scholarly journals Protective Effects of Cannabidiol on the Membrane Proteome of UVB-Irradiated Keratinocytes

Antioxidants ◽  
2021 ◽  
Vol 10 (3) ◽  
pp. 402
Author(s):  
Sinemyiz Atalay ◽  
Agnieszka Gęgotek ◽  
Elżbieta Skrzydlewska
Keyword(s):  
Cell Proliferation ◽  
Ribosomal Proteins ◽  
Biological Membranes ◽  
Protein Translation ◽  
Degradation Process ◽  
Redox Balance ◽  
Antioxidant Response ◽  
Protein Adducts ◽  
Protective Effects ◽  
Uvb Radiation

Ultraviolet (UV) radiation contained in sunlight disturbs the redox state of skin cells, leading to changes in the structures and functions of macromolecules including components of biological membranes. Cannabidiol (CBD), which accumulates in biomembranes, may be a promising protective antioxidant compound. Accordingly, the aim of this study was to compare the effects of short-term (24 h) and long-term (48 h) CBD application on the proteomic profile of biological membranes in UVB-irradiated keratinocytes. The data obtained show that UVB radiation quantitatively and qualitatively modified cell membrane proteins, with a particular research focus on adducts of proteins with the lipid peroxidation products malondialdehyde (MDA) or 4-hydroxynonenal (4-HNE). CBD application reduced the UVB-enhanced level of these protein adducts. This was particularly notable amongst proteins related to cell proliferation and apoptosis. Moreover, CBD dramatically increased the UVB-induced expression of proteins involved in the regulation of protein translation and cell proliferation (S3a/L13a/L7a ribosomal proteins), the inflammatory response (S100/S100-A6 proteins), and maintenance of redox balance (peroxiredoxin-1, carbonyl reductase 1, and aldo-keto reductase family 1 members). In contrast, CBD effects on the level of 4-HNE-protein adducts involved in the antioxidant response and proteasomal degradation process indicate that CBD may protect keratinocytes in connection with protein catabolism processes or pro-apoptotic action.

scholarly journals Role of Nrf2 and Its Activators in Respiratory Diseases

2019 ◽  
Vol 2019 ◽  
pp. 1-17 ◽  
Author(s):  
Qinmei Liu ◽  
Yun Gao ◽  
Xinxin Ci
Keyword(s):  
Respiratory Diseases ◽  
Respiratory Infections ◽  
Redox Balance ◽  
Antioxidant Response ◽  
Experimental Models ◽  
26S Proteasome ◽  
Chronic Obstructive ◽  
Related Factor ◽  
Protective Effects ◽  
Obstructive Pulmonary Disease

Transcription factor nuclear factor erythroid 2-related factor 2 (Nrf2) is a major regulator of antioxidant response element- (ARE-) driven cytoprotective protein expression. The activation of Nrf2 signaling plays an essential role in preventing cells and tissues from injury induced by oxidative stress. Under the unstressed conditions, natural inhibitor of Nrf2, Kelch-like ECH-associated protein 1 (Keap1), traps Nrf2 in the cytoplasm and promotes the degradation of Nrf2 by the 26S proteasome. Nevertheless, stresses including highly oxidative microenvironments, impair the ability of Keap1 to target Nrf2 for ubiquitination and degradation, and induce newly synthesized Nrf2 to translocate to the nucleus to bind with ARE. Due to constant exposure to external environments, including diverse pollutants and other oxidants, the redox balance maintained by Nrf2 is fairly important to the airways. To date, researchers have discovered that Nrf2 deletion results in high susceptibility and severity of insults in various models of respiratory diseases, including bronchopulmonary dysplasia (BPD), respiratory infections, acute respiratory distress syndrome (ARDS), chronic obstructive pulmonary disease (COPD), asthma, idiopathic pulmonary fibrosis (IPF), and lung cancer. Conversely, Nrf2 activation confers protective effects on these lung disorders. In the present review, we summarize Nrf2 involvement in the pathogenesis of the above respiratory diseases that have been identified by experimental models and human studies and describe the protective effects of Nrf2 inducers on these diseases.

