Journal of Bioenergetics and Biomembranes最新文献

{"title":"Resveratrol regulates the inflammation and oxidative stress of granulosa cells in PCOS via targeting TLR2.","authors":"Ben Yuan,&nbsp;Shuhong Luo,&nbsp;Liulian Feng,&nbsp;Junling Wang,&nbsp;Junbiao Mao,&nbsp;Bingbing Luo","doi":"10.1007/s10863-022-09942-7","DOIUrl":"https://doi.org/10.1007/s10863-022-09942-7","url":null,"abstract":"<p><p>Polycystic ovary syndrome (PCOS) is featured as a common endocrine disorder in reproductive-aged women, while its pathophysiology is not fully illustrated. This study examined potential actions of resveratrol in PCOS cellular model and explored the underlying interaction between resveratrol and toll-like receptor 2 (TLR2). This study performed the bioinformatics analysis on two microarray datasets (GSE34526 and GSE138518). We found that TLR2 was one of potential hub genes that may be associated with PCOS. Further examination showed that TLR2 was highly expressed in granulosa cells from PCOS group compared with control. The in vitro studies showed that LPS intervention caused an increased expression of TLR2 and the pro-inflammatory mediators, and induced oxidative stress in the granulosa cells, which was concentration-dependently antagonized by resveratrol treatment. TLR2 silence significantly attenuated LPS-induced increase TNF-α, IL-1β, IL-6 and IL-8 expression and oxidative stress of granulosa cells. Furthermore, TLR2 overexpression promoted inflammatory response and oxidative stress in the granulosa cells, which was antagonized by resveratrol treatment. In conclusion, resveratrol could attenuate LPS-induced inflammation and oxidative stress in granulosa cells, and the underlying mechanisms may be related to the inhibitory effect of resveratrol on TLR2 expression in granulosa cells.</p>","PeriodicalId":15080,"journal":{"name":"Journal of Bioenergetics and Biomembranes","volume":null,"pages":null},"PeriodicalIF":3.0,"publicationDate":"2022-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40506117","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}

{"title":"The potential role of circulating exosomes in protecting myocardial injury in acute myocardial infarction via regulating miR-190a-3p/CXCR4/CXCL12 pathway.","authors":"Chun-Yuan Jiang,&nbsp;Ting-Ting Zhong,&nbsp;Lu-Wen Qiu,&nbsp;Yan-Feng Liu,&nbsp;Hui-Hua Zuo,&nbsp;Xiao-Fei Huang","doi":"10.1007/s10863-022-09944-5","DOIUrl":"https://doi.org/10.1007/s10863-022-09944-5","url":null,"abstract":"<p><p>Exosomes of different origins have been found to be protective against ischemic-induced myocardial injury. This study examined the protective effects of circulating exosomes in the mice model of acute myocardial infarction (AMI) and explored the underlying molecular mechanisms. The effects of exosomes on myocardial injury were assessed in the AMI mice model. The in vivo studies showed that circulating exosomes reduced the infarcted size, improved the morphology of heart tissues and also reduced apoptosis of the heart tissues. In addition, the model mice showed an increase in the CD34 + /VEGFR2 + cell population and CD31, CXCR4 and CXCL12 expression after exosomes treatment. MiR-190a-3p was significantly down-regulated in the exosomes derived from the culture medium of hypoxia-treated human cardiomyocytes (HCMs). Further analysis revealed that miR-190a-3p could physically interact with CXCR4/CXCL12 by targeting the respective 3'UTRs. These exosomes could up-regulated CXCR4 and CXCL12 expression in the EPCs; in addition, miR-190a-3p mimics repressed CXCR4/CXCL12 expression in EPCs, while its inhibitor had opposite effects. The in vitro functional assays showed that miR-190a-3p overexpression suppressed the cell viability, proliferation, migration, adhesion and tube formation of EPCs; while miR-190a-3p inhibitor had the opposite effects; exosomes derived from the culture medium of hypoxia-treated HCMs exhibited similar actions of miR-190a-3p inhibitor. Moreover, miR-190a-3p was down-regulated in exosomes from serum in the AMI group when compared to that from sham group. Treatment with exosomes from serum in the AMI group promoted cell proliferation, migration, adhesion and tube formation of EPCs when compared to that in the sham group. More importantly, IT1t attenuated the enhanced effects of miR-190a-3p inhibition on EPC proliferation, migration, adhesion and tube formation. In conclusion, circulating exosomes exerted protective effects on myocardial injury in the AMI mice model, and down-regulation of miR-190a-3p in the circulating exosomes may exert protective effects against myocardial injury. Hypoxia induced the downregulation of miR-190a-3p in the culture medium of HCMs, and the mechanistic investigations indicated that exosomes of hypoxia-conditioned HCM culture medium promoted the cell viability, proliferation, migration, adhesion and tube formation of EPCs via regulating miR-190a-3p/CXCR4/CXCL12 pathway.</p>","PeriodicalId":15080,"journal":{"name":"Journal of Bioenergetics and Biomembranes","volume":null,"pages":null},"PeriodicalIF":3.0,"publicationDate":"2022-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40528979","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}

