FEBS Open Bio最新文献

Cost-effective and simple flow cytometry quantification of receptor-mediated autophagy using fluorescent tagging.

IF 2.8 4区生物学

FEBS Open Bio Pub Date : 2024-12-23 DOI: 10.1002/2211-5463.13958

Mija Marinković, Ana Rožić, Denis Polančec, Ivana Novak

{"title":"Cost-effective and simple flow cytometry quantification of receptor-mediated autophagy using fluorescent tagging.","authors":"Mija Marinković, Ana Rožić, Denis Polančec, Ivana Novak","doi":"10.1002/2211-5463.13958","DOIUrl":"https://doi.org/10.1002/2211-5463.13958","url":null,"abstract":"Mitophagy, a selective clearance of damaged or superfluous mitochondria via autophagy machinery and lysosomal degradation, is an evolutionarily conserved process essential for various physiological functions, including cellular differentiation and immune responses. Defects in mitophagy are implicated in numerous human diseases, such as neurodegenerative disorders, cancer, and metabolic conditions. Despite significant advancements in mitophagy research over recent decades, novel and robust methodologies are necessary to elucidate its molecular mechanisms comprehensively. In this study, we present a detailed protocol for quantitatively assessing mitophagy through flow cytometry using a mitochondria-targeted fluorescent mitophagy receptor, GFP-BNIP3L/NIX. This method offers a rapid alternative to conventional microscopy or immunoblotting techniques for analyzing mitophagy activity. Additionally, this approach can theoretically be adapted to utilize any fluorescent-tagged selective autophagy receptor, enabling the direct and rapid analysis of various types of receptor-mediated selective autophagy.","PeriodicalId":12187,"journal":{"name":"FEBS Open Bio","volume":" ","pages":""},"PeriodicalIF":2.8,"publicationDate":"2024-12-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142881643","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

NPC1 promotes the progression of hepatocellular carcinoma by mediating the accumulation of neutrophils into the tumor microenvironment.

IF 2.8 4区生物学

FEBS Open Bio Pub Date : 2024-12-20 DOI: 10.1002/2211-5463.13951

Songhai Yang, Jiangming Chen, Kun Xie, Fubao Liu

{"title":"NPC1 promotes the progression of hepatocellular carcinoma by mediating the accumulation of neutrophils into the tumor microenvironment.","authors":"Songhai Yang, Jiangming Chen, Kun Xie, Fubao Liu","doi":"10.1002/2211-5463.13951","DOIUrl":"https://doi.org/10.1002/2211-5463.13951","url":null,"abstract":"Hepatocellular carcinoma remains a significant threat to human health. Recent studies have found that the intake of cellular cholesterol contributes to the development and progression of hepatocellular carcinoma, although the exact mechanisms remain unclear. Our analysis of transcriptomic and proteomic databases has identified increased mRNA and protein expression levels of NPC1, a cholesterol intracellular transporter protein, in hepatocellular carcinoma tissues. This increase is significantly associated with a worse prognosis for patients. To corroborate these findings, we performed immunohistochemical staining of NPC1 on liver tissue samples from patients, revealing significantly higher expression levels of NPC1 in hepatocellular carcinoma tissues compared to normal tissues. Subsequent investigations have revealed that NPC1 expression does not significantly influence the proliferation of hepatocellular carcinoma cells in vitro. However, it has a substantial inhibitory effect on the progression of hepatocellular carcinoma tumors when observed in vivo. Utilizing flow cytometry to monitor cellular changes within the tumor microenvironment has led us to discover that NPC1 plays a crucial role in the regulation of neutrophil recruitment within the tumor. Using further neutrophil depletion experiments, we determined that the role of NPC1 in advancing hepatocellular carcinoma progression truly relies on neutrophils. These observations are further reinforced by a comprehensive analysis of clinical databases alongside immunohistochemistry findings. In conclusion, our research suggests that NPC1's overexpression could contribute to hepatocellular carcinoma progression by promoting neutrophil recruitment, positioning NPC1 as a promising new biomarker and therapeutic target for hepatocellular carcinoma.","PeriodicalId":12187,"journal":{"name":"FEBS Open Bio","volume":" ","pages":""},"PeriodicalIF":2.8,"publicationDate":"2024-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142871936","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Dexmedetomidine suppresses glucose-stimulated insulin secretion in pancreatic β-cells.

