Molecular Responses of Lactobacilli to Plant Phenolic Compounds: A Comparative Review of the Mechanisms Involved

Lactobacilli are well-studied bacteria that can undergo oxidative selective pressures by plant phenolic compounds (PPCs) in plants, during some food fermentations or in the gastrointestinal tract of animals via dietary inputs. Lactobacilli are known to be more tolerant to PPCs than other bacterial groups and, therefore, must have mechanisms to cope with the effects of these metabolites. In this review, we intend to present what is currently known about the basics beyond the responses of Lactobacillus spp. to individual PPCs. We review the molecular mechanisms that are engaged in the PPC-modulated responses studied to date in these bacteria that have been mainly characterized by system-based strategies, and we discuss their differences and similarities. A wide variety of mechanisms are induced to increase the oxidative stress response highlighting the antimicrobial nature of PPCs. However other uncovered mechanisms that are involved in the response to these compounds are reviewed, including the capacity of PPCs to modulate the expression of molecular functions used by lactobacilli to adapt to host environments. This shows that these phytochemicals can act as more than just antimicrobial agents in the dual interaction with lactobacilli.

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Functional crosstalk between myeloid Foxo1–β-catenin axis and Hedgehog/Gli1 signaling in oxidative stress response

Cell Death and Differentiation ◽

10.1038/s41418-020-00695-7 ◽

2020 ◽

Author(s):

Changyong Li ◽

Mingwei Sheng ◽

Yuanbang Lin ◽

Dongwei Xu ◽

Yizhu Tian ◽

...

Keyword(s):

Oxidative Stress ◽

Stress Response ◽

Molecular Mechanisms ◽

Ischemia Reperfusion Injury ◽

Cell Metabolism ◽

Ischemia Reperfusion ◽

Neutrophil Infiltration ◽

Oxidative Stress Response ◽

Proinflammatory Mediators ◽

Hepatocellular Damage

AbstractFoxo1 transcription factor is an evolutionarily conserved regulator of cell metabolism, oxidative stress, inflammation, and apoptosis. Activation of Hedgehog/Gli signaling is known to regulate cell growth, differentiation, and immune function. However, the molecular mechanisms by which interactive cell signaling networks restrain oxidative stress response and necroptosis are still poorly understood. Here, we report that myeloid-specific Foxo1 knockout (Foxo1M-KO) mice were resistant to oxidative stress-induced hepatocellular damage with reduced macrophage/neutrophil infiltration, and proinflammatory mediators in liver ischemia/reperfusion injury (IRI). Foxo1M-KO enhanced β-catenin-mediated Gli1/Snail activity, and reduced receptor-interacting protein kinase 3 (RIPK3) and NIMA-related kinase 7 (NEK7)/NLRP3 expression in IR-stressed livers. Disruption of Gli1 in Foxo1M-KO livers deteriorated liver function, diminished Snail, and augmented RIPK3 and NEK7/NLRP3. Mechanistically, macrophage Foxo1 and β-catenin colocalized in the nucleus, whereby the Foxo1 competed with T-cell factor (TCF) for interaction with β-catenin under inflammatory conditions. Disruption of the Foxo1–β-catenin axis by Foxo1 deletion enhanced β-catenin/TCF binding, activated Gli1/Snail signaling, leading to inhibited RIPK3 and NEK7/NLRP3. Furthermore, macrophage Gli1 or Snail knockout activated RIPK3 and increased hepatocyte necroptosis, while macrophage RIPK3 ablation diminished NEK7/NLRP3-driven inflammatory response. Our findings underscore a novel molecular mechanism of the myeloid Foxo1–β-catenin axis in regulating Hedgehog/Gli1 function that is key in oxidative stress-induced liver inflammation and necroptosis.

