Background and objectiveAutophagy is the fundamental cell survival machinery that enables cells to respond to metabolic stress by recycling and degrading intracellular components to generate energy and macromolecular precursors. Bone marrow-derived mesenchymal stem cells (MSCs), possess the unique ability of self-renewal and development into specialized cells, and long-lived cells with specific metabolic needs. It has been demonstrated that autophagy is essential for MSC differentiation, quiescence, activation, and self-renewal. Thus, the hypothesis that autophagy influences bone marrow-derived MSC post-novodrin-prompted liver dysfunction was investigated in the present study.
{"title":"Multipotent Stromal Stem Cell Approach in Alleviating Autophagy Beclin-1/XBP-1/STAT5A/PTEN Signaling Pathways in Novodrin-induced Liver Dysfunction","authors":"Mai O. Kadry, Rehab M. Abdel-Megeed","doi":"10.14218/ge.2023.00052","DOIUrl":"https://doi.org/10.14218/ge.2023.00052","url":null,"abstract":"Background and objectiveAutophagy is the fundamental cell survival machinery that enables cells to respond to metabolic stress by recycling and degrading intracellular components to generate energy and macromolecular precursors. Bone marrow-derived mesenchymal stem cells (MSCs), possess the unique ability of self-renewal and development into specialized cells, and long-lived cells with specific metabolic needs. It has been demonstrated that autophagy is essential for MSC differentiation, quiescence, activation, and self-renewal. Thus, the hypothesis that autophagy influences bone marrow-derived MSC post-novodrin-prompted liver dysfunction was investigated in the present study.","PeriodicalId":12502,"journal":{"name":"Gene expression","volume":"76 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-10-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135854711","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}
Farzaneh Koohyanizadeh, Sara Falahi, Seyed Hamid Reza Mortazavi, Farhad Salari, Alireza Rezaiemanesh, Ali Gorgin Karaji
Background and objectivesInterleukin 27 (IL-27) is a cytokine consisting of two subunits, p28 and EBI3, and is a key mediator in regulating the differentiation of TCD4 + cells while playing a crucial role in immune-related disorders. This study aims to elucidate the possible association between IL-27p28 single nucleotide polymorphisms (SNPs), IL-27 serum levels, and the risk of allergic rhinitis (AR).
{"title":"Correlation between IL-27p28 Genetic Polymorphisms and Risk of Allergic Rhinitis","authors":"Farzaneh Koohyanizadeh, Sara Falahi, Seyed Hamid Reza Mortazavi, Farhad Salari, Alireza Rezaiemanesh, Ali Gorgin Karaji","doi":"10.14218/ge.2023.00019","DOIUrl":"https://doi.org/10.14218/ge.2023.00019","url":null,"abstract":"Background and objectivesInterleukin 27 (IL-27) is a cytokine consisting of two subunits, p28 and EBI3, and is a key mediator in regulating the differentiation of TCD4 + cells while playing a crucial role in immune-related disorders. This study aims to elucidate the possible association between IL-27p28 single nucleotide polymorphisms (SNPs), IL-27 serum levels, and the risk of allergic rhinitis (AR).","PeriodicalId":12502,"journal":{"name":"Gene expression","volume":"17 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-10-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"136296161","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}
Madhav Jadhav, Shailendra Sharma, Vaishnavi Kalmegh, Saumya Kapoor, Amit Shard
Hepatic diseases have constituted a significant global problem for over two decades, numerous factors contribute to these diseases, and most eventually result in hepatocellular carcinoma. A particular pivotal factor responsible for hepatic diseases is the abnormal functioning of various metabolic processes. Pyruvate kinase is a crucial regulator of the glycolytic pathway, and overexpression of pyruvate kinase isoform M2 (PKM2) has been observed with various hepatic abnormalities due to genetic malfunctioning and other contributing factors. The present scenario for diagnosing and treating hepatic diseases includes surgery and immunosuppressant therapies. Kinase modulation may also be a potential therapeutic measure for rectifying hepatic diseases, and this can serve as a potential approach. This review summarizes the malfunctions and significance of PKM2 regulation and explores the potential of PKM2 as a target for treating hepatic abnormalities.