IF 2.8 4区生物学

FEBS Open Bio Pub Date : 2024-12-20 DOI: 10.1002/2211-5463.13960

Munenori Kusunoki, Kiichi Hirota, Tomohiro Shoji, Takeo Uba, Yoshiyuki Matsuo, Mikio Hayashi

{"title":"Dexmedetomidine suppresses glucose-stimulated insulin secretion in pancreatic β-cells.","authors":"Munenori Kusunoki, Kiichi Hirota, Tomohiro Shoji, Takeo Uba, Yoshiyuki Matsuo, Mikio Hayashi","doi":"10.1002/2211-5463.13960","DOIUrl":"https://doi.org/10.1002/2211-5463.13960","url":null,"abstract":"Proper glycemic control is crucial for patient management in critical care, including perioperative care, and can influence patient prognosis. Blood glucose concentration determines insulin secretion and sensitivity and affects the intricate balance between the glucose metabolism. Human and other animal studies have demonstrated that perioperative drugs, including volatile anesthetics and intravenous anesthetics, affect glucose-stimulated insulin secretion (GSIS). Dexmedetomidine (DEX) decreases insulin release and affects glucose metabolism; however, the specific mechanism underlying this phenomenon remains largely unknown. Thus, we investigated the effect and mechanism of DEX on insulin secretion using mouse and rat pancreatic β-cell-derived MIN6 and INS-1 cell lines and primary pancreatic β-cells/islets extracted from mice. The amount of insulin secreted into the culture medium was determined using an enzyme-linked immunosorbent assay. Cell viability, cytotoxicity, and electrophysiological effects were investigated. Clinically relevant doses of DEX suppressed GSIS in MIN6 cells, INS-1 cells, and pancreatic β-cells/islets. Furthermore, DEX suppressed insulin secretion facilitated by insulinotropic factors. There was no significant difference in oxygen consumption rate, intracellular ATP levels, or caspase-3/7 activity. Electrophysiological evaluation using the patch-clamp method showed that DEX did not affect ATP-sensitive potassium (KATP) channels, voltage-dependent potassium channels, or voltage-gated calcium channels. We demonstrated that clinically relevant doses of DEX significantly suppressed GSIS. These findings suggest that DEX inhibits a signaling pathway via α2-adrenoceptor or insulin vesicle exocytosis, resulting in GSIS suppression. Our results support the hypothesis that DEX suppresses insulin secretion and reveal some underlying mechanisms.","PeriodicalId":12187,"journal":{"name":"FEBS Open Bio","volume":" ","pages":""},"PeriodicalIF":2.8,"publicationDate":"2024-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142863892","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Evaluating frailty scores across experimental groups in rodent models: bridging physical and cognitive domains.

IF 2.8 4区生物学

FEBS Open Bio Pub Date : 2024-12-19 DOI: 10.1002/2211-5463.13955

Aleksandra Mladenovic, Smilja Pracer

{"title":"Evaluating frailty scores across experimental groups in rodent models: bridging physical and cognitive domains.","authors":"Aleksandra Mladenovic, Smilja Pracer","doi":"10.1002/2211-5463.13955","DOIUrl":"https://doi.org/10.1002/2211-5463.13955","url":null,"abstract":"Frailty, a reversible clinical geriatric syndrome, impairs the ability to maintain homeostasis, leading to severe consequences such as hospitalization and death. Cognitive frailty, characterized by the co-occurrence of physical frailty and cognitive impairment, has garnered increasing attention in recent years. Preclinical models, especially rodent studies, are essential for understanding frailty and developing interventions to mitigate associated conditions. Traditionally, animal studies have focused solely on physical frailty. We have pioneered the inclusion of cognitive parameters by developing a novel physical-cognitive frailty score (FS) in animal research, in order to assess the effectiveness of anti-aging interventions. Here, we provide a detailed example of the FS calculation at the group level, which can serve as a guide for other studies. This dual-focus approach also helps in understanding how physical frailty and cognitive impairment interact to exacerbate adverse health outcomes and provides an opportunity to evaluate potential interventions that target both physical and cognitive dimensions of frailty more reliably.","PeriodicalId":12187,"journal":{"name":"FEBS Open Bio","volume":" ","pages":""},"PeriodicalIF":2.8,"publicationDate":"2024-12-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142863893","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Synergistic antibacterial activity of baicalin in combination with oxacillin sodium against methicillin-resistant Staphylococcus aureus.

