Journal of Bioenergetics and Biomembranes最新文献_第6页

In vitro evaluation of 2-(1H-pyrazol-1-yl)-1,3,4-thiadiazole derivatives against replicative and infective stages of Trypanosoma cruzi. 2-（1H-吡唑-1-基）-1,3,4-噻二唑衍生物对克氏锥虫复制期和感染期的体外评价。

IF 3 4区生物学

Journal of Bioenergetics and Biomembranes Pub Date : 2023-12-01 Epub Date: 2023-11-03 DOI: 10.1007/s10863-023-09982-7

Ana Flávia Martins Faria, Caroline de Souza Ferreira Pereira, Guilherme Pegas Teixeira, Raíssa Maria Dos Santos Galvão, Paulo Anastácio F Pacheco, Murilo Lamim Bello, Daiane Hardoim de Jesus, Kátia Calabrese, Daniel Tadeu Gomes Gonzaga, Nubia Boechat, Robson Xavier Faria

{"title":"In vitro evaluation of 2-(1H-pyrazol-1-yl)-1,3,4-thiadiazole derivatives against replicative and infective stages of Trypanosoma cruzi.","authors":"Ana Flávia Martins Faria, Caroline de Souza Ferreira Pereira, Guilherme Pegas Teixeira, Raíssa Maria Dos Santos Galvão, Paulo Anastácio F Pacheco, Murilo Lamim Bello, Daiane Hardoim de Jesus, Kátia Calabrese, Daniel Tadeu Gomes Gonzaga, Nubia Boechat, Robson Xavier Faria","doi":"10.1007/s10863-023-09982-7","DOIUrl":"10.1007/s10863-023-09982-7","url":null,"abstract":"Current treatment of Chagas disease (CD) is based on two substances, nifurtimox (NT) and benzonidazole (BZ), both considered unsatisfactory mainly due to their low activities and high toxicity profile. One of the main challenges faced in CD management concerns the identification of new drugs active in the acute and chronic phases and with good pharmacokinetic profiles. In this work, we studied the bioactivity of twenty 2-(1H-pyrazol-1-yl)-1,3,4-thiadiazole derivatives against Trypanosoma cruzi epimastigotes and trypomastigotes. We identified seven derivatives with promising activity against epimastigote forms with IC50 values ranging from 6 µM to 44 µM. Most of the compounds showed no significant toxicity against murine macrophages. Our initial investigation on the mechanism of action indicates that this series of compounds may exert their anti-parasitic effect, inducing cell membrane damage. The results in trypomastigotes showed that one derivative, PDAN 78, satisfactorily inhibited metabolic alteration at all concentrations. Moreover, we used molecular modeling to understand how tridimensional and structural aspects might influence the observed bioactivities. Finally, we also used in silico approaches to assess the potential pharmacokinetic and toxicological properties of the most active compounds. Our initial results indicate that this molecular scaffold might be a valuable prototype for novel and safe trypanocidal compounds.","PeriodicalId":15080,"journal":{"name":"Journal of Bioenergetics and Biomembranes","volume":null,"pages":null},"PeriodicalIF":3.0,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"71423757","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

DMPP attenuates lipopolysaccharide-induced lung injury by inhibiting glycocalyx degradation through activation of the cholinergic anti-inflammatory pathway. DMPP通过激活胆碱能抗炎途径抑制糖盏降解，从而减轻脂多糖诱导的肺损伤。

IF 3 4区生物学

Journal of Bioenergetics and Biomembranes Pub Date : 2023-12-01 Epub Date: 2023-10-18 DOI: 10.1007/s10863-023-09989-0

