Journal of Bioenergetics and Biomembranes最新文献_第2页

Nigericin modifies the mechanism of the uncoupling action of bile acids in rat liver mitochondria by converting ΔpH into Δψ. 尼日利亚菌素通过将ΔpH转化为Δψ来改变胆汁酸在大鼠肝脏线粒体中解偶联作用的机制。

IF 2.9 4区生物学

Journal of Bioenergetics and Biomembranes Pub Date : 2025-02-01 Epub Date: 2024-12-19 DOI: 10.1007/s10863-024-10048-5

Evgeniya K Pavlova, Victor N Samartsev, Mikhail V Dubinin

{"title":"Nigericin modifies the mechanism of the uncoupling action of bile acids in rat liver mitochondria by converting ΔpH into Δψ.","authors":"Evgeniya K Pavlova, Victor N Samartsev, Mikhail V Dubinin","doi":"10.1007/s10863-024-10048-5","DOIUrl":"10.1007/s10863-024-10048-5","url":null,"abstract":"Cholestasis caused by impaired bile secretion in the liver is associated with the accumulation of primary bile acids (BA): cholic acid (CA) and chenodeoxycholic acid (CDCA) in the cells of this organ. The paper studies the uncoupling effect of the CA and CDCA on the succinate-fueled rat liver mitochondria under conditions of ΔpH to Δψ conversion by nigericin. It has been established that without nigericin, the dependence of the resting-state (state 4) respiration rate on the concentrations of these BA is nonlinear and is described by a parabolic equation. Under these conditions, the specific inhibitor of the ADP/ATP-antiporter - carboxyatractylate and the substrate of the aspartate/glutamate-antiporter - glutamate do not affect the state 4 respiration of mitochondria stimulated by these BA. It is suggested that without nigericin, the protonophore action of BA is due to the formation of a dimeric complex of their anion with the acid. In the presence of nigericin, the dependence of state 4 respiration rate on BA concentration is linear. Under these conditions, carboxyatractylate inhibits BA-stimulated respiration. Unlike the CDCA, the uncoupling action of CA is also suppressed by the substrates of the aspartate/glutamate-antiporter. The obtained results are considered as evidence that in the presence of nigericin, uncoupling action of CDCA is carried out primarily with the participation of ADP/ATP-antiporter. Both ADP/ATP-antiporter and aspartate/glutamate-antiporter are involved in the uncoupling action of CA. It is concluded that nigericin modifies the mechanism of the uncoupling action of BA in liver mitochondria by converting ΔpH to Δψ.","PeriodicalId":15080,"journal":{"name":"Journal of Bioenergetics and Biomembranes","volume":" ","pages":"39-48"},"PeriodicalIF":2.9,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142853433","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

Lithium compromises the bioenergetic reserve of cardiomyoblasts mitochondria.

IF 2.9 4区生物学

Journal of Bioenergetics and Biomembranes Pub Date : 2025-02-01 Epub Date: 2025-01-24 DOI: 10.1007/s10863-024-10050-x

Marian Grman, Maria Balazova, Anton Horvath, Katarina Polcicova, Katarina Ondacova, Jakub Stepanovsky, Zuzana Sevcikova Tomaskova

{"title":"Lithium compromises the bioenergetic reserve of cardiomyoblasts mitochondria.","authors":"Marian Grman, Maria Balazova, Anton Horvath, Katarina Polcicova, Katarina Ondacova, Jakub Stepanovsky, Zuzana Sevcikova Tomaskova","doi":"10.1007/s10863-024-10050-x","DOIUrl":"10.1007/s10863-024-10050-x","url":null,"abstract":"Lithium is used in the long-term treatment of bipolar disorder, exhibiting a beneficial effect on the neuronal cells. The concentration of lithium in the blood serum can vary and can easily approach a level that is related to cardiotoxic adverse effects. This is due to its narrow therapeutic index. In this study, we investigated the effect of higher than therapeutic dose of lithium. Rat cardiomyoblast cells were treated with 2 mM LiCl for 48 h, after which the mitochondrial parameters of the cells were analyzed. Lithium exposure reduced maximal respiratory capacity by diminishing reserve respiratory capacity (RRC), linked to a decrease in complex I (NADH dehydrogenase) activity and elevated superoxide radical levels. In addition, lithium treatment altered the composition of cellular membranes, including mitochondrial cardiolipin, a lipid essential for mitochondrial function. These findings suggest that impaired complex I activity, oxidative stress, and cardiolipin depletion collectively impair the ability of cells to meet high energy demands.","PeriodicalId":15080,"journal":{"name":"Journal of Bioenergetics and Biomembranes","volume":" ","pages":"27-38"},"PeriodicalIF":2.9,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11829843/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143028849","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

