / Krause, Mauricio / Porto, Rossana Rosa / Schroeder, Helena Trevisan

Biochimie. 2020 Jan., v. 168

2020

Abstract: Chronic obesity imposes an organismal state of low-grade inflammation because the physiological resolution of inflammation is progressively repressed giving rise to cellular senescence and its accompanying Senescence-Associated Secretory Phenotype (SASP), ...

Abstract	Chronic obesity imposes an organismal state of low-grade inflammation because the physiological resolution of inflammation is progressively repressed giving rise to cellular senescence and its accompanying Senescence-Associated Secretory Phenotype (SASP), which avoids apoptosis but perpetuates the relay of inflammatory signals from adipose tissue toward the rest of the body. Conversely, resolution of inflammation depends on the integrity of heat shock response (HSR) pathway that leads to the expression of cytoprotective and anti-inflammatory protein chaperones of the 70 kDa family (HSP70). However, chronic exposure to the aforementioned injuring factors leads to SASP, which, in turn, suppresses the HSR. A main metabolic tissue severely jeopardized by obesity-related dysfunctions is the endocrine pancreas, particularly β-cells of the islets of Langerhans. Because exercise is a powerful inducer of HSR and predicted to alleviate negative health outcomes of obesity, we sought whether obesity influence HSP70 expression in pancreatic islets and other metabolic tissues (adipose tissue and skeletal muscle) of adult B6.129SF2/J mice fed on a high-fat diet (HFD) for 13 weeks since the weaning and whether acute exercise as well as moderate-intensity exercise training (8 weeks) could interfere with this scenario. We showed that acute exercise of moderate intensity protects pancreatic islets against cytokine-induced cell death. In addition, acute exercise challenge time-dependently increased islet HSP70 that peaked at 12 h post-exercise in both trained and untrained mice fed on a control diet, suggesting an adequate HSR to exercise training. Unexpectedly, however, neither exercise training nor acute exercise challenges were able to increase islet HSP70 contents in trained mice submitted to HFD, but only in untrained HFD animals. In parallel, HFD disrupted glycemic status which is accompanied by loss of muscular mass resembling sarcopenic obesity that could not be rescued by exercise training. These results suggest that exercise influences HSR in pancreatic islets but obesity undermines islet, muscle and adipose tissue HSR, which is associated with metabolic abnormalities observed in such tissues.
Keywords	adipose tissue ; adults ; animal disease models ; apoptosis ; cell senescence ; chronic exposure ; exercise ; heat shock response ; high fat diet ; inflammation ; islets of Langerhans ; mice ; muscles ; obesity ; phenotype ; sarcopenia ; skeletal muscle ; weaning
Language	English
Dates of publication	2020-01
Size	p. 28-40.
Publishing place	Elsevier B.V.
Document type	Article
ZDB-ID	120345-9
ISSN	0300-9084
ISSN	0300-9084
DOI	10.1016/j.biochi.2019.10.015
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: A-family anti-inflammatory cyclopentenone prostaglandins: A novel class of non-statin inhibitors of HMG-CoA reductase.

Biochimie

2021 Volume 182, Page(s) 37–50

Abstract	Disruption of the intracellular lipid balance leading to cholesterol accumulation is one of the features of cells that participate in the development of atherosclerotic lesions. Evidence form our laboratory indicates that anti-inflammatory cyclopentenone prostaglandins (cyPGs) of A- and J-family deviate lipid metabolism from the synthesis of cholesterol and cholesteryl esters to the synthesis of phospholipids in foam-cell macrophages. cyPGs possessing an α,β-unsaturated cyclopentane ring are highly electrophilic substances able to promptly react with reactive cysteines of intracellular molecules through Michael addition. On the other hand, HMG-CoA reductase (HMGCR), the enzyme responsible for the rate-limiting step in cholesterol biosynthesis, presents critically reactive cysteines at the entry of catalytic domain, particularly Cys561, that could be target of cyPG inhibition. In the present study, we showed that cyPGs (but not other non-α,β-unsaturated PGs) physically interact with HMGCR, in a dithiothreitol- and β-mercaptoethanol-sensitive way, and block the activity of the catalytic subunit of the enzyme (IC
MeSH term(s)	Animals ; Anti-Inflammatory Agents/chemistry ; Anti-Inflammatory Agents/pharmacology ; Foam Cells/enzymology ; Humans ; Hydroxymethylglutaryl CoA Reductases/chemistry ; Hydroxymethylglutaryl CoA Reductases/metabolism ; Hydroxymethylglutaryl-CoA Reductase Inhibitors/chemistry ; Hydroxymethylglutaryl-CoA Reductase Inhibitors/pharmacology ; Male ; Prostaglandins A/chemistry ; Prostaglandins A/pharmacology ; Rats ; Rats, Wistar
Chemical Substances	Anti-Inflammatory Agents ; Hydroxymethylglutaryl-CoA Reductase Inhibitors ; Prostaglandins A ; HMGCR protein, human (EC 1.1.1.-) ; Hydroxymethylglutaryl CoA Reductases (EC 1.1.1.-) ; prostaglandin A2 (K6VT5BDY9E)
Language	English
Publishing date	2021-01-04
Publishing country	France
Document type	Journal Article
ZDB-ID	120345-9
ISSN	1638-6183 ; 0300-9084
ISSN (online)	1638-6183
ISSN	0300-9084
DOI	10.1016/j.biochi.2020.12.019
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