IF 2.8 4区生物学

FEBS Open Bio Pub Date : 2024-12-15 DOI: 10.1002/2211-5463.13952

Xin Meng, Mengna Kang, Zhiyun Yu, Changyou Li, Yang Chen, Taicheng Jin, Kai Wang, Haiyong Guo

{"title":"Synergistic antibacterial activity of baicalin in combination with oxacillin sodium against methicillin-resistant Staphylococcus aureus.","authors":"Xin Meng, Mengna Kang, Zhiyun Yu, Changyou Li, Yang Chen, Taicheng Jin, Kai Wang, Haiyong Guo","doi":"10.1002/2211-5463.13952","DOIUrl":"https://doi.org/10.1002/2211-5463.13952","url":null,"abstract":"Methicillin-resistant Staphylococcus aureus (MRSA) poses a challenge for clinical treatment and combining antibiotics with other agents might be a promising strategy to overcome this challenge. This study explored the synergistic antibacterial activity of baicalin (traditional Chinese medicine extract) and the narrow-spectrum beta-lactam antibiotic oxacillin sodium, both of which are poorly active against MRSA in vitro. The combination of baicalin and oxacillin sodium showed a synergistic effect with a fractional inhibitory concentration index of 0.5. Mechanistically, the supplementation of baicalin increased the permeability of bacterial cell walls and cell membranes, enhancing oxacillin sodium entry and bactericidal action. The combination of baicalin and oxacillin sodium also significantly inhibited MRSA USA300 biofilm formation by further reducing polysaccharide intercellular adhesion production. Therefore, the combination of baicalin and oxacillin sodium offers a new therapeutic option for addressing clinical MRSA resistance. Further studies, including clinical trials, will be required to validate the observed in vitro results.","PeriodicalId":12187,"journal":{"name":"FEBS Open Bio","volume":" ","pages":""},"PeriodicalIF":2.8,"publicationDate":"2024-12-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142827951","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Knockdown of RFC4 inhibits cell proliferation of oral squamous cell carcinoma in vitro and in vivo.

IF 2.8 4区生物学

FEBS Open Bio Pub Date : 2024-12-13 DOI: 10.1002/2211-5463.13929

Pengyue You, Di Wang, Zheng Liu, Shuzhen Guan, Ning Xiao, Haotian Chen, Xin Zhang, Lichuan Wu, Guizhen Wang, Haitao Dong

引用次数: 0

Evaluation of binding activities of a putative lipoprotein LIC_13355 of Leptospira spp.

IF 2.8 4区生物学

FEBS Open Bio Pub Date : 2024-12-12 DOI: 10.1002/2211-5463.13942

Igor R M Silva, Maria B Takahashi, Aline F Teixeira, Ana L T O Nascimento

{"title":"Evaluation of binding activities of a putative lipoprotein LIC_13355 of Leptospira spp.","authors":"Igor R M Silva, Maria B Takahashi, Aline F Teixeira, Ana L T O Nascimento","doi":"10.1002/2211-5463.13942","DOIUrl":"https://doi.org/10.1002/2211-5463.13942","url":null,"abstract":"Pathogenic Leptospira is the etiological cause of the zoonotic life-threatening infection called leptospirosis. The disease is spread worldwide with higher risk in tropical regions. Although leptospirosis represents a burden to the health of humans and animals, the pathogenic mechanisms of Leptospira infection are yet to be clarified. Leptospirosis infection is multifactorial, involving functionally redundant proteins with the capability to invade, disseminate, and escape the host's immune response. In this work, we describe a putative lipoprotein encoded by the gene LIC_13355, genome annotated as hypothetical of unknown function. The coding sequence is conserved among pathogenic Leptospira spp. with high percentage of coverage and identity. The recombinant protein, rLIC_13355, was expressed in Escherichia coli host system in its insoluble form. The circular dichroism spectrum of the refolded protein showed it containing a mixture of secondary structures. rLIC_13355 interacts with extracellular matrix (ECM) component laminin and binds plasminogen (PLG), generating plasmin (PLA), thus possibly participating during the adhesion and dissemination processes. The rLIC_13355 has the ability to interact with Ea.hy926 and HMEC-1 endothelial cells either in monolayer or suspension. The binding of rLIC_13355 with monolayer cells is dose-dependent on protein concentration. Taken together, our data suggest that this is presumably an adhesion lipoprotein that may play diverse roles in host-Leptospira interactions by mediating the interaction with host components and with endothelial cell.","PeriodicalId":12187,"journal":{"name":"FEBS Open Bio","volume":" ","pages":""},"PeriodicalIF":2.8,"publicationDate":"2024-12-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142812453","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Using TECHnology to predict the future of biomedical education.