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4-PHENYLBUTYRATE: MOLECULAR MECHANISMS AND AGING INTERVENTION POTENTIAL

Innovation in Aging ◽

10.1093/geroni/igz038.379 ◽

2019 ◽

Vol 3 (Supplement_1) ◽

pp. S101-S101

Author(s):

Michael R Bene ◽

Kevin Thyne ◽

Jonathan Dorigatti ◽

Adam B Salmon

Keyword(s):

Oxidative Stress ◽

Stress Response ◽

Molecular Mechanisms ◽

Oxidative Stress Response ◽

Chemical Chaperone ◽

Mouse Muscle ◽

Age Related ◽

Primary Mouse ◽

Wide Range

Abstract 4-Phenylbutyrate (PBA) is a FDA approved drug for treating patients with urea cycle disorders. Additionally, PBA acts upon several pathways thought of as important modifiers of aging including: histone deacetylation, proteostasis as a chemical chaperone, and stress resistance by regulating expression of oxidative stress response proteins. PBA has also been shown to extend lifespan and improve markers of age-related health in Drosophila. Due to its wide range of effects PBA has been investigated for use in numerous age-related disorders including neurodegenerative and cardiovascular diseases. To better understand the effects of PBA on the molecular level, we used both in cellulo and in vivo studies. Treatment of primary mouse fibroblasts, C2C12 mouse muscle cells, and NCTC 1469 mouse liver cells with PBA demonstrated differential responses among cell lines to upregulation of oxidative stress response and histone acetylation. Specifically, upregulation of the oxidative stress response protein DJ-1 by PBA was found to have a corresponding dose response curve to histone H3 acetylation in primary fibroblasts. To study effects of PBA in vivo, four cohorts of HET3 mice were treated with PBA at different doses in drinking water for 4 weeks. PBA was well tolerated and led to different effects on body composition dependent on the sex of mice. We are currently investigating the molecular effects of PBA treatment in multiple tissues samples from these mice. The potential of PBA to alter many fundamental pathways, and specifically those related to stress responses, make it an attractive prospect for treatment of many age-related disorders.

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p62/SQSTM1-droplet serves as a platform for autophagosome formation and anti-oxidative stress response

Nature Communications ◽

10.1038/s41467-020-20185-1 ◽

2021 ◽

Vol 12 (1) ◽

Author(s):

Shun Kageyama ◽

Sigurdur Runar Gudmundsson ◽

Yu-Shin Sou ◽

Yoshinobu Ichimura ◽

Naoki Tamura ◽

...

Keyword(s):

Oxidative Stress ◽

Molecular Mechanisms ◽

Oxidative Stress Response ◽

Liquid Droplets ◽

Autophagosome Formation ◽

Selective Autophagy ◽

Selective Degradation ◽

Physiological Relevance ◽

Related Proteins

AbstractAutophagy contributes to the selective degradation of liquid droplets, including the P-Granule, Ape1-complex and p62/SQSTM1-body, although the molecular mechanisms and physiological relevance of selective degradation remain unclear. In this report, we describe the properties of endogenous p62-bodies, the effect of autophagosome biogenesis on these bodies, and the in vivo significance of their turnover. p62-bodies are low-liquidity gels containing ubiquitin and core autophagy-related proteins. Multiple autophagosomes form on the p62-gels, and the interaction of autophagosome-localizing Atg8-proteins with p62 directs autophagosome formation toward the p62-gel. Keap1 also reversibly translocates to the p62-gels in a p62-binding dependent fashion to activate the transcription factor Nrf2. Mice deficient for Atg8-interaction-dependent selective autophagy show that impaired turnover of p62-gels leads to Nrf2 hyperactivation in vivo. These results indicate that p62-gels are not simple substrates for autophagy but serve as platforms for both autophagosome formation and anti-oxidative stress.

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Gene bb0318 Is Critical for the Oxidative Stress Response and Infectivity of Borrelia burgdorferi

Infection and Immunity ◽

10.1128/iai.00430-16 ◽

2016 ◽

Vol 84 (11) ◽

pp. 3141-3151 ◽

Cited By ~ 7

Author(s):

Adrienne C. Showman ◽

George Aranjuez ◽

Philip P. Adams ◽

Mollie W. Jewett

Keyword(s):