{"title":"Disruption of mitochondrial functions involving mitochondrial permeability transition pore opening caused by maleic acid in rat kidney.","authors":"Ana Cristina Roginski,&nbsp;Ângela Beatris Zemniaçak,&nbsp;Rafael Aguiar Marschner,&nbsp;Simone Magagnin Wajner,&nbsp;Rafael Teixeira Ribeiro,&nbsp;Moacir Wajner,&nbsp;Alexandre Umpierrez Amaral","doi":"10.1007/s10863-022-09945-4","DOIUrl":"https://doi.org/10.1007/s10863-022-09945-4","url":null,"abstract":"<p><p>Propionic acid (PA) predominantly accumulates in tissues and biological fluids of patients affected by propionic acidemia that may manifest chronic renal failure along development. High urinary excretion of maleic acid (MA) has also been described. Considering that the underlying mechanisms of renal dysfunction in this disorder are poorly known, the present work investigated the effects of PA and MA (1-5 mM) on mitochondrial functions and cellular viability in rat kidney and cultured human embryonic kidney (HEK-293) cells. Mitochondrial membrane potential (∆ψm), NAD(P)H content, swelling and ATP production were measured in rat kidney mitochondrial preparations supported by glutamate or glutamate plus malate, in the presence or absence of Ca²⁺. MTT reduction and propidium iodide (PI) incorporation were also determined in intact renal cells pre-incubated with MA or PA for 24 h. MA decreased Δψm and NAD(P)H content and induced swelling in Ca²⁺-loaded mitochondria either respiring with glutamate or glutamate plus malate. Noteworthy, these alterations were fully prevented by cyclosporin A plus ADP, suggesting the involvement of mitochondrial permeability transition (mPT). MA also markedly inhibited ATP synthesis in kidney mitochondria using the same substrates, implying a strong bioenergetics impairment. In contrast, PA only caused milder changes in these parameters. Finally, MA decreased MTT reduction and increased PI incorporation in intact HEK-293 cells, indicating a possible association between mitochondrial dysfunction and cell death in an intact cell system. It is therefore presumed that the MA-induced disruption of mitochondrial functions involving mPT pore opening may be involved in the chronic renal failure occurring in propionic acidemia.</p>","PeriodicalId":15080,"journal":{"name":"Journal of Bioenergetics and Biomembranes","volume":null,"pages":null},"PeriodicalIF":3.0,"publicationDate":"2022-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10775499","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}