Feng Qi, Chengwei Duan, Tianpeng Chen, Feng Li, Jinsong Zhang

{"title":"DMPP attenuates lipopolysaccharide-induced lung injury by inhibiting glycocalyx degradation through activation of the cholinergic anti-inflammatory pathway.","authors":"Feng Qi, Chengwei Duan, Tianpeng Chen, Feng Li, Jinsong Zhang","doi":"10.1007/s10863-023-09989-0","DOIUrl":"10.1007/s10863-023-09989-0","url":null,"abstract":"The study aimed to investigate the therapeutic potential of 1,1-dimethyl-4-phenylpiperazinium iodide (DMPP), an agonist of nicotinic acetylcholine receptor (nAChR), in treating acute lung injury (ALI) induced by lipopolysaccharide (LPS). A murine ALI model was developed utilizing intraperitoneal injection of LPS. We evaluated the therapeutic efficacy of DMPP treatment in LPS-induced lung injury using various approaches, including pathohistological evaluation, appraisal of pulmonary edema, and measurement of inflammatory cytokine levels and their associated pathways within lung tissues. The gene chip data of LPS-induced acute lung injury mice were retrieved from the Gene Expression Omnibus (GEO) database for gene differential expression analysis and Gene Set Enrichment Analysis (GSEA) analysis. The impact of DMPP on glycocalyx shedding was assessed by measuring the expression levels of syndecan-1 (SDC-1) and matrix metalloproteinase-9 (MMP-9). DMPP treatment significantly improved pathomorphological changes and pathological lung injury scores in the LPS-induced ALI mouse model. The genes expressed differentially in the LPS-induced ALI group in GSE2411 were found to be involved in multiple processes, including the NF-κB signaling pathway, NOD-like receptor signaling pathway, Toll-like receptor signaling pathway, as well as the JAK-STAT signaling pathway. DMPP treatment effectively downregulated pro-inflammatory cytokines, suppressed the NF-κB signaling pathway, and effectively restrained the LPS-induced upregulation of MMP-9 and shedding of syndecan-1, thereby contributing to the preservation of endothelial glycocalyx and attenuation of endothelial barrier dysfunction. The administration of DMPP has been shown to confer protection against LPS-induced acute lung injury via a cholinergic anti-inflammatory pathway, which effectively inhibits endothelial glycocalyx degradation.","PeriodicalId":15080,"journal":{"name":"Journal of Bioenergetics and Biomembranes","volume":null,"pages":null},"PeriodicalIF":3.0,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41235553","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

NFE2L1 restrains ferroptosis by transcriptionally regulating HJURP and participates in the progress of oral squamous cell carcinoma. NFE2L1通过转录调节HJURP抑制脱铁性贫血，并参与口腔鳞状细胞癌的进展。

IF 3 4区生物学

Journal of Bioenergetics and Biomembranes Pub Date : 2023-12-01 Epub Date: 2023-10-18 DOI: 10.1007/s10863-023-09987-2

Meixia Zhang, Zhonghou Wang, Guang Yang, Linfu Han, Xiaofeng Wang

{"title":"NFE2L1 restrains ferroptosis by transcriptionally regulating HJURP and participates in the progress of oral squamous cell carcinoma.","authors":"Meixia Zhang, Zhonghou Wang, Guang Yang, Linfu Han, Xiaofeng Wang","doi":"10.1007/s10863-023-09987-2","DOIUrl":"10.1007/s10863-023-09987-2","url":null,"abstract":"Oral squamous cell carcinoma (OSCC) is a common head and neck malignancy with increasing mortality and high recurrence. In this work, we aim to explore the functional role of NFE2 like bZIP transcription factor 1 (NFE2L1) in OSCC progression. Based on databases analysis, we found that NFE2L1 was overexpressed in OSCC tumor tissues, and elevated NFE2L1 level induced poor prognosis of OSCC patients. Our results showed that NFE2L1 is upregulated in OSCC cells and overexpression of NFE2L1 promotes cell proliferation, and reduces the sensitivity of OSCC cells to erastin-induced ferroptosis. NFE2L1 upregulation decreased the levels of Fe2+, lipid reactive oxygen species and content of malondialdehyde, and increased the level of the key negative regulator of ferroptosis, GPX4 and SLC7A11. In NFE2L1 suppressed cells, these trends were reversed. Further results of dual luciferase reporter and chromatin immunoprecipitation assays confirmed that NFE2L1 could bind to the promoter of Holliday junction recognition protein (HJURP) to increase the transcriptional activity of HJURP, thus upregulating its expression. Inhibition of HJURP attenuated the proliferation and ferroptosis inhibition in NFE2L1 upregulated cells. In vivo tumorigenicity assay further proved that NFE2L1 promotes OSCC tumor growth. In summary, NFE2L1 restrains ferroptosis by transcriptionally regulating HJURP and participates in the progress of OSCC. Thus, NFE2L1 plays a key role in OSCC development and may be a promising therapeutic target for OSCC.","PeriodicalId":15080,"journal":{"name":"Journal of Bioenergetics and Biomembranes","volume":null,"pages":null},"PeriodicalIF":3.0,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41235554","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