IF 2.8 4区生物学

FEBS Open Bio Pub Date : 2024-12-12 DOI: 10.1002/2211-5463.13953

Robert A Harris, Hasan Kazdağlı

引用次数: 0

A white paper from the FEBS Education and Training Conference: challenges, opportunities, and action plans for transforming molecular life sciences education.

IF 2.8 4区生物学

FEBS Open Bio Pub Date : 2024-12-12 DOI: 10.1002/2211-5463.13916

Ly Villo, Nino Sincic, Luciane V Mello, Manuel Joao Costa, Didier Picard, Francesco Malatesta, Jerka Dumic, Ferhan G Sagin

{"title":"A white paper from the FEBS Education and Training Conference: challenges, opportunities, and action plans for transforming molecular life sciences education.","authors":"Ly Villo, Nino Sincic, Luciane V Mello, Manuel Joao Costa, Didier Picard, Francesco Malatesta, Jerka Dumic, Ferhan G Sagin","doi":"10.1002/2211-5463.13916","DOIUrl":"https://doi.org/10.1002/2211-5463.13916","url":null,"abstract":"The inaugural FEBS Education and Training Conference (ETC) was held in Türkiye, in 2024. This first-ever Molecular Life Sciences Education Conference in Europe was organized by the FEBS Education and Training Committee and it was a groundbreaking event that brought together educators and scientists to explore how to enhance education and training in molecular life sciences. The conference explored a wide range of critical themes, for example-digital revolution, active learning and student engagement, multidisciplinary teaching and learning, transitions and inclusivity in education, students' self-assessment, and self-regulated learning. The discussions and presentations underscored the pressing need for transformation in how academics and researchers approach teaching and learning. Such shift is driven by rapid technological advancements, societal shifts, and the evolving demands of the scientific landscape. This document synthesizes key insights, discussions, and recommendations from the conference and proposes actionable strategies for all stakeholders in the field-institutions, educators and students-to address current challenges in education and training in molecular life sciences.","PeriodicalId":12187,"journal":{"name":"FEBS Open Bio","volume":" ","pages":""},"PeriodicalIF":2.8,"publicationDate":"2024-12-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142812451","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Delta-9 desaturase reduction in gastrointestinal cells induced to senescence by doxorubicin.

IF 2.8 4区生物学

FEBS Open Bio Pub Date : 2024-12-10 DOI: 10.1002/2211-5463.13945

Valentina De Nunzio, Emanuela Aloisio Caruso, Matteo Centonze, Giuliano Pinto, Miriam Cofano, Ilenia Saponara, Maria Notarnicola

{"title":"Delta-9 desaturase reduction in gastrointestinal cells induced to senescence by doxorubicin.","authors":"Valentina De Nunzio, Emanuela Aloisio Caruso, Matteo Centonze, Giuliano Pinto, Miriam Cofano, Ilenia Saponara, Maria Notarnicola","doi":"10.1002/2211-5463.13945","DOIUrl":"https://doi.org/10.1002/2211-5463.13945","url":null,"abstract":"The condition of cellular senescence has specific features, including an altered lipid metabolism. Delta-9 desaturase (Δ9) catalyzes the conversion of saturated fatty acids, such as palmitic acid and stearic acid, into their monounsaturated forms, palmitoleic and oleic acid, respectively. Δ9 activity is important for most lipid functions, such as membrane fluidity, lipoprotein metabolism and energy storage. The present study aimed to investigate differences in the expression of Δ9 in senescence-induced pancreatic (MIA-PaCa-2 and PANC-1) and hepatic (Hepa-RG and HLF) cancer cell lines. Cellular senescence was induced by growing cells in the presence of the chemotherapic drug doxorubicin. Senescence status was determined by the senescence-associated beta-galactosidase activity assay kit combined with the p21 and senescence associated secretory phenotype protein assay. Δ9 was downregulated in all senescence-induced cell lines compared to control cells, in both the lipidomic analysis and when measuring protein levels via western blotting. Hence, our findings demonstrate that the study of membrane lipid composition and the expression levels of Δ9 could potentially form the basis for future applications investigating the state of cellular senescence.","PeriodicalId":12187,"journal":{"name":"FEBS Open Bio","volume":" ","pages":""},"PeriodicalIF":2.8,"publicationDate":"2024-12-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142827939","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0