{"title":"CircZNF644 aggravates lipopolysaccharide-induced HK-2 cell impairment via the miR-140-5p/MLKL axis.","authors":"Jing Xing,&nbsp;Songtao Fan,&nbsp;Hongyang Liu,&nbsp;Su Zhang,&nbsp;Nan Li","doi":"10.1007/s10863-022-09946-3","DOIUrl":"https://doi.org/10.1007/s10863-022-09946-3","url":null,"abstract":"<p><p>Circular RNAs (circRNAs) play vital roles in human diseases, including acute kidney injury (AKI). In this paper, we focused on the effect of circRNA zinc finger protein 644 (circZNF644) on AKI cell model progression. qRT-PCR was conducted for the levels of circZNF644, ZNF644, miR-140-5p and mixed lineage kinase domain like pseudokinase (MLKL). RNase R assay, actinomycin D assay and subcellular fraction analysis were conducted to analyze the features of circZNF644. CCK-8 assay and EdU assay were used to explore cell proliferation. Flow cytometry analysis was conducted to analyze cell cycle and cell apoptosis. Western blot assay was executed for protein levels. ELISA was performed for the levels of inflammatory cytokines. The relationships among circZNF644, miR-140-5p and MLKL were analyzed by dual-luciferase reporter assay and RIP assay. CircZNF644 was upregulated in LPS-stimulated HK-2 cells. LPS-mediated inhibitory effects on cell proliferation and cell cycle and promotional effects on apoptosis and inflammation were reversed by circZNF644 knockdown. CircZNF644 directly interacted with miR-140-5p and MLKL was the target gene of miR-140-5p. The impact of circZNF644 knockdown on HK-2 cell injury was relieved by miR-140-5p inhibition. Moreover, miR-140-5p enhancement alleviated LPS-triggered HK-2 cell damage, while MLKL elevation reversed the effect. CircZNF644 knockdown protected HK-2 cells from LPS-induced injury by altering miR-140-5p/MLKL pathway, suggesting that circZNF644 may be a hopeful therapeutic target for AKI.</p>","PeriodicalId":15080,"journal":{"name":"Journal of Bioenergetics and Biomembranes","volume":null,"pages":null},"PeriodicalIF":3.0,"publicationDate":"2022-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10535831","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}

{"title":"Correction to: Chronic exposure to ozone induces cardiac antioxidant response and overexpression of either mitochondrial fsion protein DRP1 and hipertrophyc-related proteins.","authors":"Nancy P Gómez-Crisóstomo,&nbsp;Selva Rivas-Arancibia,&nbsp;Erika Rodríguez-Martínez,&nbsp;Erick N De la Cruz-Hernández,&nbsp;Corazón de María Márquez Álvarez,&nbsp;Pablo Alexis Estrada Caraveo,&nbsp;Noemí Gelista Herrera,&nbsp;Marlen Valdés-Fuentes,&nbsp;Eduardo Martínez-Abundis","doi":"10.1007/s10863-022-09943-6","DOIUrl":"https://doi.org/10.1007/s10863-022-09943-6","url":null,"abstract":"","PeriodicalId":15080,"journal":{"name":"Journal of Bioenergetics and Biomembranes","volume":null,"pages":null},"PeriodicalIF":3.0,"publicationDate":"2022-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40578632","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}

{"title":"SKA-31-induced activation of small-conductance calcium-activated potassium channels decreased modulation of detrusor smooth muscle function in a rat model of obesity","authors":"Jingyu Li, T. Liu, Ning Li, Fengming Dong, Ping Wang","doi":"10.1007/s10863-022-09939-2","DOIUrl":"https://doi.org/10.1007/s10863-022-09939-2","url":null,"abstract":"","PeriodicalId":15080,"journal":{"name":"Journal of Bioenergetics and Biomembranes","volume":null,"pages":null},"PeriodicalIF":3.0,"publicationDate":"2022-04-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42862233","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}

{"title":"CircCDC6 restrains tumor growth and glycolysis energy metabolism in colorectal cancer via regulating miR-3187-3p and downstream PRKAA2","authors":"Chunxiang Zhao, Hong Chen, Kai Min","doi":"10.1007/s10863-022-09938-3","DOIUrl":"https://doi.org/10.1007/s10863-022-09938-3","url":null,"abstract":"","PeriodicalId":15080,"journal":{"name":"Journal of Bioenergetics and Biomembranes","volume":null,"pages":null},"PeriodicalIF":3.0,"publicationDate":"2022-04-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43939209","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}