Modifications of the respiratory chain of Bacillus licheniformis as an alkalophilic and cyanide-degrading microorganism. 地衣芽孢杆菌作为一种嗜碱和降解氰化物微生物的呼吸链改造。

IF 2.9 4区生物学

Journal of Bioenergetics and Biomembranes Pub Date : 2024-12-01 Epub Date: 2024-11-05 DOI: 10.1007/s10863-024-10041-y

Daniel Uribe-Ramírez, Lucero Romero-Aguilar, Héctor Vázquez-Meza, Eliseo Cristiani-Urbina, Juan Pablo Pardo

{"title":"Modifications of the respiratory chain of Bacillus licheniformis as an alkalophilic and cyanide-degrading microorganism.","authors":"Daniel Uribe-Ramírez, Lucero Romero-Aguilar, Héctor Vázquez-Meza, Eliseo Cristiani-Urbina, Juan Pablo Pardo","doi":"10.1007/s10863-024-10041-y","DOIUrl":"10.1007/s10863-024-10041-y","url":null,"abstract":"Bacillus licheniformis can use cyanide as a nitrogen source for its growth. However, it can also carry out aerobic respiration in the presence of this compound, a classic inhibitor of mammalian cytochrome c oxidase, indicating that B. licheniformis has a branched respiratory chain with various terminal oxidases. Here, we studied the modifications in the respiratory chain of B. licheniformis when cells were cultured in Nutrient Broth, an alkaline medium with ammonium, or an alkaline medium with cyanide. Then, we measured oxygen consumption in intact cells and membranes, enzyme activities, carried out 1D and 2D-BN-PAGE, followed by mass spectrometry analysis of BN-PAGE bands associated with NADH, NADPH, and succinate dehydrogenase activities. We found that cell growth was favored in a nutrient medium than in an alkaline medium with cyanide. In parallel, respiratory activity progressively decreased in cells cultured in the rich medium, alkaline medium with ammonium, and the lowest activity was in the cells growing in the alkaline medium with cyanide. B. licheniformis membranes contain NADH, NADPH, and succinate dehydrogenases, and the proteomic analysis detected the nitrate reductase and the bc, caa3, aa3, and bd complexes. The succinate dehydrogenase migrated with a molecular mass of 375 kDa, indicating its association with the nitrate reductase (115 kDa + 241 kDa, respectively). The NADH dehydrogenase of B. licheniformis forms aggregates of different molecular mass.","PeriodicalId":15080,"journal":{"name":"Journal of Bioenergetics and Biomembranes","volume":" ","pages":"591-605"},"PeriodicalIF":2.9,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11624218/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142575759","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

PRKN-mediated the ubiquitination of IQGAP3 regulates cell growth, metastasis and ferroptosis in early-onset colorectal cancer. PRKN 介导的 IQGAP3 泛素化调节早期结直肠癌的细胞生长、转移和铁变态反应。

IF 2.9 4区生物学

Journal of Bioenergetics and Biomembranes Pub Date : 2024-12-01 Epub Date: 2024-09-30 DOI: 10.1007/s10863-024-10039-6