Transcriptomics profiling reveal the heterogeneity of white and brown adipocyte. 转录组学分析揭示了白色和棕色脂肪细胞的异质性。

IF 3 4区生物学

Journal of Bioenergetics and Biomembranes Pub Date : 2023-12-01 Epub Date: 2023-10-31 DOI: 10.1007/s10863-023-09990-7

Zhongxiao Zhang, Liling Xu, Ling Zhang, Jingxian Lu, Zhou Peng, Xirong Guo, Jianfang Gao

{"title":"Transcriptomics profiling reveal the heterogeneity of white and brown adipocyte.","authors":"Zhongxiao Zhang, Liling Xu, Ling Zhang, Jingxian Lu, Zhou Peng, Xirong Guo, Jianfang Gao","doi":"10.1007/s10863-023-09990-7","DOIUrl":"10.1007/s10863-023-09990-7","url":null,"abstract":"The marker genes associated with white adipocytes and brown adipocytes have been previously identified; however, these markers have not been updated in several years, and the differentiation process of preadipocytes remains relatively fixed. Consequently, there has been a lack of exploration into alternative differentiation schemes. In this particular study, we present a transcriptional signature specific to brown adipocytes and white adipocytes. Notably, our findings reveal that ZNF497, ZIC1, ZFY, UTY, USP9Y, TXLNGY, TTTY14, TNNT3, TNNT2, TNNT1, TNNI1, TNNC1, TDRD15, SOX11, SLN, SFRP2, PRKY, PAX3KLHL40, PAX3, INKA2-AS1, SOX11, and TDRD15 exhibit high expression levels in brown adipocytes. XIST, HOXA10, PCAT19, HOXA7, PLSCR3, and AVPR1A exhibited high expression levels in white adipocytes, suggesting their potential as novel marker genes for the transition from white to brown adipocytes. Furthermore, our analysis revealed the coordinated activation of several pathways, including the PPAR signaling pathway, focal adhesion, retrograde endocannabinoid signaling, oxidative phosphorylation, PI3K-Akt signaling pathway, and thermogenesis pathways, in brown adipocytes. Moreover, in contrast to prevailing culture techniques, we conducted a comparative analysis of the differentiation protocols for white preadipocytes and brown preadipocytes, revealing that the differentiation outcome remained unaffected by the diverse culture schemes employed. However, the expression levels of certain marker genes in both adipocyte types were found to be altered. This investigation not only identified potential novel marker genes for adipocytes but also examined the impact of different differentiation methods on preadipocyte maturation. Consequently, these findings offer significant insights for further research on the differentiation processes of diverse adipocyte subtypes.","PeriodicalId":15080,"journal":{"name":"Journal of Bioenergetics and Biomembranes","volume":null,"pages":null},"PeriodicalIF":3.0,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"71423758","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

USP10 suppresses ABCG2-induced malignant characteristics of doxorubicin-resistant thyroid cancer by inhibiting PI3K/AKT pathway. USP10通过抑制PI3K/AKT途径抑制ABCG2诱导的阿霉素耐药甲状腺癌症的恶性特征。