{"title":"miR-29b ameliorates atrial fibrosis in rats with atrial fibrillation by targeting TGFβRΙ and inhibiting the activation of Smad-2/3 pathway.","authors":"Xinyuan Han,&nbsp;Shunda Wang,&nbsp;Zhijun Yong,&nbsp;Xueting Zhang,&nbsp;Xuanqi Wang","doi":"10.1007/s10863-022-09934-7","DOIUrl":"https://doi.org/10.1007/s10863-022-09934-7","url":null,"abstract":"<p><strong>Objective: </strong>Atrial fibrillation (AF) is a major cause of stroke with lifetime risks. microRNAs (miRNAs) are associated with AF attenuation, yet the mechanism remains unknown. This study investigated the functional mechanism of miR-29b in atrial fibrosis in AF.</p><p><strong>Methods: </strong>The AF rat model was established by a 7-day intravenous injection of Ach-CaCl₂ mixture. AF rats were injected with adeno-associated virus (AAv)-miR-29b and TGFβRΙ overexpression plasmid. AF duration was recorded by electrocardiogram. Atrial fibrosis was observed by Masson staining. Expressions of COL1A1, COL3A1, TGFβRΙ, TGFβΙ, miR-29b and Smad-2/3 pathway-related proteins in atrial tissues were detected by RT-qPCR and Western blot. Binding sites of miR-29b and TGFβRΙ were predicted and their target relationship was verified by dual-luciferase reporter assay.</p><p><strong>Results: </strong>miR-29b was poorly expressed and expressions of COL1A1, COL3A1, TGFβRΙ, and TGFβ1 were increased in atrial tissues of AF rats. miR-29b overexpression alleviated atrial fibrosis, reduced expressions of COL1A1, COL3A1, and TGFβ1, and shortened AF duration in AF rats. TGFβRΙ was highly expressed in atrial tissues of AF rats. miR-29b targeted TGFβRΙ. TGFβRΙ overexpression overcame the improving effect of miR-29b overexpression on AF. miR-29b overexpression decreased ratios of p-Smad-2/3 and Smad-2/3 and inhibited the Smad-2/3 pathway.</p><p><strong>Conclusion: </strong>miR-29b might mitigate atrial fibrosis in AF rats by targeting TGFβRΙ and inhibiting the Smad-2/3 pathway.</p>","PeriodicalId":15080,"journal":{"name":"Journal of Bioenergetics and Biomembranes","volume":null,"pages":null},"PeriodicalIF":3.0,"publicationDate":"2022-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40318414","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}

{"title":"Circ_0001093 promotes glutamine metabolism and cancer progression of esophageal squamous cell carcinoma by targeting miR-579-3p/glutaminase axis.","authors":"Cui-Juan Qian,&nbsp;Yi-Yang Tong,&nbsp;Yi-Chao Wang,&nbsp;Xiao-Sheng Teng,&nbsp;Jun Yao","doi":"10.1007/s10863-022-09935-6","DOIUrl":"https://doi.org/10.1007/s10863-022-09935-6","url":null,"abstract":"<p><p>Increasing studies indicate that circular RNAs (circRNAs) play critical roles in tumor metabolism of multiple cancers. However, the contribution of circRNAs in glutamine metabolism of esophageal squamous cell carcinoma (ESCC) remains elusive. The objective of this research was to investigate the role and mechanism of circRNA hsa_circ_0001093 (circ_0001093) in the glutamine metabolism and tumorigenesis of ESCC. Circ_0001093, microRNA-579-3p (miR-579-3p) and glutaminase (GLS) expressions in ESCC tissues and cell lines were measured by qRT-PCR, tissue array or Western blot. Cell proliferation, invasion and migration were assessed by CCK-8 or transwell assays. Glutamine consumption, glutamate and ATP production were detected by indicated assay kits. The relationships between circ_0001093 and miR-579-3p or GLS mRNA were investigated by bioinformatics analysis, RNA pull-down, luciferase reporter and RNA immunoprecipitation (RIP) assays. Here, we found that circ_0001093 expression was up-regulated in ESCC tissues and cell lines. Increased circ_0001093 expression predicted an unfavourable prognosis, and was associated with the lymph node metastasis, TNM staging and tumor size in ESCC tissues. Circ_0001093 knockdown suppressed cell proliferation, invasion, migration and glutamine metabolism of ESCC cells, while circ_0001093 over-expression showed the opposite effects. Mechanistically, circ_0001093 acted as a competing endogenous RNA (ceRNA) by sponging miR-579-3p, thereby increasing GLS expression. Furthermore, the inhibitory effects of circ_0001093 knockdown on the invasion, migration and glutamine metabolism were partly rescued by miR-579-3p inhibition or GLS over-expression in ESCC cells. Additionally, miR-579-3p expression was down-regulated in ESCC tissues, while GLS expression was up-regulated. In conclusion, this study first provides evidence that the circ_0001093/miR-579-3p/GLS regulatory network can affect glutamine metabolism and malignant phenotype of ESCC, which can further impact ESCC progression.</p>","PeriodicalId":15080,"journal":{"name":"Journal of Bioenergetics and Biomembranes","volume":null,"pages":null},"PeriodicalIF":3.0,"publicationDate":"2022-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40318413","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}

