Journal of physiology and biochemistry最新文献

The importance of growth differentiation factor 15 and interleukin 6 serum levels in inflammatory bowel diseases. 生长分化因子 15 和白细胞介素 6 血清水平在炎症性肠病中的重要性。

IF 3.7 3区生物学

Journal of physiology and biochemistry Pub Date : 2024-11-19 DOI: 10.1007/s13105-024-01057-4

Evgenia Koureta, Pantelis Karatzas, Panagiotis N Kanellopoulos, Angeliki Papapanagiotou, Vasileios Lekakis, Giorgos Bamias, George Karamanolis, Jiannis Vlachogiannakos, Athanasios G Papavassiliou, George V Papatheodoridis

{"title":"The importance of growth differentiation factor 15 and interleukin 6 serum levels in inflammatory bowel diseases.","authors":"Evgenia Koureta, Pantelis Karatzas, Panagiotis N Kanellopoulos, Angeliki Papapanagiotou, Vasileios Lekakis, Giorgos Bamias, George Karamanolis, Jiannis Vlachogiannakos, Athanasios G Papavassiliou, George V Papatheodoridis","doi":"10.1007/s13105-024-01057-4","DOIUrl":"10.1007/s13105-024-01057-4","url":null,"abstract":"There are only scarce recent reports about the role of growth differentiation factor 15 (GDF-15) and some more data about interleukin-6 (IL-6) in inflammatory bowel diseases (IBD). We assessed GDF-15 and IL-6 serum levels in patients with IBD and associations with their characteristics. We included 122 and 71 stored samples from patients with Crohn's disease (CD) and ulcerative colitis (UC), respectively, and regular follow-up and 44 samples from healthy controls. Data regarding epidemiologic and disease characteristics were recorded. In CD, both GDF-15 and IL-6 levels were higher in active disease or all patients than controls (P ≤ 0.020) as well as patients with elevated CRP (P ≤ 0.008), endoscopically active disease (P ≤ 0.017), age ≥ 40 years (P ≤ 0.005) and active smokers (P ≤ 0.050) and were positively correlated with hospitalization numbers (P ≤ 0.019). GDF-15 levels were also positively correlated with flares within year-1 (P < 0.001). In UC, both GDF-15 and IL-6 levels were higher in clinically active or all patients than controls (P < 0.001), but they shared no other association with patient characteristics except for positive correlation with CRP. Only IL-6 levels were higher in active than inactive UC either clinically (P = 0.047) or endoscopically (P < 0.001) and were positively correlated with stool calprotectin (P = 0.021). GDF-15 was positively correlated to IL-6 levels only in UC (rs=0.591, P < 0.001) but not in CD. In conclusion, in CD, GDF-15 and IL-6 levels could constitute indexes of activity and even offer a prognostic index of disease progression. In UC, IL-6 could also represent an activity index, but the role of GDF-15 needs further evaluation.","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":" ","pages":""},"PeriodicalIF":3.7,"publicationDate":"2024-11-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142667833","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}

引用次数: 0

Prognostic model development using novel genetic signature associated with adenosine metabolism and immune status for patients with hepatocellular carcinoma. 利用与腺苷代谢和免疫状态相关的新型基因特征，为肝细胞癌患者建立预后模型。

IF 3.7 3区生物学

Journal of physiology and biochemistry Pub Date : 2024-11-15 DOI: 10.1007/s13105-024-01061-8

Yidan Chen, Kemei Wang, Xingyun Zhang, Dongying Tao, Yulong Shang, Ping Wang, Qiang Li, Yansheng Liu