IF 3 4区生物学

Journal of Bioenergetics and Biomembranes Pub Date : 2023-12-01 Epub Date: 2023-11-03 DOI: 10.1007/s10863-023-09986-3

Jianwei Sun, Qian Xiang, Ding Ding, Nan Yan

{"title":"USP10 suppresses ABCG2-induced malignant characteristics of doxorubicin-resistant thyroid cancer by inhibiting PI3K/AKT pathway.","authors":"Jianwei Sun, Qian Xiang, Ding Ding, Nan Yan","doi":"10.1007/s10863-023-09986-3","DOIUrl":"10.1007/s10863-023-09986-3","url":null,"abstract":"Doxorubicin (DOX) is the most extensively used drug in the chemotherapy of thyroid cancer (TC). However, the existence of DOX resistance is not conducive to TC treatment. Here, we investigated the role of USP10 in DOX-resistant TC and explored the underlying molecular mechanism. CCK-8 assay was used to measure cell viability in thyroid cancer FTC133 and DOX-resistant FTC133-DOX cells. RT-qPCR and western blot were used to evaluate USP10 expression. Cell migration, invasion, and apoptotic assays were conducted. Western blot was used to detect cellular signaling proteins, EMT-related proteins, and apoptosis-related proteins. We found a lower expression of USP10 in the human TC cell line FTC133 as compared to the normal human thyroid Htori-3 cells. Notably, USP10 expression was further reduced in DOX-resistant (FTC133-DOX) cells compared to the FTC133 cells. FTC133-DOX cells had increased invasion, migration, and EMT properties while less apoptosis by activating the PI3K/AKT pathway. Interestingly, overexpressing USP10 increased the chemosensitivity of FTC133 cells to DOX therapy. Overexpressing USP10 inhibited invasion, migration, and EMT properties of FTC133-DOX cells and promoted apoptosis. Mechanistically, overexpressing USP10 inhibited PI3K/AKT pathway by activating PTEN. Furthermore, overexpressed USP10 controlled all these processes by downregulating ABCG2. This study demonstrates that USP10 could reduce DOX-induced resistance of TC cells to DOX therapy and could suppress TC malignant behavior by inhibiting the PI3K/AKT pathway. Furthermore, USP10 targeted ABCG2 to inhibit all these malignant processes, therefore, either increasing USP10 expression or inhibiting ABCG2 could be used as novel targets for treating DOX-resistant thyroid cancer.","PeriodicalId":15080,"journal":{"name":"Journal of Bioenergetics and Biomembranes","volume":null,"pages":null},"PeriodicalIF":3.0,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10682060/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"71423759","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Computational prediction of analog compounds of the membrane protein MCHR1 antagonists ALB-127158 and KRX-104130. 膜蛋白MCHR1拮抗剂ALB-127158和KRX-104130的类似化合物的计算预测。

IF 3 4区生物学

Journal of Bioenergetics and Biomembranes Pub Date : 2023-12-01 Epub Date: 2023-11-09 DOI: 10.1007/s10863-023-09993-4