scholarly journals Protective Effect of Mitochondrial ND2 C5178A Gene Mutation on Cell and Mitochondrial Functions

2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
Liuyang Tian ◽  
Chao Zhu ◽  
Huanwan Yang ◽  
Yang Li ◽  
Yuqi Liu
Keyword(s):  
Cell Proliferation ◽  
Gene Mutation ◽  
Atp Synthesis ◽  
Protein Translation ◽  
Control Group ◽  
Protective Effects ◽  
Mitochondrial Oxidative Stress ◽  
Nadh Dehydrogenase Subunit 2 ◽  
Mitochondrial Functions ◽  
Significant Difference

Background. Mitochondrial NADH dehydrogenase subunit 2 (MT-ND2) m. 5178C>A gene mutation has protective effects against various diseases, but the molecular mechanism is still unclear. In previous study, we found a heteroplasmy level of MT-ND2 m. 5178C>A mutation in normotensive controls. Peripheral blood samples were obtained from essential hypertension individuals carrying the mutation and healthy controls without gene mutation to establish immortalized lymphocyte lines. To investigate the effect of the MT-ND2 m. 5178C>A gene mutation, comparative analyses of the two group cell lines were performed, including measurements of cell proliferation, viability, ATP synthesis, mitochondrial oxidative stress, and oxidative phosphorylation. Results. The cell proliferation rate and viability of the MT-ND2 m. 5178C>A mutant lymphocyte line were higher than those of the control group. Mitochondrial functions of the MT-ND2 m. 5178C>A mutant lymphocyte were increased, including increased ATP synthesis, decreased ROS production, increased mitochondrial membrane potential and Bcl-2 gene transcription and protein translation, decreased Caspase 3/7 activity, and decreased early apoptosis and late apoptosis. The oxygen consumption rate (OCR) of the mutant lymphocyte line was higher than that of the control group, including basal OCR, ATP-linked OCR, maximal OCR, proton leak OCR, and reserve OCR, and there was no significant difference in nonmitochondrial OCR. The activity of Mitochondrial Complex I of the mutant group was increased than that of the control group. Conclusions. The MT-ND2 m. 5178C>A mutation is a protective mutation that may be related to improvement of mitochondrial functions and decrease in apoptosis.

scholarly journals Exploring the Protective Effects of Phaeodactylum tricornutum Extract on LPS-Treated Fibroblasts

Cosmetics ◽  
2021 ◽  
Vol 8 (3) ◽  
pp. 76
Author(s):  
Dimitra Mosxou ◽  
Sophia Letsiou
Keyword(s):  
Cell Proliferation ◽  
Phaeodactylum Tricornutum ◽  
Skin Inflammation ◽  
Rice Flour ◽  
Antioxidant Response ◽  
Dermal Fibroblasts ◽  
Protective Effects ◽  
Omega 3 ◽  
Transcript Accumulation ◽  
Anti Inflammatory

Background: Microalgal extracts are an important source of bioactive compounds with antioxidant and anti-inflammatory properties that can be used in cosmetics. The microalgae Phaeodactylum tricornutum (PT) is known for its high content of omega-3 fatty acids, which are known to attenuate inflammation. Here, we explore the effects of aqueous microencapsulated extract of PT on lipopolysaccharide (LPS)-stimulated normal human dermal fibroblasts (NHDF) to underline its application as an active ingredient in cosmetics. Methods: We assessed cell viability using MTT assay, so as to target any potential cytotoxicity of the extract. Moreover, with the aid of RT-qPCR, we studied the transcript accumulation of genes involved in cell antioxidant response, cell proliferation, and inflammation. Results: Our results revealed that the hydrolyzed rice flour-encapsulated (HRF) PT extract promotes anti-inflammatory and antioxidant response, increasing cell proliferation in NHDF cells. Conclusions: Our data indicate a promising use of HRF-encapsulated PT extract in cosmetics by reducing skin inflammation.