Gun Chen, Linghua Cong, Chijiang Gu, Ping Li

{"title":"PRKN-mediated the ubiquitination of IQGAP3 regulates cell growth, metastasis and ferroptosis in early-onset colorectal cancer.","authors":"Gun Chen, Linghua Cong, Chijiang Gu, Ping Li","doi":"10.1007/s10863-024-10039-6","DOIUrl":"10.1007/s10863-024-10039-6","url":null,"abstract":"High IQ motif-containing GTPase activating protein 3 (IQGAP3) expression is considered to be associated with poor prognosis of colorectal cancer (CRC). However, its role in early-onset CRC (EOCRC) progress is unclear. The mRNA and protein levels of IQGAP3 and Parkin (PRKN) were examined by qRT-PCR and western blot. Cell proliferation, apoptosis and metastasis were determined by CCK8 assay, EdU assay, flow cytometry and transwell assay. ROS, MDA, GSH, Fe2+, ACSL4 and SLC7A11 levels were detected to assess cell ferroptosis. The interaction between PRKN and IQGAP3 was assessed by Co-IP assay and ubiquitination assay. Xenograft tumor models were constructed to explore the effect of PRKN and IQGAP3 on the tumorigenesis in vivo. IQGAP3 was upregulated, while PRKN was downregulated in EOCRC tissues and cells. IQGAP3 knockdown inhibited CRC cell proliferation, migration and invasion, while enhanced apoptosis and ferroptosis. PRKN ubiquitinated IQGAP3 to promote its degradation. PRKN overexpression suppressed CRC cell growth, metastasis and promoted ferroptosis, while these effects were reversed by upregulating IQGAP3. In animal study, upregulation of PRKN reduced CRC tumorigenesis by decreasing IQGAP3 expression in vivo. IQGAP3, ubiquitinated by PRKN, promoted EOCRC progression by enhancing cell proliferation, metastasis, repressing apoptosis and ferroptosis, which provided a novel target for EOCRC treatment.","PeriodicalId":15080,"journal":{"name":"Journal of Bioenergetics and Biomembranes","volume":" ","pages":"645-655"},"PeriodicalIF":2.9,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142347206","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

N⁶-methyladenosine (m⁶A) reader HNRNPA2B1 accelerates the cervical cancer cells aerobic glycolysis. N6-甲基腺苷（m6A）阅读器 HNRNPA2B1 可加速宫颈癌细胞的有氧糖酵解。

IF 2.9 4区生物学

Journal of Bioenergetics and Biomembranes Pub Date : 2024-12-01 Epub Date: 2024-10-19 DOI: 10.1007/s10863-024-10042-x

Mengke Wen, Na Yi, Bulabiyamu Mijiti, Shihong Zhao, Guqun Shen

{"title":"N6-methyladenosine (m6A) reader HNRNPA2B1 accelerates the cervical cancer cells aerobic glycolysis.","authors":"Mengke Wen, Na Yi, Bulabiyamu Mijiti, Shihong Zhao, Guqun Shen","doi":"10.1007/s10863-024-10042-x","DOIUrl":"10.1007/s10863-024-10042-x","url":null,"abstract":"N6-methyladenosine (m6A) modification is, a more common epigenetic modification, mainly found in mRNA. More and more researches have shown the important functions of m6A on human cancers. This study seeks to explore the role of hnRNPA2B1 and m6A-dependent mechanism in cervical cancer. Elevated hnRNPA2B1 indicated the poor prognosis of cervical cancer patients. Enforced hnRNPA2B1 reduced the apoptosis, and accelerated the proliferation and migration of cervical cancer cells in vitro. Besides, hnRNPA2B1 promoted the aerobic glycolysis of cervical cancer cells, including the lactate secretion, glucose uptake, ATP production, extracellular acidification rate (ECAR) and oxygen consumption rate (OCR). LDHA was found as the downstream target of hnRNPA2B1 by m6A site. Moreover, hnRNPA2B1 enhanced the mRNA stability of LDHA through m6A-dependent manner. LDHA inhibitor (FX-11) could reverse the effect of hnRNPA2B1. Taken together, the data revealed that hnRNPA2B1 promoted the proliferation, migration and aerobic glycolysis of cervical cancer cells by m6A/LDHA-dependent manner. These findings might bring a new idea for cervical cancer treatment.","PeriodicalId":15080,"journal":{"name":"Journal of Bioenergetics and Biomembranes","volume":" ","pages":"657-668"},"PeriodicalIF":2.9,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142466166","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

Effects of MMP2 and its inhibitor TIMP2 on DNA damage, apoptosis and senescence of human lens epithelial cells induced by oxidative stress. MMP2 及其抑制剂 TIMP2 对氧化应激诱导的人晶状体上皮细胞 DNA 损伤、凋亡和衰老的影响

IF 2.9 4区生物学

Journal of Bioenergetics and Biomembranes Pub Date : 2024-12-01 Epub Date: 2024-11-14 DOI: 10.1007/s10863-024-10044-9