{"title":"Prognostic model development using novel genetic signature associated with adenosine metabolism and immune status for patients with hepatocellular carcinoma.","authors":"Yidan Chen, Kemei Wang, Xingyun Zhang, Dongying Tao, Yulong Shang, Ping Wang, Qiang Li, Yansheng Liu","doi":"10.1007/s13105-024-01061-8","DOIUrl":"https://doi.org/10.1007/s13105-024-01061-8","url":null,"abstract":"The high mortality rate of hepatocellular carcinoma (HCC) is partly due to advanced diagnosis, emphasizing the need for effective predictive tools in HCC treatment. The aim of this study is to propose a novel prognostic model for HCC based on adenosine metabolizing genes and explore the potential relationship between them. Regression analysis was performed to identify differentially expressed genes associated with adenosine metabolism in HCC patients using RNA sequencing data obtained from a public database. Adenosine metabolism-related risk score (AMrisk) was derived using the least absolute shrinkage and selection operator (LASSO) Cox regression and verified using another database. Changes in adenosine metabolism in HCC were analyzed using functional enrichment analysis and multiple immune scores. The gene expression levels in patient samples were validated using quantitative reverse transcription polymerase chain reaction. Thirty adenosine metabolism-related differentially expressed genes were identified in HCC, and six genes (ADA, P2RY4, P2RY6, RPIA, SLC6A3, and VEGFA) were used to calculate the AMrisk score; the higher the risk scores, the lower the overall survival. Moreover, immune infiltration activation and immune checkpoints were considerably higher in the high-risk group. Additional in vitro experiments validated the enhanced expression of these six genes in HCC. The established predictive model demonstrated that adenosine metabolism-related genes was significantly associated with prognosis in HCC patients.","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":" ","pages":""},"PeriodicalIF":3.7,"publicationDate":"2024-11-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142639265","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}

引用次数: 0

Histone demethylase JMJD1C advances macrophage foam cell formation and atherosclerosis progression by promoting the transcription of PCSK9. 组蛋白去甲基化酶 JMJD1C 通过促进 PCSK9 的转录，推动巨噬细胞泡沫细胞的形成和动脉粥样硬化的进展。

IF 3.7 3区生物学

Journal of physiology and biochemistry Pub Date : 2024-11-08 DOI: 10.1007/s13105-024-01058-3

Yiming Wang, Yifei Chen, Jianbo Yang, Wei Sun, Xiaoning Zhang

{"title":"Histone demethylase JMJD1C advances macrophage foam cell formation and atherosclerosis progression by promoting the transcription of PCSK9.","authors":"Yiming Wang, Yifei Chen, Jianbo Yang, Wei Sun, Xiaoning Zhang","doi":"10.1007/s13105-024-01058-3","DOIUrl":"https://doi.org/10.1007/s13105-024-01058-3","url":null,"abstract":"Macrophage is considered as a critical driving factor in the progression of atherosclerosis (AS), and epigenetic heterogeneity contributes important mechanisms in this process. Here, we identified that a histone demethylase jumonji domain-containing protein 1 C (JMJD1C) is a promising biomarker for atherosclerotic cerebral infarction through clinical analysis. Then, AOPE-/- mice fed with a high fat diet and RAW264.7 cells induced by oxidized low-density lipoprotein (ox-LDL) were used as AS models to verify the function of JMJD1C in AS development in vivo and in vitro. JMJD1C knockdown significantly reduced plaque area, inflammation and endothelial damage in AS model mice, and also alleviated foam cell formation, inflammatory cytokines production and cell apoptosis in ox-LDL-treated RAW264.7 cells. Mechanistically, JMJD1C promoted the transcription of proprotein convertase subtilisin/kexin type 9 (PCSK9) through mediating H3 Lysine 9 demethylation. The effects of JMJD1C knockdown on ox-LDL-induced macrophages were blocked by PCSK9 overexpression. Altogether, our study proves that JMJD1C advances macrophage foam cell formation, inflammation and apoptosis to accelerate AS progression through H3 demethylation of PCSK9. The findings underscore the important role of JMJD1C-mediated histone modification in macrophage regulation and AS progression, which brings a new insight into the pathobiology of AS.","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":" ","pages":""},"PeriodicalIF":3.7,"publicationDate":"2024-11-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142603715","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}

引用次数: 0

Apelin/APJ signaling in IGF-1-induced acute mitochondrial and antioxidant effects in spontaneously hypertensive rat myocardium. 自发性高血压大鼠心肌中 IGF-1 诱导的急性线粒体和抗氧化效应中的凋亡素/APJ 信号传导。