{"title":"Moonlighting Effects of Pyruvate Kinase M2 in Chronic Liver Diseases","authors":"Madhav Jadhav, Shailendra Sharma, Vaishnavi Kalmegh, Saumya Kapoor, Amit Shard","doi":"10.14218/ge.2023.00038","DOIUrl":"https://doi.org/10.14218/ge.2023.00038","url":null,"abstract":"Hepatic diseases have constituted a significant global problem for over two decades, numerous factors contribute to these diseases, and most eventually result in hepatocellular carcinoma. A particular pivotal factor responsible for hepatic diseases is the abnormal functioning of various metabolic processes. Pyruvate kinase is a crucial regulator of the glycolytic pathway, and overexpression of pyruvate kinase isoform M2 (PKM2) has been observed with various hepatic abnormalities due to genetic malfunctioning and other contributing factors. The present scenario for diagnosing and treating hepatic diseases includes surgery and immunosuppressant therapies. Kinase modulation may also be a potential therapeutic measure for rectifying hepatic diseases, and this can serve as a potential approach. This review summarizes the malfunctions and significance of PKM2 regulation and explores the potential of PKM2 as a target for treating hepatic abnormalities.","PeriodicalId":12502,"journal":{"name":"Gene expression","volume":"14 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135425481","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}
Background and ObjectivesNanoparticle (NP) drug delivery systems have been developed recently to resolve the obstacle of drug resistance, contributing to the effective drug delivery to the target organ. A comparative study was carried out herein between doxorubicin (DOX), doxorubicin-loaded titanium NPs, DOX-loaded lactoferrin NPs, DOX-NPs, and PEGylated-doxorubicin (PEG-DOX) on the reno-carcinogenic impact of 3-methylcholanthrene (CA).
{"title":"Titanium-nanostructured and PEGylated Doxorubicin Diminish Chemotherapeutic Resistance in 3-Methylcholanthrene Renal Epithelial Cell Carcinoma via KRAS/FKBP5/P53/JAK2 Signaling","authors":"Mai O. Kadry, Rehab M. Abdel-Megeed","doi":"10.14218/ge.2023.00069","DOIUrl":"https://doi.org/10.14218/ge.2023.00069","url":null,"abstract":"Background and ObjectivesNanoparticle (NP) drug delivery systems have been developed recently to resolve the obstacle of drug resistance, contributing to the effective drug delivery to the target organ. A comparative study was carried out herein between doxorubicin (DOX), doxorubicin-loaded titanium NPs, DOX-loaded lactoferrin NPs, DOX-NPs, and PEGylated-doxorubicin (PEG-DOX) on the reno-carcinogenic impact of 3-methylcholanthrene (CA).","PeriodicalId":12502,"journal":{"name":"Gene expression","volume":"232 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135343582","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}
Many (+)RNA viruses employ translational recoding mechanisms, such as programmed ribosomal readthrough and ribosomal frameshifting, to direct a fraction of translating ribosomes in the infected cell to recode or bypass a stop codon in the zero reading frame and continue translation, thus producing protein isoforms with distinct functions. This creates a means to regulate both the quantity and time of synthesis of canonical and fusion proteins. The viral programmed ribosomal readthrough and ribosomal frameshifting signals are variable, with some being just short RNA sequences encompassing a stop codon, whereas others require elaborate RNA-RNA and RNA-protein interactions. Within virus evolutionary lineages, a given type of recoding signal is not universal, and its presence may be specific to a virus family, species, or even strain. It is possible that the establishment of virus recoding mechanisms and expression patterns occurs after the appearance of extant virus lineages, and these recoding signals might be acquired on multiple occasions during evolution. Recoding signals are the key regulators of gene expression in several clinically important viruses, such as human immunodeficiency viruses 1 and 2, human T-cell lymphotropic retroviruses, and severe acute respiratory syndrome coronavirus 2, as well as in a number of other animal and plant viruses of concern. The knowledge of viral recoding mechanisms is expected to provide new perspectives for the development of antiviral and synthetic biology strategies.
