I. Aggeletopoulou, C. Konstantakis, Christos Triantos
{"title":"Chronic Atrophic Autoimmune Gastritis: The Evolving Role of Vitamin D","authors":"I. Aggeletopoulou, C. Konstantakis, Christos Triantos","doi":"10.31083/j.fbl2907252","DOIUrl":"https://doi.org/10.31083/j.fbl2907252","url":null,"abstract":"Vitamin D possesses a crucial role in preserving bone health, modulating the immune system responses, and supporting various physiological functions throughout the body. Chronic atrophic autoimmune gastritis (CAAG) constitutes an autoimmune condition marked by inflammation and damage to the stomach cells, often resulting in a decreased ability to absorb certain nutrients, including vitamin B12 and iron. Although, vitamin D is not directly affected by this condition, the sufficiency of this micronutrient seems to have important implications for overall health and management of the disease. The aim of the current review was to assess the incidence and related features of vitamin D deficiency in patients with CAAG and to elucidate the complex regulatory role of this nutrient, in an effort to improve patient outcomes. Vitamin D greatly contributes to the regulation of the immune system. In patients with CAAG, the immune system attacks the stomach lining; thus, the maintenance of a healthy and balanced immune response is important. In autoimmune conditions such as CAAG, where inflammation plays a decisive role in disease progression, vitamin D could potentially exert a role in managing and controlling the associated symptoms. Adequate vitamin D levels may help in regulating the immune response and reducing inflammation. In addition, patients with CAAG are at risk of nutrient deficiencies, including vitamin B12 and iron, which can lead to anemia and bone health issues. As vitamin D is critical for calcium absorption and bone health, assurance of sufficient levels of this micronutrient can be beneficial in preventing or mitigating bone-related complications. In conclusion, regular monitoring of vitamin D levels, among other nutrients, and appropriate supplementation, when necessary, can help improve overall health and well-being in these patients.","PeriodicalId":503756,"journal":{"name":"Frontiers in Bioscience-Landmark","volume":" 4","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-07-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141830540","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Sonia Carta, Maddalena Ghelardoni, Francesca Vitale, Silvia Ravera, Vanessa Cossu, N. Bertola, Serena Losacco, Jonathan Martinelli, Edoardo Dighero, M. Riondato, A. Orengo, Matteo Bauckneht, Sabrina Chiesa, G. Sambuceti, Cecilia Marini
{"title":"The Glucose-Glutamine Metabolic Interplay in MCF-7 Cells, a Hormone-Sensitive Breast Cancer Model","authors":"Sonia Carta, Maddalena Ghelardoni, Francesca Vitale, Silvia Ravera, Vanessa Cossu, N. Bertola, Serena Losacco, Jonathan Martinelli, Edoardo Dighero, M. Riondato, A. Orengo, Matteo Bauckneht, Sabrina Chiesa, G. Sambuceti, Cecilia Marini","doi":"10.31083/j.fbl2907251","DOIUrl":"https://doi.org/10.31083/j.fbl2907251","url":null,"abstract":"Background : Selective deprivation of glutamine has been shown to accelerate the generation of reactive oxygen species (ROS) and to impair the activity of a specific pentose phosphate pathway (PPP) located within the endoplasmic reticulum (ER). The consequent oxidative damage suggests that glucose flux through this reticular pathway might contribute to the redox stress of breast cancer cells. We thus evaluated whether this response is reproduced when the glutamine shortage is coupled with the glucose deprivation. Methods : Cancer growth, metabolic plasticity and redox status were evaluated under saturating conditions and after 48 h starvation (glucose 2.5 mM, glutamine 0.5 mM). The Seahorse technology was used to estimate adenosine triphosphate (ATP)-linked and ATP-independent oxygen consumption rate (OCR) as well as proton efflux rate (PER). 18 F-fluoro-deoxy-glucose (FDG) uptake was evaluated through the LigandTracer device. Proliferation rate was estimated by the carboxyfluorescein-diacetate-succinimidyl ester (CFSE) staining, while cell viability by the propidium iodide exclusion assay. Results : Starvation reduced the proliferation rate of MCF-7 cells without affecting their viability. It also decreased lactate release and PER. Overall OCR was left unchanged although ATP-synthase dependent fraction was increased under nutrient shortage. Glutaminolysis inhibition selectively impaired the ATP-independent and the oligomycin-sensitive OCR in control and starved cultures, respectively. The combined nutrient shortage decreased the cytosolic and