Xinran Deng, Yan Zhang, Xiwei He, Li Li, Zhongbin Yue, Yong Liang, Yue Huang

{"title":"Effects of MMP2 and its inhibitor TIMP2 on DNA damage, apoptosis and senescence of human lens epithelial cells induced by oxidative stress.","authors":"Xinran Deng, Yan Zhang, Xiwei He, Li Li, Zhongbin Yue, Yong Liang, Yue Huang","doi":"10.1007/s10863-024-10044-9","DOIUrl":"10.1007/s10863-024-10044-9","url":null,"abstract":"Oxidative stress-induced lens epithelial cells (LECs) death plays a pivotal role in pathogenesis of age-related cataract (ARC), causing significant visual impairment. Apoptosis of porcine granulosa cells mediated by MMP2 is linked to DNA damage. The current study aimed to investigate the potential mechanism of MMP2 in DNA damage, apoptosis and senescence of lens epithelial cells caused by oxidative stress. HLE-B3 cells were treated with different doses of H2O2 for 24 h, and CCK-8 was used to detect cell viability. Furthermore, western blotting was used to detect the expressions of MMP2, Bcl2, Bax, cleaved caspase3, γ-H2AX, p16, p21, and TIMP2. DCFH-DA staining was used to assess ROS levels. Moreover, EdU staining was used to detect cell proliferation, and flow cytometry was used to detect cell apoptosis. Then, 15A3 immunofluorescence staining and γ-H2AX staining were used to detect DNA damage. In addition, SA-β-gal staining was used to observe cell senescence. The present findings suggest that oxidative stress triggers damage to LECs viability and elevates the expression of MMP2. Furthermore, MMP2 interference attenuates H2O2-induced active damage, apoptosis, DNA damage, and cellular senescence in LECs. Additionally, TIMP2 expression is down-regulated in H2O2-induced LECs, which suppresses the expression of MMP2 induced by H2O2. These findings highlight the crucial role of MMP2 and TIMP2 in the modulation of oxidative stress-induced cellular responses in LECs. Collectively, TIMP2 alleviates H2O2-induced lens epithelial cell viability damage, apoptosis, DNA damage and cell senescence in LECs by inhibiting MMP2.","PeriodicalId":15080,"journal":{"name":"Journal of Bioenergetics and Biomembranes","volume":" ","pages":"619-630"},"PeriodicalIF":2.9,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142621070","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

TRIM46 accelerates H1N1 influenza virus-induced ferroptosis and inflammatory response by regulating SLC7A11 ubiquitination. TRIM46通过调节SLC7A11泛素化加速甲型H1N1流感病毒诱导的铁变态反应和炎症反应。

IF 2.9 4区生物学

Journal of Bioenergetics and Biomembranes Pub Date : 2024-12-01 Epub Date: 2024-11-12 DOI: 10.1007/s10863-024-10043-w

Chao Zhou, Genchong Bao, Yanfei Chen

{"title":"TRIM46 accelerates H1N1 influenza virus-induced ferroptosis and inflammatory response by regulating SLC7A11 ubiquitination.","authors":"Chao Zhou, Genchong Bao, Yanfei Chen","doi":"10.1007/s10863-024-10043-w","DOIUrl":"10.1007/s10863-024-10043-w","url":null,"abstract":"Influenza A (H1N1) virus is an acute respiratory infection responsible for enormous morbidity and mortality worldwide. The tripartite motif-containing protein 46 (TRIM46) has an antiviral function that inhibits various viral infections. This study is designed to explore the role and mechanism of TRIM46 in the progress of H1N1 infection. Herein, we infected A549 or 16HBE cells with the H1N1 virus at different times to assess TRIM46 and solute carrier family 7 member 11 (SLC7A11) expression. TRIM46 and Influenza A nucleoprotein mRNA levels were detected by real-time quantitative polymerase chain reaction (RT-qPCR). TRIM46, solute carrier family 7 member 11 (SLC7A11), and Nucleoprotein protein levels were detected using protein level were detected by western blot assay. Cell virulence was determined using Virulence assay (TCID50) assay. Cell viability was determined using Cell Counting Kit-8 (CCK-8) assay. Reactive oxygen species (ROS), intracellular iron content, Malondialdehyde (MDA), and Glutathione (GSH) levels were determined using special assay kits. The stability of SLC7A11 was assessed by Cycloheximide (CHX) assay. Interaction between TRIM46 and SLC7A11 was verified using Co-immunoprecipitation (CoIP) assay. The biological role of TRIM46 was assessed in H1N1 virus-challenged lung injury mice in vivo. TRIM46 level was significantly increased during H1N1 virus infection, and SLC7A11 expression was decreased. TRIM46 downregulation could suppress H1N1 virus replication and relieve H1N1 infection-induced ferroptosis and inflammation in A549 or 16HBE cells. Mechanistically, TRIM46 could promote SLC7A11 ubiquitination and decrease its stability. TRIM46 knockdown repressed H1N1 virus-induced lung injury in vivo. TRIM46 could contribute to influenza A H1N1 virus infection by promoting SLC7A11 ubiquitination in A549 cells, which indicates that targeting TRIM46 may improve the prognosis of patients.","PeriodicalId":15080,"journal":{"name":"Journal of Bioenergetics and Biomembranes","volume":" ","pages":"631-643"},"PeriodicalIF":2.9,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142621074","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