scholarly journals The transcription factor SlHY5 regulates the ripening of tomato fruit at both the transcriptional and translational levels

2021 ◽  
Vol 8 (1) ◽  
Author(s):  
Weihao Wang ◽  
Peiwen Wang ◽  
Xiaojing Li ◽  
Yuying Wang ◽  
Shiping Tian ◽  
...  
Keyword(s):  
Fruit Ripening ◽  
Nutritional Quality ◽  
Ribosomal Proteins ◽  
Anthocyanin Biosynthesis ◽  
Tomato Fruit ◽  
Critical Role ◽  
Regulation Of Gene Expression ◽  
Protein Translation ◽  
Transcriptional Level ◽  
Translation Efficiency

AbstractLight plays a critical role in plant growth and development, but the mechanisms through which light regulates fruit ripening and nutritional quality in horticultural crops remain largely unknown. Here, we found that ELONGATED HYPOCOTYL 5 (HY5), a master regulator in the light signaling pathway, is required for normal fruit ripening in tomato (Solanum lycopersicum). Loss of function of tomato HY5 (SlHY5) impairs pigment accumulation and ethylene biosynthesis. Transcriptome profiling identified 2948 differentially expressed genes, which included 1424 downregulated and 1524 upregulated genes, in the Slhy5 mutants. In addition, genes involved in carotenoid and anthocyanin biosynthesis and ethylene signaling were revealed as direct targets of SlHY5 by chromatin immunoprecipitation. Surprisingly, the expression of a large proportion of genes encoding ribosomal proteins was downregulated in the Slhy5 mutants, and this downregulation pattern was accompanied by a decrease in the abundance of ribosomal proteins. Further analysis demonstrated that SlHY5 affected the translation efficiency of numerous ripening-related genes. These data indicate that SlHY5 regulates fruit ripening both at the transcriptional level by targeting specific molecular pathways and at the translational level by affecting the protein translation machinery. Our findings unravel the regulatory mechanisms of SlHY5 in controlling fruit ripening and nutritional quality and uncover the multifaceted regulation of gene expression by transcription factors.

scholarly journals Impact of sex in the prevalence and progression of glioblastomas: the role of gonadal steroid hormones

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Claudia Bello-Alvarez ◽  
Ignacio Camacho-Arroyo
Keyword(s):  
Cell Proliferation ◽  
Steroid Hormones ◽  
Physiological State ◽  
Migration And Invasion ◽  
Low Grade ◽  
Main Body ◽  
Protective Effects ◽  
Gonadal Steroid Hormones ◽  
Gonadal Steroid

Abstract Background As in other types of cancers, sex is an essential factor in the origin and progression of glioblastomas. Research in the field of endocrinology and cancer suggests that gonadal steroid hormones play an important role in the progression and prevalence of glioblastomas. In the present review, we aim to discuss the actions and mechanism triggered by gonadal steroid hormones in glioblastomas. Main body Glioblastoma is the most common malignant primary brain tumor. According to the epidemiological data, glioblastomas are more frequent in men than in women in a 1.6/1 proportion both in children and adults. This evidence, and the knowledge about sex influence over the prevalence of countless diseases, suggest that male gonadal steroid hormones, such as testosterone, promote glioblastomas growth. In contrast, a protective role of female gonadal steroid hormones (estradiol and progesterone) against glioblastomas has been questioned. Several pieces of evidence demonstrate a variety of effects induced by female and male gonadal steroid hormones in glioblastomas. Several studies indicate that pregnancy, a physiological state with the highest progesterone and estradiol levels, accelerates the progression of low-grade astrocytomas to glioblastomas and increases the symptoms associated with these tumors. In vitro studies have demonstrated that progesterone has a dual role in glioblastoma cells: physiological concentrations promote cell proliferation, migration, and invasion while very high doses (out physiological range) reduce cell proliferation and increases cell death. Conclusion Gonadal steroid hormones can stimulate the progression of glioblastomas through the increase in proliferation, migration, and invasion. However, the effects mentioned above depend on the concentrations of these hormones and the receptor involved in hormone actions. Estradiol and progesterone can exert promoter or protective effects while the role of testosterone has been always associated to glioblastomas progression.