Oxidative Stress ◽

Stress Response ◽

Borrelia Burgdorferi ◽

Molecular Mechanisms ◽

De Novo ◽

Oxidative Stress Response ◽

Growth Defect ◽

Content Type

A greater understanding of the molecular mechanisms that Borrelia burgdorferi uses to survive during mammalian infection is critical for the development of novel diagnostic and therapeutic tools to improve the clinical management of Lyme disease. By use of an in vivo expression technology (IVET)-based approach to identify B. burgdorferi genes expressed in vivo , we discovered the bb0318 gene, which is thought to encode the ATPase component of a putative riboflavin ABC transport system. Riboflavin is a critical metabolite enabling all organisms to maintain redox homeostasis. B. burgdorferi appears to lack the metabolic capacity for de novo synthesis of riboflavin and so likely relies on scavenging riboflavin from the host environment. In this study, we sought to investigate the role of bb0318 in B. burgdorferi pathogenesis. No in vitro growth defect was observed for the Δ bb0318 clone. However, the mutant spirochetes displayed reduced levels of survival when exposed to exogenous hydrogen peroxide or murine macrophages. Spirochetes lacking bb0318 were found to have a 100-fold-higher 50% infectious dose than spirochetes containing bb0318 . In addition, at a high inoculum dose, bb0318 was found to be important for effective spirochete dissemination to deep tissues for as long as 3 weeks postinoculation and to be critical for B. burgdorferi infection of mouse hearts. Together, these data implicate bb0318 in the oxidative stress response of B. burgdorferi and indicate the contribution of bb0318 to B. burgdorferi mammalian infectivity.

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Kluyveromyces lactis: A Suitable Yeast Model to Study Cellular Defense Mechanisms against Hypoxia-Induced Oxidative Stress

Oxidative Medicine and Cellular Longevity ◽

10.1155/2012/634674 ◽

2012 ◽

Vol 2012 ◽

pp. 1-14 ◽

Cited By ~ 10

Author(s):

M. Isabel González Siso ◽

M. Esperanza Cerdán

Keyword(s):

Oxidative Stress ◽

Defense Mechanisms ◽

Molecular Mechanisms ◽

Kluyveromyces Lactis ◽

Oxidative Stress Response ◽

Unicellular Eukaryote ◽

Extended Model ◽

Cellular Defense ◽

Health Disorders ◽

Fermentative Yeast

Studies about hypoxia-induced oxidative stress in human health disorders take advantage from the use of unicellular eukaryote models. A widely extended model is the fermentative yeastSaccharomyces cerevisiae. In this paper, we describe an overview of the molecular mechanisms induced by a decrease in oxygen availability and their interrelationship with the oxidative stress response in yeast. We focus on the differential characteristics betweenS. cerevisiaeand the respiratory yeastKluyveromyces lactis, a complementary emerging model, in reference to multicellular eukaryotes.

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Black and yellow soybean: Contribution of seed quality to oxidative stress response during plant development

Genetika ◽

10.2298/gensr1902495k ◽

2019 ◽

Vol 51 (2) ◽

pp. 495-510

Author(s):

Biljana Kiprovski ◽

Jegor Miladinovic ◽

Anamarija Koren ◽

Djordje Malencic ◽

Maja Mikulic-Petkovsek

Keyword(s):

Oxidative Stress ◽

Stress Response ◽

Phenolic Compounds ◽

Seed Quality ◽

Oxidative Stress Response ◽

Oxidative Stresses ◽

Conventional Production ◽

Reproduction Period ◽

Excellent Source

The purpose of this paper was to compare quality of seeds of two black and yellow soybean and the response of plants developed from these seeds to oxidative stress during vegetation and reproduction period. Content of carbohydrates: cellulose, starch, total and reduced sugars, as well as oil and protein content varied among all varieties, irrespective the colour. Bearing in mind all differences in seed quality, as well as response to oxidative stresses during development, black cultivars could be proposed as an excellent source of phenolic compounds (flavan-3-ols, antocyanins, genistein, glycitein, quercetin, laricitrin and isorhamnetin derivatives). Due to extreme fluctuation in precipitation amounts in the last years, information on the better performance of soybean varieties in oxidative stress conditions is of great importance to organic and conventional production of this cultivar.

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Novel lncRNA AL033381.2 Promotes Hepatocellular Carcinoma Progression by Upregulating PRKRA Expression

Oxidative Medicine and Cellular Longevity ◽

10.1155/2022/1125932 ◽

2022 ◽

Vol 2022 ◽

pp. 1-24

Author(s):

Feiran Wang ◽

Lirong Zhu ◽

Qiang Xue ◽

Chong Tang ◽

Weidong Tang ◽

...

