Biochemistry and Cell Biology最新文献

{"title":"Astrocyte-specific Ca²⁺ activity: Mechanisms of action, experimental tools, and roles in ethanol-induced dysfunction.","authors":"O R Coulter, C D Walker, M-L Risher","doi":"10.1139/bcb-2023-0008","DOIUrl":"10.1139/bcb-2023-0008","url":null,"abstract":"<p><p>Astrocytes are a subtype of non-neuronal glial cells that reside in the central nervous system. Astrocytes have extensive peripheral astrocytic processes that ensheathe synapses to form the tripartite synapse. Through a multitude of pathways, astrocytes can influence synaptic development and structural maturation, respond to neuronal signals, and modulate synaptic transmission. Over the last decade, strong evidence has emerged demonstrating that astrocytes can influence behavioral outcomes in various animal models of cognition. However, the full extent of how astrocytes influence brain function is still being revealed. Astrocyte calcium (Ca²⁺) signaling has emerged as an important driver of astrocyte-neuronal communication allowing intricate crosstalk through mechanisms that are still not fully understood. Here, we will review the field's current understanding of astrocyte Ca²⁺ signaling and discuss the sophisticated state-of-the-art tools and approaches used to continue unraveling astrocytes' interesting role in brain function. Using the field of pre-clinical ethanol (EtOH) studies in the context of alcohol use disorder, we focus on how these novel approaches have helped to reveal an important role for astrocyte Ca²⁺ function in regulating EtOH consumption and how astrocyte Ca²⁺ dysfunction contributes to the cognitive deficits that emerge after EtOH exposure in a rodent model.</p>","PeriodicalId":8775,"journal":{"name":"Biochemistry and Cell Biology","volume":" ","pages":"410-421"},"PeriodicalIF":2.4,"publicationDate":"2023-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10010321","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Analysis of financial challenges faced by graduate students in Canada.","authors":"Sarah Jane Laframboise,&nbsp;Thomas Bailey,&nbsp;Anh-Thu Dang,&nbsp;Mercedes Rose,&nbsp;Zier Zhou,&nbsp;Matthew D Berg,&nbsp;Stephen Holland,&nbsp;Sami Aftab Abdul,&nbsp;Kaela O'Connor,&nbsp;Sara El-Sahli,&nbsp;Dominique M Boucher,&nbsp;Garrett Fairman,&nbsp;Jacky Deng,&nbsp;Katherine Shaw,&nbsp;Nathaniel Noblett,&nbsp;Alexa D'Addario,&nbsp;Madelaine Empey,&nbsp;Keaton Sinclair","doi":"10.1139/bcb-2023-0021","DOIUrl":"10.1139/bcb-2023-0021","url":null,"abstract":"<p><p>Graduate students are vital to the creation of research and innovation in Canada. The National Graduate Student Finance Survey was launched in 2021 by the Ottawa Science Policy Network to investigate the financial realities of Canadian graduate students. Closing in April 2022, the survey received 1305 responses from graduate students representing various geographical locations, years of study, fields of education, and demographic backgrounds. The results capture a snapshot into graduate student finances, including an in-depth analysis of stipends, scholarships, debt, tuition, and living expenses. In its entirety, we found that the majority of graduate students are facing serious financial concerns. This is largely due to stagnant funding for students both from federal and provincial granting agencies and from within their institutions. This reality is even worse for international students, members of historically underrepresented communities, and those with dependents, all of whom experience additional challenges that impact their financial security. Based on our findings, we propose several recommendations to the Tri-Council agencies (Natural Sciences and Engineering Research Council, Social Science and Humanities Research Council, and Canadian Institute for Health Research) and academic institutions to strengthen graduate student finances and help sustain the future of research in Canada.</p>","PeriodicalId":8775,"journal":{"name":"Biochemistry and Cell Biology","volume":"101 4","pages":"326-360"},"PeriodicalIF":2.9,"publicationDate":"2023-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9900386","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Retraction: Role of the TSLP-DC-OX40L pathway in asthma pathogenesis and airway inflammation in mice.","authors":"","doi":"10.1139/bcb-2023-0071","DOIUrl":"10.1139/bcb-2023-0071","url":null,"abstract":"","PeriodicalId":8775,"journal":{"name":"Biochemistry and Cell Biology","volume":"101 4","pages":"377"},"PeriodicalIF":2.9,"publicationDate":"2023-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9900658","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Retraction: MiR-204 suppresses cell proliferation and promotes apoptosis in ovarian granulosa cells via targeting TPT1 in polycystic ovary syndrome.","authors":"","doi":"10.1139/bcb-2023-0070","DOIUrl":"https://doi.org/10.1139/bcb-2023-0070","url":null,"abstract":"","PeriodicalId":8775,"journal":{"name":"Biochemistry and Cell Biology","volume":"101 4","pages":"378"},"PeriodicalIF":2.9,"publicationDate":"2023-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9900659","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Retraction: MiR-301b promotes the proliferation, mobility, and epithelial-to-mesenchymal transition of bladder cancer cells by targeting <i>EGR1</i>.","authors":"","doi":"10.1139/bcb-2023-0074","DOIUrl":"10.1139/bcb-2023-0074","url":null,"abstract":"","PeriodicalId":8775,"journal":{"name":"Biochemistry and Cell Biology","volume":"101 4","pages":"379"},"PeriodicalIF":2.9,"publicationDate":"2023-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9900665","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"High concentrations of fructose cause brain damage in mice.","authors":"Anderson Cargnin-Carvalho,&nbsp;Mariella Reinol Silva,&nbsp;Ana Beatriz Costa,&nbsp;Nicole Alessandra Engel,&nbsp;Bianca Xavier Farias,&nbsp;Joice Benedet Bressan,&nbsp;Kassiane Mathiola Backes,&nbsp;Francielly de Souza,&nbsp;Naiana da Rosa,&nbsp;Aloir Neri de Oliveira Junior,&nbsp;Mariana Pereira de Souza Goldim,&nbsp;Maria Eduarda Anastácio Borges Corrêa,&nbsp;Ligia Milanez Venturini,&nbsp;Jucélia Jeremias Fortunato,&nbsp;Josiane Somariva Prophiro,&nbsp;Fabricia Petronilho,&nbsp;Paulo Cesar Lock Silveira,&nbsp;Gabriela Kozuchovski Ferreira,&nbsp;Gislaine Tezza Rezin","doi":"10.1139/bcb-2022-0088","DOIUrl":"10.1139/bcb-2022-0088","url":null,"abstract":"<p><p>Excessive fructose consumption is associated with the incidence of obesity and systemic inflammation, resulting in increased oxidative damage and failure to the function of brain structures. Thus, we hypothesized that fructose consumption will significantly increase inflammation, oxidative damage, and mitochondrial dysfunction in the mouse brain and, consequently, memory damage. The effects of different fructose concentrations on inflammatory and biochemical parameters in the mouse brain were evaluated. Male Swiss mice were randomized into four groups: control, with exclusive water intake, 5%, 10%, and 20% fructose group. The 10% and 20% fructose groups showed an increase in epididymal fat, in addition to higher food consumption. Inflammatory markers were increased in epididymal fat and in some brain structures. In the evaluation of oxidative damage, it was possible to observe significant increases in the hypothalamus, prefrontal cortex, and hippocampus. In the epididymal fat and in the prefrontal cortex, there was a decrease in the activity of the mitochondrial respiratory chain complexes and an increase in the striatum. Furthermore, short memory was impaired in the 10% and 20% groups but not long memory. In conclusion, excess fructose consumption can cause fat accumulation, inflammation, oxidative damage, and mitochondrial dysfunction, which can damage brain structures and consequently memory.</p>","PeriodicalId":8775,"journal":{"name":"Biochemistry and Cell Biology","volume":"101 4","pages":"313-325"},"PeriodicalIF":2.9,"publicationDate":"2023-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9897190","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Evaluation of biochemical profile and oxidative damage to lipids and proteins in patients with lysosomal acid lipase deficiency.","authors":"Gilian Guerreiro, Marion Deon, Carmen Regla Vargas","doi":"10.1139/bcb-2022-0330","DOIUrl":"10.1139/bcb-2022-0330","url":null,"abstract":"<p><p>Lysosomal acid lipase deficiency (LALD) is an inborn error of metabolism that lacks satisfactory treatment, which leads to the development of severe hepatic and cardiac complications and may even lead to death. In this sense, knowledge of the mechanisms involved in the pathophysiology of this disorder becomes essential to allow the search for new therapeutic strategies. There are no studies in the literature investigating the role of reactive species and inflammatory processes in the pathophysiology of this disorder. Therefore, the aim of this work was to investigate parameters of oxidative and inflammatory stress in LALD patients. In this work, we obtained results that demonstrate that LALD patients are susceptible to oxidative stress caused by an increase in the production of free radicals, observed by the increase of 2-7-dihydrodichlorofluorescein. The decrease in sulfhydryl content reflects oxidative damage to proteins, as well as a decrease in antioxidant defenses. Likewise, the increase in urinary levels of di-tyrosine observed also demonstrates oxidative damage to proteins. Furthermore, the determination of chitotriosidase activity in the plasma of patients with LALD was significantly higher, suggesting a pro-inflammatory state. An increase in plasma oxysterol levels was observed in patients with LALD, indicating an important relationship between this disease and cholesterol metabolism and oxidative stress. Also, we observed in LALD patients increased levels of nitrate production. The positive correlation found between oxysterol levels and activity of chitotriosidase in these patients indicates a possible link between the production of reactive species and inflammation. In addition, an increase in lipid profile biomarkers such as total and low-density lipoprotein cholesterol were demonstrated in the patients, which reinforces the involvement of cholesterol metabolism. Thus, we can assume that, in LALD, oxidative and nitrosative damage, in addition to inflammatory process, play an important role in its evolution and future clinical manifestations. In this way, we can suggest that the study of the potential benefit of the use of antioxidant and anti-inflammatory substances as an adjuvant tool in the treatment will be important, which should be associated with the already recommended therapy.