scholarly journals Stress Responses in Down Syndrome Neurodegeneration: State of the Art and Therapeutic Molecules

Biomolecules ◽  
2021 ◽  
Vol 11 (2) ◽  
pp. 266
Author(s):  
Chiara Lanzillotta ◽  
Fabio Di Domenico
Keyword(s):  
Down Syndrome ◽  
Stress Response ◽  
Stress Responses ◽  
Redox Balance ◽  
Antioxidant Response ◽  
Chromosome 21 ◽  
Therapeutic Approaches ◽  
Genomic Disorder ◽  
Therapeutic Molecules ◽  
Early Alzheimer’S Disease

Down syndrome (DS) is the most common genomic disorder characterized by the increased incidence of developing early Alzheimer’s disease (AD). In DS, the triplication of genes on chromosome 21 is intimately associated with the increase of AD pathological hallmarks and with the development of brain redox imbalance and aberrant proteostasis. Increasing evidence has recently shown that oxidative stress (OS), associated with mitochondrial dysfunction and with the failure of antioxidant responses (e.g., SOD1 and Nrf2), is an early signature of DS, promoting protein oxidation and the formation of toxic protein aggregates. In turn, systems involved in the surveillance of protein synthesis/folding/degradation mechanisms, such as the integrated stress response (ISR), the unfolded stress response (UPR), and autophagy, are impaired in DS, thus exacerbating brain damage. A number of pre-clinical and clinical studies have been applied to the context of DS with the aim of rescuing redox balance and proteostasis by boosting the antioxidant response and/or inducing the mechanisms of protein re-folding and clearance, and at final of reducing cognitive decline. So far, such therapeutic approaches demonstrated their efficacy in reverting several aspects of DS phenotype in murine models, however, additional studies aimed to translate these approaches in clinical practice are still needed.

Beetroot and leaf extracts present protective effects against prostate cancer cells, inhibiting cell proliferation, migration, and growth signaling pathways

2021 ◽  
Author(s):  
Mariana Camargo Silva Mancini ◽  
Luis Gustavo Saboia Ponte ◽  
Cayo Henrique Rocha Silva ◽  
Isabella Fagundes ◽  
Isadora Carolina Betim Pavan ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Signaling Pathways ◽  
Protective Effects ◽  
Prostate Cancer Cells ◽  
Leaf Extracts

scholarly journals Total flavonoids from Astragalus alleviate endothelial dysfunction by activating the Akt/eNOS pathway

2017 ◽  
Vol 46 (6) ◽  
pp. 2096-2103 ◽  
Author(s):  
Qian Liu ◽  
Ling Zhang ◽  
Qiyuan Shan ◽  
Yuxia Ding ◽  
Zhaocai Zhang ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Vascular Endothelial Cells ◽  
Ex Vivo ◽  
Umbilical Vein ◽  
Cell Counting ◽  
Total Flavonoids ◽  
Vascular Endothelial ◽  
Protective Effects ◽  
Hypoxic Conditions ◽  
Underlying Mechanisms