IF 3.7 3区生物学

Journal of physiology and biochemistry Pub Date : 2024-10-25 DOI: 10.1007/s13105-024-01055-6

Alejandra M Yeves, Joshua Godoy Coto, Erica V Pereyra, Andrés J Medina, Luisa F González Arbelaez, Fiorella A Cavalli, Irene L Ennis

{"title":"Apelin/APJ signaling in IGF-1-induced acute mitochondrial and antioxidant effects in spontaneously hypertensive rat myocardium.","authors":"Alejandra M Yeves, Joshua Godoy Coto, Erica V Pereyra, Andrés J Medina, Luisa F González Arbelaez, Fiorella A Cavalli, Irene L Ennis","doi":"10.1007/s13105-024-01055-6","DOIUrl":"https://doi.org/10.1007/s13105-024-01055-6","url":null,"abstract":"IGF-1 and apelin are released in response to exercise training with beneficial effects. Previously we demonstrated that a swimming routine is effective to convert pathological into physiological cardiac hypertrophy, and that IGF-1 improves contractility and the redox state, in spontaneously hypertensive rats (SHR). Now, we hypothesize that the apelinergic pathway is involved in the cardioprotective effects of IGF-1 in the SHR. We assessed the redox state and mitochondrial effects of IGF-1 or apelin in the presence/absence of AG1024 or ML221 [pharmacological antagonists of IGF1 (IGF1R) and apelin (APJ) receptors, respectively] in SHR isolated cardiomyocytes or perfused hearts. Acute IGF-1 (10 nmol/L) significantly: -reduced H2O2 production (IGF-1:62 ± 6; control:100 ± 8.1, %), -increased the activity of superoxide dismutase (IGF-1:193 ± 17, control: 100 ± 13,%), -prevented H2O2-induced ΔΨm loss (TMREF10min/F0 min: IGF-1:0.93 ± 0.017, control: 0.72 ± 0.029), -reduced mitochondrial permeability transition pore (mPTP) opening estimated by the calcium retention capacity (nmol/mg protein, IGF-1:251 ± 34, control:112 ± 5), and -increased P-AMPK (IGF-1:129 ± 0.9, control: 100 ± 2%) and P-AKT (IGF-1:143 ± 17 control:100 ± 6, %). These effects were suppressed not only by the antagonism of IGF1R but also of APJ. Moreover, IGF-1 significantly increased APJ (IGF-1:198 ± 29 control:100 ± 15,%) and apelin mRNAs (IGF-1:251 ± 48, control:100 ± 6,%). On the other hand, an equipotent dose of exogenous apelin (50 nmol/L) emulated IGF-1 effects being cancelled by the antagonism of APJ however not by AG1024. IGF-1/IGF1R stimulates the apelinergic pathway, improving the redox balance and mitochondria status in the pathologically hypertrophied myocardium of the SHR.","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":" ","pages":""},"PeriodicalIF":3.7,"publicationDate":"2024-10-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142502601","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}

引用次数: 0

TAF15 inhibits p53 nucleus translocation and promotes HCC cell 5-FU resistance via post-transcriptional regulation of UBE2N. TAF15 通过转录后调控 UBE2N 抑制 p53 核转位并促进 HCC 细胞对 5-FU 的耐受。

IF 3.7 3区生物学

Journal of physiology and biochemistry Pub Date : 2024-10-24 DOI: 10.1007/s13105-024-01053-8