</p>","PeriodicalId":8775,"journal":{"name":"Biochemistry and Cell Biology","volume":"101 4","pages":"294-302"},"PeriodicalIF":2.9,"publicationDate":"2023-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9916495","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hedgehog signal activates AMPK via Smoothened to promote autophagy and lipid degradation in hepatocytes.","authors":"Yixing Yao,&nbsp;Tianyuan Li,&nbsp;Tingting Yu,&nbsp;Xin Yang,&nbsp;Yue Wang,&nbsp;Jing Cai,&nbsp;Steven Y Cheng,&nbsp;Chen Liu,&nbsp;Shen Yue","doi":"10.1139/bcb-2022-0345","DOIUrl":"10.1139/bcb-2022-0345","url":null,"abstract":"<p><p>Studies in the past decade have shown that lipid droplets stored in liver cells under starvation are encapsulated by autophagosomes and fused to lysosomes via the endocytic system. Autophagy responds to a variety of environmental factors inside and outside the cell, so it has a complex signal regulation network. To this end, we first explored the role of Hedgehog (Hh) in autophagy and lipid metabolism. Treatment of normal mouse liver cells with SAG and GDC-0449 revealed elevated phosphorylation of AMP-activated protein kinase (AMPK) and increased lipidation of LC3. SAG, and GDC-0449 were agonist and antagonist of Smoothened (Smo) in canonical Hh pathway, respectively, but they played a consistent role in the regulation of autophagy in hepatocytes. Moreover, SAG and GDC-0449 did not affect the expression of glioma-associated oncogene (Gli1) and patched 1, suggesting the absence of canonical Hh signaling in hepatocytes. We further knocked down the Smo and found that the effects of SAG and GDC-0449 disappeared, indicating that the non-canonical Smo pathway was involved in the regulation of autophagy in hepatocytes. In addition, SAG and GDC-0449 promoted lipid degradation and inhibited lipid production signals. Knockdown of Smo slowed down the rate of lipid degradation rather than Sufu or Gli1, indicating that Hh signaling regulated the lipid metabolism via Smo. In summary, activates AMPK via Smo to promote autophagy and lipid degradation.</p>","PeriodicalId":8775,"journal":{"name":"Biochemistry and Cell Biology","volume":"101 4","pages":"284-293"},"PeriodicalIF":2.9,"publicationDate":"2023-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9970485","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"SARS-CoV-2 E protein-induced THP-1 pyroptosis is reversed by Ruscogenin.","authors":"Houda Huang,&nbsp;Xiuzhen Li,&nbsp;Duoduo Zha,&nbsp;Hongru Lin,&nbsp;Lingyi Yang,&nbsp;Yihan Wang,&nbsp;Luyan Xu,&nbsp;Linsiqi Wang,&nbsp;Tianhua Lei,&nbsp;Zhou Zhou,&nbsp;Yun-Fei Xiao,&nbsp;Hong-Bo Xin,&nbsp;Mingui Fu,&nbsp;Yisong Qian","doi":"10.1139/bcb-2022-0359","DOIUrl":"10.1139/bcb-2022-0359","url":null,"abstract":"<p><p>Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), an emerging pathogenic coronavirus, has been reported to cause excessive inflammation and dysfunction in multiple cells and organs, but the underlying mechanisms remain largely unknown. Here we showed exogenous addition of SARS-CoV-2 envelop protein (E protein) potently induced cell death in cultured cell lines, including THP-1 monocytic leukemia cells, endothelial cells, and bronchial epithelial cells, in a time- and concentration-dependent manner. SARS-CoV-2 E protein caused pyroptosis-like cell death in THP-1 and led to GSDMD cleavage. In addition, SARS-CoV-2 E protein upregulated the expression of multiple pro-inflammatory cytokines that may be attributed to activation of NF-κB, JNK and p38 signal pathways. Notably, we identified a natural compound, Ruscogenin, effectively reversed E protein-induced THP-1 death via inhibition of NLRP3 activation and GSDMD cleavage. In conclusion, these findings suggested that Ruscogenin may have beneficial effects on preventing SARS-CoV-2 E protein-induced cell death and might be a promising treatment for the complications of COVID-19.</p>","PeriodicalId":8775,"journal":{"name":"Biochemistry and Cell Biology","volume":"101 4","pages":"303-312"},"PeriodicalIF":2.9,"publicationDate":"2023-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10276182","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Retraction: Profibrogenic phenotype in caveolin-1 deficiency via differential regulation of STAT-1/3 proteins.","authors":"","doi":"10.1139/bcb-2023-0089","DOIUrl":"10.1139/bcb-2023-0089","url":null,"abstract":"","PeriodicalId":8775,"journal":{"name":"Biochemistry and Cell Biology","volume":"101 4","pages":"380"},"PeriodicalIF":2.9,"publicationDate":"2023-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9891337","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}