LncRNA UCA1 enhances NRF2 expression through the m⁶A pathway to mitigate oxidative stress and ferroptosis in aging cardiomyocytes. LncRNA UCA1通过m6A途径增强NRF2的表达，从而缓解衰老心肌细胞中的氧化应激和铁变态反应。

IF 2.9 4区生物学

Journal of Bioenergetics and Biomembranes Pub Date : 2024-12-01 Epub Date: 2024-11-14 DOI: 10.1007/s10863-024-10045-8

Kunli Jiao, Jiahao Cheng, Qi Wang, Mingxiu Hao

{"title":"LncRNA UCA1 enhances NRF2 expression through the m6A pathway to mitigate oxidative stress and ferroptosis in aging cardiomyocytes.","authors":"Kunli Jiao, Jiahao Cheng, Qi Wang, Mingxiu Hao","doi":"10.1007/s10863-024-10045-8","DOIUrl":"10.1007/s10863-024-10045-8","url":null,"abstract":"To explore the regulatory mechanism of lncRNA UCA1 and NRF2 in cardiomyocyte aging. In this study, we explored how lncRNA UCA1 regulates NRF2 and its effect on cardiomyocyte aging. H9c2 cardiomyocytes were cultured and treated with H2O2 to simulate cardiomyocyte aging in vitro. The expression levels of lncRNA UCA1 and NRF2 in cells were detected using qRT-PCR. Cell viability was assessed using the CCK8 assay, and cell aging was detected via Sa-β-gal staining. The levels of oxidative stress markers (SOD, MDA, ROS) and the expressions of ferroptosis-related proteins (ACSL4, TFR1, FTH1, GPX4) were measured. The regulatory mechanism between UCA1 and NRF2 was investigated using RIP-qPCR. Additionally, changes in m6A modification levels and the expression of m6A modification-related proteins in cells after UCA1 overexpression were analyzed by western blot. Our results indicate that H2O2 treatment significantly downregulated the expression of lncRNA UCA1 and NRF2. UCA1 overexpression promoted H9c2 cell proliferation, inhibited cell aging, increased SOD activity and the expression of FTH1 and GPX4 proteins, and decreased MDA and ROS content as well as ACSL4 and TFR1 protein expression. RIP-qPCR verified that UCA1 can promote the expression of NRF2 in cells. Overexpression of UCA1 significantly increased the expression of the demethylase FTO, leading to a reduction in m6A modification levels. Furthermore, there was significant enrichment between FTO and NRF2, and overexpression of FTO improved the expression of NRF2 protein in cells. Taken together, lncRNA UCA1 inhibits oxidative stress and ferroptosis, thereby preventing cardiomyocyte aging. This protective effect is likely mediated by increasing the expression of demethylase FTO and reducing m6A modification, which promotes the expression of NRF2.","PeriodicalId":15080,"journal":{"name":"Journal of Bioenergetics and Biomembranes","volume":" ","pages":"607-617"},"PeriodicalIF":2.9,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142621072","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

The effect of intra spinal administration of cerium oxide nanoparticles on central pain mechanism: An experimental study. 脊髓内注射氧化铈纳米颗粒对中枢疼痛机制的影响：一项实验研究。

IF 2.9 4区生物学

Journal of Bioenergetics and Biomembranes Pub Date : 2024-10-01 Epub Date: 2024-08-05 DOI: 10.1007/s10863-024-10033-y

Ahmad Mostaar, Zahra Behroozi, Ali MotamedNezhad, Sourosh Taherkhani, Negin Mojarad, Fatemeh Ramezani, Atousa Janzadeh, Pooya Hajimirzaie