Jiayan Fang, Mengqi Zou, Mei Yang, Yejia Cui, Rong Pu, Yufeng Yang

{"title":"TAF15 inhibits p53 nucleus translocation and promotes HCC cell 5-FU resistance via post-transcriptional regulation of UBE2N.","authors":"Jiayan Fang, Mengqi Zou, Mei Yang, Yejia Cui, Rong Pu, Yufeng Yang","doi":"10.1007/s13105-024-01053-8","DOIUrl":"https://doi.org/10.1007/s13105-024-01053-8","url":null,"abstract":"Chemotherapy resistance is an important factor responsible for the low 5-year survival rate of hepatocellular carcinoma (HCC) patients. Ubiquitin-conjugating enzyme E2N (UBE2N) is a cancer-associated ubiquitin-conjugating enzyme that is expressed in HCC tissues, and its high expression is associated with a poor prognosis. This study explored the role played by UBE2N in development of 5-fluorouracil (5-FU) resistance in HCC cells. Three HCC cell lines (HepG2 [p53 wild type], Huh7 [p53 point mutant type], Hep3B [p53 non-expression type]), and one normal liver cell line (MIHA) were used in our present study. The IC50 value of 5-FU was determined using a cell counting kit-8 (CCK-8) assay. Cell viability was assessed by colony formation assays. TUNEL assays and flow cytometry were used to analyze cell apoptosis. RNA pull-down and RNA immunoprecipitation (RIP) assays were performed to confirm the binding relationship between UBE2N mRNA and TAF15 protein. Our results showed that TAF15 and UBE2N were highly expressed in HCC cells. UBE2N inhibited the translocation of p53 protein into the cell nucleus to increase 5-FU resistance, as reflected by an increased IC50 value, an increase in cell viability, and a reduction in cell apoptosis. Overexpression of p53 reduced 5-FU resistance, but that effect could be reversed by UBE2N overexpression. TAF15 protein bound to and stabilized UBE2N mRNA, thereby inhibiting p53 translocation into the nucleus and promoting 5-FU resistance in HCC cells. Collectively, our present study identified a novel mechanism by which TAF15/UBE2N regulates p53 distribution to increase 5-FU resistance. Our results also suggest potential therapeutic strategies for treating HCC.","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":" ","pages":""},"PeriodicalIF":3.7,"publicationDate":"2024-10-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142502602","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}

引用次数: 0

Renal denervation ameliorates atrial remodeling in type 2 diabetic rats by regulating mitochondrial dynamics. 通过调节线粒体动力学，肾脏去神经化可改善 2 型糖尿病大鼠的心房重塑。

IF 3.7 3区生物学

Journal of physiology and biochemistry Pub Date : 2024-10-22 DOI: 10.1007/s13105-024-01054-7

Jun-Yu Huo, Can Hou, Xiao-Long Li, Ling Yang, Wan-Ying Jiang

{"title":"Renal denervation ameliorates atrial remodeling in type 2 diabetic rats by regulating mitochondrial dynamics.","authors":"Jun-Yu Huo, Can Hou, Xiao-Long Li, Ling Yang, Wan-Ying Jiang","doi":"10.1007/s13105-024-01054-7","DOIUrl":"https://doi.org/10.1007/s13105-024-01054-7","url":null,"abstract":"There is no effective treatment for diabetes-related atrial remodeling currently. This study aimed to investigate the effects of renal denervation (RDN) on diabetes-related atrial remodeling and explore the related mechanisms. A type 2 diabetes mellitus model was established by high-fat diet feeding and low-dose streptozotocin injection in Sprague‒Dawley rats. After successful modeling, the diabetic rats were randomly assigned to two groups according to whether they were subjected to RDN or sham RDN surgery. At the end of the experiment, cardiac function and structure were evaluated by echocardiography and histology, respectively. Mitochondrial morphology, function and mitochondrial dynamics were assessed by multiple methods. Mdivi1 was used to verify the mechanism by which RDN improves atrial remodeling. In the 10th week, diabetic rats exhibited obvious atrial remodeling, including atrial enlargement and diastolic dysfunction. Pathological staining showed that diabetic rats had cardiomyocyte hypertrophy and interstitial fibrosis in atrial tissues. In terms of mitochondrial morphology and function, diabetic rats exhibited fragmented mitochondria, reduced adenosine triphosphate production and decreased mitochondrial membrane potential levels. Abnormal mitochondrial dynamics in diabetic rats were characterized by the inhibition of mitochondrial fusion, excessive mitochondrial fission, and the suppression of mitophagy. However, RDN effectively ameliorated diabetes-induced pathological atrial remodeling. In addition, RDN significantly improved mitochondrial morphological and functional abnormalities and corrected the disorders of mitochondrial dynamics. Furthermore, the protective effects of RDN against atrial remodeling were related to the regulation of mitochondrial dynamics. RDN prevented diabetes-induced atrial remodeling. These protective effects might be related to improvements in mitochondrial dynamics.","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":" ","pages":""},"PeriodicalIF":3.7,"publicationDate":"2024-10-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142468326","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}