Emrah Sariyer, Ayşegül Saral Sariyer

{"title":"Computational prediction of analog compounds of the membrane protein MCHR1 antagonists ALB-127158 and KRX-104130.","authors":"Emrah Sariyer, Ayşegül Saral Sariyer","doi":"10.1007/s10863-023-09993-4","DOIUrl":"10.1007/s10863-023-09993-4","url":null,"abstract":"Obesity, which is already pervasive throughout the world, endangers public health by raising the prevalence of metabolic disorders and making their treatment more difficult. The development of drugs to treat obesity is a focus of effort. Melanin concentrated hormone receptor 1 (MCHR1) is the target of some of these therapeutic possibilities since as increased levels of melanin concentrated hormone have been found in obesity models. Known MCHR1 antagonists include BMS-830216, GW-856464, NGD-4715, ALB-127158, and AMG 076, but many have failed phase-I clinical studies. As a potential treatment for cardiotoxicity, KRX-104130 has only recently been identified. As MCH system is potentially effective target for treatment of obesity, in silico research into interaction between MCHR1 and its antagonists at molecular level was the primary goal of this study. Analogues ALB-127158 and KRX-104130 were screened among the RealEnamine library. The complexes obtained by molecular docking were embedded in mimics brain-cell membrane and simulated for 540 ns, and then MM-GBSA were calculated with MMPBSA.py. With all these computational studies, similar or different aspects of selected analogous compounds to ALB-127158 and KRX-104130 were investigated. The specificity of this study was that it analyzed MCHR1 protein as embedded in membrane. It was concluded that KRX-104130's analogue Z1922310273 and ALB-127158's analogue PV-002757495233 did not cause a difference in terms of phospholipid membrane properties. In addition, all ligands remained stable in putative binding site. It has been suggested that PV-002757495233 and Z1922310273 compounds can be evaluated as MCHR1 antagonists when all these outputs are considered in melting pots.","PeriodicalId":15080,"journal":{"name":"Journal of Bioenergetics and Biomembranes","volume":null,"pages":null},"PeriodicalIF":3.0,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"71521559","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

Mir-25-3p in extracellular vesicles from fibroblast-like synoviocytes alleviates pyroptosis of chondrocytes in knee osteoarthritis. 成纤维细胞样滑膜细胞的细胞外小泡中的Mir-25-3p减轻膝骨关节炎软骨细胞的焦下垂。

IF 3 4区生物学

Journal of Bioenergetics and Biomembranes Pub Date : 2023-10-01 Epub Date: 2023-09-19 DOI: 10.1007/s10863-023-09964-9

Jianhang Wang, Tao Sun

{"title":"Mir-25-3p in extracellular vesicles from fibroblast-like synoviocytes alleviates pyroptosis of chondrocytes in knee osteoarthritis.","authors":"Jianhang Wang, Tao Sun","doi":"10.1007/s10863-023-09964-9","DOIUrl":"https://doi.org/10.1007/s10863-023-09964-9","url":null,"abstract":"Knee osteoarthritis (KOA) is defined as a joint disease that occurs mostly among elderly people. Fibroblast-like synoviocytes-derived extracellular vesicles (FLS-EVs) have impacts on the treatment of OA. This study elucidated the mechanism of miR-25-3p in pyroptosis of chondrocytes in KOA. FLSs and EVs were extracted from neonatal mice; destabilization of the medial meniscus (DMM) was used to simulate KOA in mice, followed by the evaluation of cartilage damage and the contents of MMP-3 and MMP-13 in KOA mice. Lipopolysaccharide (LPS) was used to induce inflammation damage in mouse chondrocytes ATDC5, and the cell viability and the expressions of NLRP3, Cleaved-Caspase-1, GSDMD-N, IL-18, and IL-1β were examined. We found that FLS-EV treatment mitigated the knee-joint damage and symptoms of KOA mice, decreased MMP-3 and MMP-13, and inhibited pyroptosis of chondrocytes in DMM mice and LPS-induced ATD5 cells. Then, Cy3-labeled miR-25-3p in mice chondrocytes was observed and the expressions and the binding relation of miR-25-3p and cytoplasmic polyadenylation element-binding protein 1 (CPEB1) were verified. It showed that FLS-EVs carried miR-25-3p into chondrocytes, and upregulated miR-25-3p expression while inhibited CPEB1 transcription, resulting in mitigation of pyroptosis of chondrocytes, and CPEB1 overexpression reversed the inhibition of FLS-EVs on pyroptosis of chondrocytes in KOA.","PeriodicalId":15080,"journal":{"name":"Journal of Bioenergetics and Biomembranes","volume":null,"pages":null},"PeriodicalIF":3.0,"publicationDate":"2023-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41112236","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: 1

Blockage of PHLPP1 protects against myocardial ischemia/reperfusion injury in diabetic mice via activation of STAT3 signaling. PHLPP1的阻断通过STAT3信号的激活保护糖尿病小鼠免受心肌缺血/再灌注损伤。