{"title":"The effect of intra spinal administration of cerium oxide nanoparticles on central pain mechanism: An experimental study.","authors":"Ahmad Mostaar, Zahra Behroozi, Ali MotamedNezhad, Sourosh Taherkhani, Negin Mojarad, Fatemeh Ramezani, Atousa Janzadeh, Pooya Hajimirzaie","doi":"10.1007/s10863-024-10033-y","DOIUrl":"10.1007/s10863-024-10033-y","url":null,"abstract":"This study investigated Cerium oxide nanoparticles (CeONPs) effect on central neuropathic pain (CNP). The compressive method of spinal cord injury (SCI) model was used for pain induction. Three groups were formed by a random allocation of 24 rats. In the treatment group, CeONPs were injected above and below the lesion site immediately after inducing SCI. pain symptoms were evaluated using acetone, Radian Heat, and Von Frey tests weekly for six weeks. Finally, we counted fibroblasts using H&E staining. We evaluated the expression of Cx43, GAD65 and HDAC2 proteins using the western blot method. The analysis of results was done by PRISM software. At the end of the study, we found that CeONPs reduced pain symptoms to levels similar to those observed in normal animals. CeONPs also increased the expression of GAD65 and Cx43 proteins but did not affect HDAC2 inhibition. CeONPs probably have a pain-relieving effect on chronic pain by potentially preserving GAD65 and Cx43 protein expression and hindering fibroblast infiltration.","PeriodicalId":15080,"journal":{"name":"Journal of Bioenergetics and Biomembranes","volume":" ","pages":"505-515"},"PeriodicalIF":2.9,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141889340","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

WTAP promotes fibroblast-like synoviocyte pyroptosis in Rheumatoid arthritis by upregulating N6-methyladenosine modification of NLRP3. WTAP 通过上调 NLRP3 的 N6-甲基腺苷修饰，促进类风湿性关节炎中成纤维细胞样滑膜细胞的脓毒症。

IF 2.9 4区生物学

Journal of Bioenergetics and Biomembranes Pub Date : 2024-10-01 Epub Date: 2024-08-27 DOI: 10.1007/s10863-024-10035-w

Xiuchan Liu, Zhenjuan Xia, Lei Liu, Dongyun Ren

{"title":"WTAP promotes fibroblast-like synoviocyte pyroptosis in Rheumatoid arthritis by upregulating N6-methyladenosine modification of NLRP3.","authors":"Xiuchan Liu, Zhenjuan Xia, Lei Liu, Dongyun Ren","doi":"10.1007/s10863-024-10035-w","DOIUrl":"10.1007/s10863-024-10035-w","url":null,"abstract":"Rheumatoid arthritis (RA) is a chronic condition characterized by inflammation and an abnormal immune response. N6-methyladenosine (m6A) methylation has altered nucleotide-binding oligomerization domain, leucine-rich repeat, and pyrin domain-containing (NLRP) 3. This change is implicated in the regulation of cell pyroptosis and inflammation. WTAP has a crucial role in regulating NLRP3 m6A. In this work, we used a rat model of collagen-induced arthritis (CIA) to investigate the involvement of WTAP in the evolution of inflammation in RA. The purpose of silencing or overexpressing WTAP in RA-fibroblast-like synoviocytes (RA-FLSs) treated with TNF-α was to identify its impact on pyroptosis, NLRP3 inflammasome-related proteins, the secretion of pro-inflammatory cytokines and migration. Bioinformatics techniques were used to pinpoint the exact target controlled by WTAP. To assess WTAP and NLRP3's role in RA-FLSs, we used methylated RNA immunoprecipitation, LDH test, flow cytometry, RT-qPCR, Western blotting, and Transwell. Our results show that WTAP expression is upregulated in both RA rats and cell models. Cell pyroptosis, NLRP3-related pro-inflammatory cytokines, and migration were reduced in TNF-α-treated RA-FLSs when WTAP was knocked down, whereas overexpression of WTAP displayed the opposite effect in RA-FLSs. WTAP mediated m6A modification in the NLRP3 mRNA and enhanced its mRNA stability. These results suggested that WTAP promoted FLSs pyroptosis and related inflammatory response via NLRP3 and identified WTAP as a potential target for treating RA.","PeriodicalId":15080,"journal":{"name":"Journal of Bioenergetics and Biomembranes","volume":" ","pages":"563-571"},"PeriodicalIF":2.9,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142072893","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