{"title":"HyfF subunit of hydrogenase 4 is crucial for regulating F_OF₁ dependent proton/potassium fluxes during fermentation of various concentrations of glucose.","authors":"Liana Vanyan,&nbsp;Karen Trchounian","doi":"10.1007/s10863-022-09930-x","DOIUrl":"https://doi.org/10.1007/s10863-022-09930-x","url":null,"abstract":"<p><p>Escherichia coli anaerobically ferment glucose and perform proton/potassium exchange at pH 7.5. The role of hyf (hydrogenase 4) subunits (HyfBDF) in sensing different concentrations of glucose (2 g L^-1 or 8 g L^-1) via regulating H⁺/K⁺ exchange was studied. HyfB, HyfD and HyfF part of a protein family of NADH-ubiquinone oxidoreductase ND2, ND4 and ND5 subunits is predicted to operate as proton pump. Specific growth rate was optimal in wild type and mutants grown on 2 g L^-1 glucose reaching ~ 0.8 h^-1. It was shown that in wild type cells proton but not potassium fluxes were stimulated ~ 1.7 fold reaching up to 1.95 mmol/min when cells were grown in the presence of 8 g L^-1 glucose. Interestingly, cells grown on peptone only had similar proton/potassium fluxes as grown on 2 g L^-1glucose. H⁺/K⁺ fluxes of the cells grown on 2 g L^-1 but not 8 g L^-1 glucose depend on externally added glucose concentration in the assays. DCCD-sensitive H⁺ fluxes were tripled and K⁺ fluxes doubled in wild type cells grown on 8 g L^-1 glucose compared to 2 g L^-1 when in the assays 2 g L^-1glucose was added. Interestingly, in hyfF mutant when cells were grown on 2 g L^-1glucose and in 2 g L^-1 assays DCCD-sensitive fluxes were not determined compared to wild type while in hyfD mutant it was doubled reaching up to 0.657 mmol/min. In hyf mutants DCCD-sensitive K⁺ fluxes were stimulated in hyfD and hyfF mutants compared to wild type but depend on external glucose concentration. DCCD-sensitive H⁺/K⁺ ratio was equal to ~ 2 except hyfF mutant grown and assayed on 2 g L^-1glucose while in 8 g L^-1 conditions role of hyfB and hyfD is considered. Taken together it can be concluded that Hyd-4 subunits (HyfBDF) play key role in sensing glucose concentration for regulation of DCCD-sensitive H⁺/K⁺ fluxes for maintaining proton motive force generation.</p>","PeriodicalId":15080,"journal":{"name":"Journal of Bioenergetics and Biomembranes","volume":null,"pages":null},"PeriodicalIF":3.0,"publicationDate":"2022-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39879494","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}