Keyword(s):

Oxidative Stress ◽

Hepatocellular Carcinoma ◽

Stress Response ◽

Stress Responses ◽

Molecular Mechanisms ◽

Oxidative Stress Response ◽

Migration And Invasion ◽

Pcr Analysis ◽

Therapeutic Effects

Hepatocellular carcinoma (HCC) is a common malignant tumor that is characterized by aggressiveness and poor prognosis. Accumulating evidence indicates that oxidative stress plays a crucial role in carcinogenesis, whereas the potential mechanism between oxidative stress and carcinogenic effects remains elusive. In recent years, long noncoding RNAs (lncRNAs) in cancers have attracted extensive attention and have been shown to be involved in oxidative stress response and carcinogenesis. Nevertheless, the roles of lncRNA AL033381.2 in regulating the development and progression of HCC still remain unclear. The purpose of our study was to evaluate the potential effects and molecular mechanisms of AL033381.2 that may be involved in oxidative stress response in HCC. Using bioinformatics analyses based on the TCGA database, we screened and identified a novel lncRNA AL033381.2 in HCC, which may be involved in oxidative stress responses. qRT-PCR analysis revealed that AL033381.2 is upregulated in HCC tissues. Through in vitro and in vivo experiments, we found that AL033381.2 dramatically facilitates the growth and metastasis of HCC. Mechanistically, RNA pull-down experiments, mass spectrometry, PathArray™, and RIP were used to determine that AL033381.2 binds to PRKRA and may be involved in AL033381.2-mediated oncogenic functions in HCC cells. Moreover, rescue experiments demonstrated that PRKRA overexpression rescues the abilities of HCC cell proliferation, migration, and invasion that were affected by AL033381.2 knockdown. Furthermore, we produced a nanoparticle-based siRNA delivery system and tested its therapeutic effects in vivo. The results showed that the in vivo growth rate of the tumors treated with the nanoparticle/AL033381.2 siRNA complexes was dramatically lower than those treated with the nanoparticle/scramble siRNA complexes. Taken together, our results suggest that the novel lncRNA AL033381.2 may be involved in oxidative stress response by targeting oxidative stress-related genes in HCC. AL033381.2 plays vital oncogenic roles in HCC progression and may be a novel therapeutic marker for HCC diagnosis and treatment.

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The Response to Oxidative Stress in Listeria monocytogenes Is Temperature Dependent

Microorganisms ◽

10.3390/microorganisms8040521 ◽

2020 ◽

Vol 8 (4) ◽

pp. 521 ◽

Cited By ~ 1

Author(s):

Beatriz Manso ◽

Beatriz Melero ◽

Beatrix Stessl ◽

Isabel Jaime ◽

Martin Wagner ◽

...

Keyword(s):

Oxidative Stress ◽

Listeria Monocytogenes ◽

Stress Response ◽

Food Processing ◽

Molecular Mechanisms ◽

Cumene Hydroperoxide ◽

Oxidative Stress Response ◽

Survival Strategies ◽

Processing Plants ◽

Dairy Plant

The stress response of 11 strains of Listeria monocytogenes to oxidative stress was studied. The strains included ST1, ST5, ST7, ST6, ST9, ST87, ST199 and ST321 and were isolated from diverse food processing environments (a meat factory, a dairy plant and a seafood company) and sample types (floor, wall, drain, boxes, food products and water machine). Isolates were exposed to two oxidizing agents: 13.8 mM cumene hydroperoxide (CHP) and 100 mM hydrogen peroxide (H2O2) at 10 °C and 37 °C. Temperature affected the oxidative stress response as cells treated at 10 °C survived better than those treated at 37 °C. H2O2 at 37 °C was the condition tested resulting in poorest L. monocytogenes survival. Strains belonging to STs of Lineage I (ST5, ST6, ST87, ST1) were more resistant to oxidative stress than those of Lineage II (ST7, ST9, ST199 and ST321), with the exception of ST7 that showed tolerance to H2O2 at 10 °C. Isolates of each ST5 and ST9 from different food industry origins showed differences in oxidative stress response. The gene expression of two relevant virulence (hly) and stress (clpC) genes was studied in representative isolates in the stressful conditions. hly and clpC were upregulated during oxidative stress at low temperature. Our results indicate that conditions prevalent in food industries may allow L. monocytogenes to develop survival strategies: these include activating molecular mechanisms based on cross protection that can promote virulence, possibly increasing the risk of virulent strains persisting in food processing plants.

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