{"title":"Where To Stop: Occurrence and Evolution of Translational Recoding Signals in RNA Viruses of Eukaryotes","authors":"Alexey A. Agranovsky","doi":"10.14218/ge.2023.00025","DOIUrl":"https://doi.org/10.14218/ge.2023.00025","url":null,"abstract":"Many (+)RNA viruses employ translational recoding mechanisms, such as programmed ribosomal readthrough and ribosomal frameshifting, to direct a fraction of translating ribosomes in the infected cell to recode or bypass a stop codon in the zero reading frame and continue translation, thus producing protein isoforms with distinct functions. This creates a means to regulate both the quantity and time of synthesis of canonical and fusion proteins. The viral programmed ribosomal readthrough and ribosomal frameshifting signals are variable, with some being just short RNA sequences encompassing a stop codon, whereas others require elaborate RNA-RNA and RNA-protein interactions. Within virus evolutionary lineages, a given type of recoding signal is not universal, and its presence may be specific to a virus family, species, or even strain. It is possible that the establishment of virus recoding mechanisms and expression patterns occurs after the appearance of extant virus lineages, and these recoding signals might be acquired on multiple occasions during evolution. Recoding signals are the key regulators of gene expression in several clinically important viruses, such as human immunodeficiency viruses 1 and 2, human T-cell lymphotropic retroviruses, and severe acute respiratory syndrome coronavirus 2, as well as in a number of other animal and plant viruses of concern. The knowledge of viral recoding mechanisms is expected to provide new perspectives for the development of antiviral and synthetic biology strategies.","PeriodicalId":12502,"journal":{"name":"Gene expression","volume":"2016 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135426613","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}
Anastasia V. Poznyak, Vasily N. Sukhorukov, Mikhail А. Popov, Yegor S Chegodaev, Anton Y. Postnov, Alexander N. Orekhov
Mitochondria are one of the most crucial components of the cell. Aging has a critical impact on mitochondria. Various studies have shown that the relationship between aging and mitochondria is multifaceted. In this review, we focused on mitochondrial DNA mutations and their impact on the cardiovascular system during aging and oxidative stress. While mitochondria contain their own DNA, part of their proteome is encoded by nuclear DNA, which further complicates the inheritance of mitochondrial diseases, making almost all methods of transmission of various pathologies possible. We provide a discussion on mitochondrial DNA mutagenesis and the most common problems associated with mitochondrial DNA mutations.
{"title":"Mitochondrial Mutations Affect the Cardiovascular System during Aging and Oxidative Stress","authors":"Anastasia V. Poznyak, Vasily N. Sukhorukov, Mikhail А. Popov, Yegor S Chegodaev, Anton Y. Postnov, Alexander N. Orekhov","doi":"10.14218/ge.2023.00039","DOIUrl":"https://doi.org/10.14218/ge.2023.00039","url":null,"abstract":"Mitochondria are one of the most crucial components of the cell. Aging has a critical impact on mitochondria. Various studies have shown that the relationship between aging and mitochondria is multifaceted. In this review, we focused on mitochondrial DNA mutations and their impact on the cardiovascular system during aging and oxidative stress. While mitochondria contain their own DNA, part of their proteome is encoded by nuclear DNA, which further complicates the inheritance of mitochondrial diseases, making almost all methods of transmission of various pathologies possible. We provide a discussion on mitochondrial DNA mutagenesis and the most common problems associated with mitochondrial DNA mutations.","PeriodicalId":12502,"journal":{"name":"Gene expression","volume":"15 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-09-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"136101508","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}
Bárbara Ferreira Khouri, Izabella Paulino de Souza Candido, Regina Célia Poli-Frederico, Paulo Roberto Bignardi
Host-specific genetics, such as epigenetic profiles and genetic variants, can contribute to the pathogenesis of infectious diseases. Strong associations have been previously identified in infections by human immunodeficiency virus (HIV), Plasmodium falciparum, norovirus, and influenza A virus. Despite the efforts to characterize the role of host genetics in severe acute respiratory syndrome virus coronavirus 2 (SARS-CoV-2) infection, this comprehension remains incipient. Coronavirus disease 2019 (COVID-19) can evolve with a wide spectrum of manifestations, ranging from asymptomatic and mild cases to severe forms with acute respiratory distress syndrome, multi-organ complications, and even death. Classic clinical risk factors only partially explain this interindividual variability, suggesting that host genetics may contribute to the heterogeneity of courses. Robust evidence has revealed the multiple associations of genes (ABO, PPP1R15A, SLC6A20, IFNAR2, OAS, TYK2, CCR2, CCR5, TLR7, ApoE, TMPRSS2, HLA, ACE2, etc.) with the susceptibility and/or severity of SARS-CoV-2 infection. In addition, the genetics behind the established risk factors have been considered: at least four loci associated with COVID-19 severity (DPP9, FOXP4, SFTPD and MUC5B) have been previously linked to lung fibrosis, interstitial lung disease, lung carcinomas, and/or decreased lung function. In summary, identifying the host-specific genetic factors may improve our knowledge of risk groups for infection and severe outcomes, as well as the biological mechanisms of therapeutic relevance. Therefore, the present literature review aims to understand the genetics underlying the patterns of susceptibility and prognosis of COVID-19.