Objective To investigate the vasodilative and endothelial-protective effects and the underlying mechanisms of total flavonoids from Astragalus (TFA). Methods The vasodilative activities of TFA were measured with a myograph ex vivo using rat superior mesenteric arterial rings. The primary human umbilical vein endothelial cell (HUVEC) viabilities were assayed using the cell counting kit-8 after hypoxia or normoxia treatment with or without TFA. Akt, P-Akt, eNOS, P-eNOS, Erk, P-Erk, Bcl-2 and Bax expression were analyzed using western blotting. Results TFA showed concentration-dependent vasodilative effects on rat superior mesenteric arterial rings, but had no effects on normal or potassium chloride precontracted arterial rings. TFA did not affect HUVEC viabilities in normoxia, but dramatically promoted cell proliferation in the concentration range of 1 to 30 µg/mL under hypoxia. Moreover, TFA significantly increased the ratios of P-Akt/Akt and P-eNOS/eNOS in vascular endothelial cells under hypoxic conditions, but did not change the P-Erk/Erk or Bcl-2/Bax ratios. Conclusions TFA might exhibit vasorelaxant and endothelial-protective effects via the Akt/eNOS signaling pathway.

scholarly journals Toward a better understanding of folate metabolism in health and disease

2018 ◽  
Vol 216 (2) ◽  
pp. 253-266 ◽  
Author(s):  
Yuxiang Zheng ◽  
Lewis C. Cantley
Keyword(s):  
Cell Proliferation ◽  
Epigenetic Regulation ◽  
Historical Perspective ◽  
Mitochondrial Protein ◽  
Protein Translation ◽  
Folate Metabolism ◽  
Cellular Functions ◽  
Biochemical Processes ◽  
Health And Disease ◽  
Thymidine Monophosphate

Folate metabolism is crucial for many biochemical processes, including purine and thymidine monophosphate (dTMP) biosynthesis, mitochondrial protein translation, and methionine regeneration. These biochemical processes in turn support critical cellular functions such as cell proliferation, mitochondrial respiration, and epigenetic regulation. Not surprisingly, abnormal folate metabolism has been causally linked with a myriad of diseases. In this review, we provide a historical perspective, delve into folate chemistry that is often overlooked, and point out various missing links and underdeveloped areas in folate metabolism for future exploration.

scholarly journals Mitochondrial Protein Translation: Emerging Roles and Clinical Significance in Disease

2021 ◽  
Vol 9 ◽  
Author(s):  
Fei Wang ◽  
Deyu Zhang ◽  
Dejiu Zhang ◽  
Peifeng Li ◽  
Yanyan Gao
Keyword(s):  
Ribosomal Proteins ◽  
Large Fraction ◽  
Mitochondrial Protein ◽  
Mitochondrial Diseases ◽  
Protein Translation ◽  
Genetic System ◽  
Mitochondrial Rna ◽  
Trna Synthetases ◽  
Translation Factors ◽  
Genes Encoding

Mitochondria are one of the most important organelles in cells. Mitochondria are semi-autonomous organelles with their own genetic system, and can independently replicate, transcribe, and translate mitochondrial DNA. Translation initiation, elongation, termination, and recycling of the ribosome are four stages in the process of mitochondrial protein translation. In this process, mitochondrial protein translation factors and translation activators, mitochondrial RNA, and other regulatory factors regulate mitochondrial protein translation. Mitochondrial protein translation abnormalities are associated with a variety of diseases, including cancer, cardiovascular diseases, and nervous system diseases. Mutation or deletion of various mitochondrial protein translation factors and translation activators leads to abnormal mitochondrial protein translation. Mitochondrial tRNAs and mitochondrial ribosomal proteins are essential players during translation and mutations in genes encoding them represent a large fraction of mitochondrial diseases. Moreover, there is crosstalk between mitochondrial protein translation and cytoplasmic translation, and the imbalance between mitochondrial protein translation and cytoplasmic translation can affect some physiological and pathological processes. This review summarizes the regulation of mitochondrial protein translation factors, mitochondrial ribosomal proteins, mitochondrial tRNAs, and mitochondrial aminoacyl-tRNA synthetases (mt-aaRSs) in the mitochondrial protein translation process and its relationship with diseases. The regulation of mitochondrial protein translation and cytoplasmic translation in multiple diseases is also summarized.

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