IF 3 4区生物学

Journal of Bioenergetics and Biomembranes Pub Date : 2023-10-01 Epub Date: 2023-08-16 DOI: 10.1007/s10863-023-09977-4

Sumin Gao, Yun Qiu, Yuming Meng, Yajuan Jia, Xuemei Lang, Hongmei Zhao, Hong Sun, Jinsong Zhang, Lianshu Ding

{"title":"Blockage of PHLPP1 protects against myocardial ischemia/reperfusion injury in diabetic mice via activation of STAT3 signaling.","authors":"Sumin Gao, Yun Qiu, Yuming Meng, Yajuan Jia, Xuemei Lang, Hongmei Zhao, Hong Sun, Jinsong Zhang, Lianshu Ding","doi":"10.1007/s10863-023-09977-4","DOIUrl":"10.1007/s10863-023-09977-4","url":null,"abstract":"Diabetes can exacerbate myocardial ischemia/reperfusion (IR) injury. However, the sensitivity to IR injury and the underlying mechanisms in diabetic hearts remain unclear. Inhibition of PH domain leucine-rich repeating protein phosphatase (PHLPP1) could reduce myocardial IR injury, our previous study demonstrated that the expression of PHLPP1 was upregulated in diabetic myocardial IR model. Thus, this study aimed to investigate the mechanism of PHLPP1 in diabetic myocardial IR injury. Nondiabetic and diabetic C57BL/6 mice underwent 45 min of coronary artery occlusion followed by 2 h of reperfusion. Male C57BL/6 mice were injected with streptozotocin for five consecutive days to establish a diabetes model. H9c2 cells were exposed to normal or high glucose and subjected to 4 h of hypoxia followed by 4 h of reoxygenation. Diabetes or hyperglycemia increased postischemic infarct size, cellular injury, release of creatine kinase-MB, apoptosis, and oxidative stress, while exacerbating mitochondrial dysfunction. This was accompanied by enhanced expression of PHLPP1 and decreased levels of p-STAT3 and p-Akt. These effects were counteracted by PHLPP1 knockdown. Moreover, PHLPP1 knockdown resulted in an increase in mitochondrial translocation of p-STAT3 Ser727 and nuclear translocation of p-STAT3 Tyr705 and p-STAT3 Ser727. However, the effect of PHLPP1 knockdown in reducing posthypoxic cellular damage was nullified by either Stattic or LY294002. Additionally, a co-immunoprecipitation assay indicated a direct interaction between PHLPP1 and p-STAT3 Ser727, but not p-STAT3 Tyr705. The abnormal expression of PHLPP1 plays a significant role in exacerbating myocardial IR injury in diabetic mice. Knockdown of PHLPP1 to activate the STAT3 signaling pathway may represent a novel strategy for alleviating myocardial IR injury in diabetes.","PeriodicalId":15080,"journal":{"name":"Journal of Bioenergetics and Biomembranes","volume":null,"pages":null},"PeriodicalIF":3.0,"publicationDate":"2023-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10007012","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

Hsa_circ_0052611 and mir-767-5p guide the warburg effect, migration, and invasion of BRCA cells through modulating SCAI. Hsa_cir_0052611和mir-767-5p通过调节SCAI指导BRCA细胞的warburg效应、迁移和侵袭。

IF 3 4区生物学

Journal of Bioenergetics and Biomembranes Pub Date : 2023-10-01 Epub Date: 2023-09-25 DOI: 10.1007/s10863-023-09985-4