{"title":"Host Genetics and COVID-19: Genes Underlying the Patterns of Susceptibility and Prognosis","authors":"Bárbara Ferreira Khouri, Izabella Paulino de Souza Candido, Regina Célia Poli-Frederico, Paulo Roberto Bignardi","doi":"10.14218/ge.2023.00026","DOIUrl":"https://doi.org/10.14218/ge.2023.00026","url":null,"abstract":"Host-specific genetics, such as epigenetic profiles and genetic variants, can contribute to the pathogenesis of infectious diseases. Strong associations have been previously identified in infections by human immunodeficiency virus (HIV), Plasmodium falciparum, norovirus, and influenza A virus. Despite the efforts to characterize the role of host genetics in severe acute respiratory syndrome virus coronavirus 2 (SARS-CoV-2) infection, this comprehension remains incipient. Coronavirus disease 2019 (COVID-19) can evolve with a wide spectrum of manifestations, ranging from asymptomatic and mild cases to severe forms with acute respiratory distress syndrome, multi-organ complications, and even death. Classic clinical risk factors only partially explain this interindividual variability, suggesting that host genetics may contribute to the heterogeneity of courses. Robust evidence has revealed the multiple associations of genes (ABO, PPP1R15A, SLC6A20, IFNAR2, OAS, TYK2, CCR2, CCR5, TLR7, ApoE, TMPRSS2, HLA, ACE2, etc.) with the susceptibility and/or severity of SARS-CoV-2 infection. In addition, the genetics behind the established risk factors have been considered: at least four loci associated with COVID-19 severity (DPP9, FOXP4, SFTPD and MUC5B) have been previously linked to lung fibrosis, interstitial lung disease, lung carcinomas, and/or decreased lung function. In summary, identifying the host-specific genetic factors may improve our knowledge of risk groups for infection and severe outcomes, as well as the biological mechanisms of therapeutic relevance. Therefore, the present literature review aims to understand the genetics underlying the patterns of susceptibility and prognosis of COVID-19.","PeriodicalId":12502,"journal":{"name":"Gene expression","volume":"47 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-09-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"136235166","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}
Despite advances in current treatment options, Hepatocellular Carcinoma (HCC) recurrence still presents as a significant clinical challenge. After initial treatment, HCC recurrence occurs in a considerable portion of patients without an available standardized protocol for managing such an incident. Recurrence of advanced liver disease may make surgical treatment options impossible, in which case, locoregional therapy should be considered as an alternative. This review article discusses recurrent HCC after initial treatment and available non-surgical treatment options. Along with systemic therapy, liver-targeted therapies for recurrent HCC including, radiofrequency, microwave ablation, transarterial chemoembolization, and stereotactic body radiation therapy are promising options. Thermal ablation with radiofrequency or microwave ablation is a suitable treatment option for patients who experience smaller tumor recurrences but are not operable because of comorbidities, impaired liver functions, or tumor locality. Transarterial chemoembolization or radioembolization using Yttrium-90 can be used for patients with an incurable disease and have comparatively low adverse effects.
{"title":"Non-surgical Treatment Options in Managing Recurrent Hepatocellular Carcinoma","authors":"Walaa Abdelhamed, Mohamed El-Kassas","doi":"10.14218/ge.2023.00010","DOIUrl":"https://doi.org/10.14218/ge.2023.00010","url":null,"abstract":"Despite advances in current treatment options, Hepatocellular Carcinoma (HCC) recurrence still presents as a significant clinical challenge. After initial treatment, HCC recurrence occurs in a considerable portion of patients without an available standardized protocol for managing such an incident. Recurrence of advanced liver disease may make surgical treatment options impossible, in which case, locoregional therapy should be considered as an alternative. This review article discusses recurrent HCC after initial treatment and available non-surgical treatment options. Along with systemic therapy, liver-targeted therapies for recurrent HCC including, radiofrequency, microwave ablation, transarterial chemoembolization, and stereotactic body radiation therapy are promising options. Thermal ablation with radiofrequency or microwave ablation is a suitable treatment option for patients who experience smaller tumor recurrences but are not operable because of comorbidities, impaired liver functions, or tumor locality. Transarterial chemoembolization or radioembolization using Yttrium-90 can be used for patients with an incurable disease and have comparatively low adverse effects.","PeriodicalId":12502,"journal":{"name":"Gene expression","volume":"93 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135011281","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":"Diagrams Describing the Evolution of Gene Expression, the Emergence of Novel Cell Types During Evolution, and Evo-devo","authors":"Andrei P. Kozlov","doi":"10.14218/ge.2023.00031","DOIUrl":"https://doi.org/10.14218/ge.2023.00031","url":null,"abstract":"","PeriodicalId":12502,"journal":{"name":"Gene expression","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44286382","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}
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