mitochondrial markers of redox stress. It also left unchanged the expression of the reticular unfolded protein marker GRP78. By contrast, starvation decreased the expression of hexose-6P-dehydrogenase (H6PD) thus decreasing the glucose flux through the ER-PPP as documented by the profound impairment in the uptake rate of FDG. Conclusions : When combined with glucose deprivation, glutamine shortage does not elicit the expected enhancement of ROS generation in the studied breast cancer cell line. Combined with the decreased activity of ER-PPP, this observation suggests that glutamine interferes with the reticular glucose metabolism to regulate the cell redox balance.","PeriodicalId":503756,"journal":{"name":"Frontiers in Bioscience-Landmark","volume":" 20","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141831562","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Jing Luo, Hongmei Yu, Zhen Yuan, Wenqing Tang, Chen Wang
{"title":"REST Promotes Autophagy in Gastric Cancer by Transcriptionally Activating FABP6 to Inhibit the Akt/mTOR Signaling Pathway","authors":"Jing Luo, Hongmei Yu, Zhen Yuan, Wenqing Tang, Chen Wang","doi":"10.31083/j.fbl2906212","DOIUrl":"https://doi.org/10.31083/j.fbl2906212","url":null,"abstract":"","PeriodicalId":503756,"journal":{"name":"Frontiers in Bioscience-Landmark","volume":"84 13","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-06-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141352785","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Xiao-Yan Pu, Yonghong Mei, Qiang Zheng, Chih-Yuan Ko
{"title":"Inhibition of Melanoma Cell Growth by Salvianolic Acid A through CHK2-CDC25A Pathway Modulation","authors":"Xiao-Yan Pu, Yonghong Mei, Qiang Zheng, Chih-Yuan Ko","doi":"10.31083/j.fbl2906213","DOIUrl":"https://doi.org/10.31083/j.fbl2906213","url":null,"abstract":"Background : This study investigated the impact of salvianolic acids, derived from Danshen, on melanoma cell growth. Specifically, we assessed the ability of salvianolic acid A (Sal A) to modulate melanoma cell proliferation. Methods : We used human melanoma A2058 and A375 cell lines to investigate the effects of Sal A on cell proliferation and death by measuring bromodeoxyuridine incorporation and lactate dehydrogenase release. We assessed cell viability and cycle progression using water soluble tetrazolium salt-1 (WST-1) mitochondrial staining and propidium iodide. Additionally, we used a phospho-kinase array to investigate intracellular kinase phosphorylation, specifically measuring the influence of Sal A on checkpoint kinase-2 (Chk-2) via western blot analysis. Results : Sal A inhibited the growth of A2058 and A375 cells dose-responsively and induced cell cycle arrest at the G2/M phase. Notably, Sal A selectively induces Chk-2 phosphorylation without affecting Chk-1, thereby degrading Chk-2-regulated genes Cdc25A and Cdc2 . However, Sal A does not affect the Chk1-Cdc25C pathway. Conclusions : Salvianolic acids, especially Sal A, effectively hinder melanoma cell growth by inducing Chk-2 phosphorylation and disrupting G2/M checkpoint regulation.","PeriodicalId":503756,"journal":{"name":"Frontiers in Bioscience-Landmark","volume":"31 9","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-06-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141353477","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
L. Longhitano, D. Tibullo, T. Zuppelli, Simone Ronsisvalle, E. La Spina, Anna Nicolosi, Maria Antoci, F. Sipala, Fabio Galvano, W. Currenti, Annalisa Santisi, A. M. Alanazi, Guido Zanghì, Emanuela Tropea, Giovanni Li Volti, I. Barbagallo
{"title":"(+)Alpha-Lipoic Acid Regulates Lipid Metabolism Gene Expression and Lipidic Profile in a Cellular Model of Fatty Acid Overload","authors":"L. Longhitano, D. Tibullo, T. Zuppelli, Simone Ronsisvalle, E. La Spina, Anna Nicolosi, Maria Antoci, F. Sipala, Fabio Galvano, W. Currenti, Annalisa Santisi, A. M. Alanazi, Guido Zanghì, Emanuela Tropea, Giovanni Li Volti, I. Barbagallo","doi":"10.31083/j.fbl2906209","DOIUrl":"https://doi.org/10.31083/j.fbl2906209","url":null,"abstract":"Background : Nonalcoholic fatty liver disease (NAFLD) is a prevalent condition characterized by hepatic fat accumulation, often progressing to severe liver injury, for which approved treatments are currently lacking. This study explores the potential therapeutic impact of alpha-lipoic acid (ALA), a natural compound crucial in lipid metabolism, on NAFLD using an in vitro model. Methods : HepG2 cells were treated with a palmitic acid:oleic acid (PA:OA) mixture, representing a cellular model of steatosis. Subsequent treatment with ALA at concentrations of 1 µM and 5 µM aimed to evaluate its effects on