Xin Wang, Zongwen Liu, Alan Chu, Rui Song, Shijia Liu, Ting Chai, Chen Sun

{"title":"Hsa_circ_0052611 and mir-767-5p guide the warburg effect, migration, and invasion of BRCA cells through modulating SCAI.","authors":"Xin Wang, Zongwen Liu, Alan Chu, Rui Song, Shijia Liu, Ting Chai, Chen Sun","doi":"10.1007/s10863-023-09985-4","DOIUrl":"10.1007/s10863-023-09985-4","url":null,"abstract":"Noncoding RNAs are key regulators in the Warburg Effect, an emerging hallmark of cancer. We intended to investigate the role and mechanism of circular RNA hsa_circ_0052611 (circ_0052611) and microRNA (miR)-767-5p in breast cancer (BRCA) hallmarks, especially the Warburg Effect. Expression of circ_0052611 and SCAI was downregulated, and miR-767-5p was upregulated in human BRCA tissues and cells; moreover, circ_0052611 acted as a miR-767-5p sponge to modulate the expression of miR-767-5p-targeted SCAI. Functionally, re-expressing circ_0052611 suppressed migration, invasion, glucose uptake, lactate production, and extracellular acidification rate (ECAR) in BRCA cells, and promoted apoptotic rate. These effects were accompanied by decreased Vimentin, N-cadherin, Bcl-2, and LDHA, and increased E-cadherin and Bax. Consistently, exhausting miR-767-5p exerted similar effects in BRCA cells. High miR-767-5p could counteract the role of circ_0052611 overexpression, and low SCAI likewise blocked the role of miR-767-5p deletion. In vivo, upregulating circ_0052611 delayed tumor growth of BRCA cells by altering miR-767-5p and SCAI expression. circ_0052611/miR-767-5p/SCAI axis might boycott the malignancy of BRCA cells.","PeriodicalId":15080,"journal":{"name":"Journal of Bioenergetics and Biomembranes","volume":null,"pages":null},"PeriodicalIF":3.0,"publicationDate":"2023-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41129768","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

Propionic and valproic acids have an impact on bacteria viability, proton flux and ATPase activity. 丙酸和丙戊酸对细菌活力、质子通量和ATP酶活性有影响。

IF 3 4区生物学

Journal of Bioenergetics and Biomembranes Pub Date : 2023-10-01 Epub Date: 2023-09-13 DOI: 10.1007/s10863-023-09983-6

Heghine Gevorgyan, Tamara Abaghyan, Margarita Mirumyan, Konstantin Yenkoyan, Karen Trchounian

{"title":"Propionic and valproic acids have an impact on bacteria viability, proton flux and ATPase activity.","authors":"Heghine Gevorgyan, Tamara Abaghyan, Margarita Mirumyan, Konstantin Yenkoyan, Karen Trchounian","doi":"10.1007/s10863-023-09983-6","DOIUrl":"10.1007/s10863-023-09983-6","url":null,"abstract":"Short-chain fatty acids like propionic (PPA) and valproic acids (VP) can alter gut microbiota, which is suggested to play a role in development of autism spectrum disorders (ASD). In this study we investigated the role of various concentrations of PPA and VP in gut enteric gram-negative Escherichia coli K12 and gram-positive Enterococcus hirae ATCC 9790 bacteria growth properties, ATPase activity and proton flux. The specific growth rate (µ) was 0.24 h-1 and 0.82 h-1 in E. coli and E. hirae, respectively. Different concentrations of PPA reduced the value of µ similarly in both strains. PPA affects membrane permeability only in E. hirae. PPA decreased DCCD-sensitive ATPase activity in the presence of K+ ions by 20% in E. coli and 40% in E. hirae suggesting the importance of the FOF1-K+ transport system in the regulation of PPA-disrupted homeostasis. Moreover, the H+ flux during PPA consumption could be the protective mechanism for enteric bacteria. VP has a selective effect on the µ depending on bacteria. The overwhelming effect of VP was detected on the K+-promoted ATPase activity in E. hirae. Taken together it can be suggested that PPA and VP have a disruptive effect on E. coli and E. hirae growth, viability, bioenergetic and biochemical properties, which are connected with the alteration of FOF1-ATPase activity and H+ flux rate or direction.","PeriodicalId":15080,"journal":{"name":"Journal of Bioenergetics and Biomembranes","volume":null,"pages":null},"PeriodicalIF":3.0,"publicationDate":"2023-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10214761","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}

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