lipid content and metabolism. Real-time polymerase chain reaction (PCR), BODIPY staining, cytofluorimetric analysis, and lipidomics were used to assess gene expression, lipid droplet accumulation, and fatty acid profiles. Results : Our results showed that ALA significantly reduced lipid droplets in PA:OA-treated HepG2 cells, with a concentration-dependent effect. Analysis of fatty acid profiles demonstrated a decrease in palmitic acid levels with ALA treatment, while oleic acid reduction was observed only at the higher concentration. Moreover, ALA modulated the expression of genes involved in cholesterol biosynthesis and low-density lipoprotein (LDL) metabolism, indicating a potential role in lipid homeostasis. Further insights into molecular mechanisms revealed that ALA modulated peroxisome proliferator activated receptors (PPARs), specifically PPAR-alpha and PPAR-gamma, involved in fatty acid metabolism and insulin sensitivity. Finally, ALA counteracted the overexpression of thermo-genic genes induced by exogenous fatty acids, suggesting a regulatory role in energy dissipation pathways. Conclusion : In conclusion, this study highlights ALA as a therapeutic agent in mitigating lipid accumulation and dysregulation in NAFLD.","PeriodicalId":503756,"journal":{"name":"Frontiers in Bioscience-Landmark","volume":"22 4","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141356769","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Pyroptosis in Spinal Cord Injury: Implications for Pathogenesis and Therapeutic Approaches","authors":"Guangjin Gu, Huaqi Yu, Huishuang Zou, Wenjuan Kou, Pingping Zhang, Guangjie Gu, Jie Lu, Weihan Shi, Pengcheng Chu, Yaning Zhang, Guangwei Sun, Jun Shang","doi":"10.31083/j.fbl2906210","DOIUrl":"https://doi.org/10.31083/j.fbl2906210","url":null,"abstract":"Traumatic spinal cord injury (SCI) is a serious disease of the central nervous system. Aside from the limited intrinsic regenerative capacity of neurons, complex microenvironmental disturbances can also lead to further cellular damage and growth inhibition. Programmed cell death regulated by pyroptosis has an important role in the pathogenesis of SCI. While there has been a wealth of new knowledge regarding cellular pyroptosis, a detailed understanding of its role in SCI and possible therapeutic strategies is still lacking. This review summarizes current advances in the regulatory role of pyroptosis-regulated cell death and inflammasome components in the inhibitory microenvironment following SCI, as well as recent therapeutic advances.","PeriodicalId":503756,"journal":{"name":"Frontiers in Bioscience-Landmark","volume":"122 47","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141360619","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"A Preliminary Investigation into the Effect of Low-Energy Lasers on Dental Pulp Stem Cell Proliferation and the Associated Mechanism","authors":"Wenting Pan, Shiwen Yan, Tiantian Li, He Jiang, Mengwen Wang, Peng Xue","doi":"10.31083/j.fbl2906211","DOIUrl":"https://doi.org/10.31083/j.fbl2906211","url":null,"abstract":"","PeriodicalId":503756,"journal":{"name":"Frontiers in Bioscience-Landmark","volume":"4 3","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141357064","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"A Predictive Model Based on the FBXO Family Reveals the Significance of Cyclin F in Hepatocellular Carcinoma","authors":"D. Gao, Suxin Li, Huahu Guo, Xianfu Liu, Zhaochen Liu, Luhao Li, Liang Bao, Xiaowei Dang","doi":"10.31083/j.fbl2905202","DOIUrl":"https://doi.org/10.31083/j.fbl2905202","url":null,"abstract":"","PeriodicalId":503756,"journal":{"name":"Frontiers in Bioscience-Landmark","volume":"8 6","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-05-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141102695","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Tao Liu, Manqi Yang, Bo Cui, Hao Ju, Jinchun Wu, Zongli Ren, Sheng Cao, Min Yan, Fan Zhang, Zheyu Liu, Shuijing He, Jiajun Zhang, R. Hiram, Feng Xiong, Mian Cheng, Gang Wu
{"title":"Alterations of Myocardial Mitochondrial Morphology and Function in a Canine Model of Premature Ventricular Contractions-Induced Cardiomyopathy","authors":"Tao Liu, Manqi Yang, Bo Cui, Hao Ju, Jinchun Wu, Zongli Ren, Sheng Cao, Min Yan, Fan Zhang, Zheyu Liu, Shuijing He, Jiajun Zhang, R. Hiram, Feng Xiong, Mian Cheng, Gang Wu","doi":"10.31083/j.fbl2905200","DOIUrl":"https://doi.org/10.31083/j.fbl2905200","url":null,"abstract":"","PeriodicalId":503756,"journal":{"name":"Frontiers in Bioscience-Landmark","volume":"97 9","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141111563","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}