引用次数: 0

Normobaric hypoxia accelerates high-intensity intermittent training-induced mitochondrial biogenesis (PGC-1α)- and dynamics (OPA1)-related protein expressions in rat gastrocnemius muscle. 常压低氧可加速高强度间歇训练诱导的大鼠腓肠肌线粒体生物生成（PGC-1α）和动力学（OPA1）相关蛋白的表达。

IF 3.7 3区生物学

Journal of physiology and biochemistry Pub Date : 2024-10-18 DOI: 10.1007/s13105-024-01052-9

Shohei Dobashi, Toshinori Yoshihara, Yuji Ogura, Hisashi Naito

{"title":"Normobaric hypoxia accelerates high-intensity intermittent training-induced mitochondrial biogenesis (PGC-1α)- and dynamics (OPA1)-related protein expressions in rat gastrocnemius muscle.","authors":"Shohei Dobashi, Toshinori Yoshihara, Yuji Ogura, Hisashi Naito","doi":"10.1007/s13105-024-01052-9","DOIUrl":"https://doi.org/10.1007/s13105-024-01052-9","url":null,"abstract":"High-intensity intermittent training (HIIT) in a normobaric hypoxic environment enhances exercise capacity, possibly by increasing the mitochondrial content in skeletal muscle; however, the molecular mechanisms underlying these adaptations are not well understood. Therefore, we investigated whether HIIT under normobaric hypoxia can enhance the expression of proteins involved in mitochondrial biogenesis and dynamics in rat gastrocnemius muscle. Five-week-old male Wistar rats (n = 24) were randomly assigned to the following four groups: (1) sedentary under normoxia (20.9% O2) (NS), (2) training under normoxia (NT), (3) sedentary under normobaric hypoxia (14.5% O2) (HS), and (4) training under normobaric hypoxia (HT). The training groups in both conditions were engaged in HIIT on a treadmill five to six days per week for nine weeks. From the fourth week of the training period, the group assigned to hypoxic conditions was exposed to normobaric hypoxia. Forty-eight hours after completing the final training session, gastrocnemius muscles were surgically removed, and mitochondrial enzyme activity and mitochondrial biogenesis and dynamics regulatory protein levels were determined. Citrate synthase (CS) activity and mitochondrial oxygen phosphorylation (OXPHOS) subunits in the gastrocnemius muscle in the HT significantly exceeded those in the other three groups. Moreover, the levels of a master regulator of mitochondrial biogenesis, peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α), and a mitochondrial fusion-related protein, optic atrophy 1 (OPA1), were significantly increased by HIIT under normobaric hypoxia. Our data indicates that HIIT and normobaric hypoxia increase the expression of mitochondrial biogenesis- and dynamics-related proteins in skeletal muscles.","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":" ","pages":""},"PeriodicalIF":3.7,"publicationDate":"2024-10-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142468216","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}

引用次数: 0

Mechanism of Mettl14 regulating AIM2 inflammasome activation and neuronal apoptosis and pyroptosis in spinal cord injury by mediating PPARγ m6A methylation. Mettl14 通过介导 PPARγ m6A 甲基化调节脊髓损伤中 AIM2 炎症小体激活、神经元凋亡和热凋亡的机制

IF 3.7 3区生物学

Journal of physiology and biochemistry Pub Date : 2024-10-14 DOI: 10.1007/s13105-024-01047-6

Fan Wu, Liqun Li, Zhigang Li, Dabiao Zhou, Zhihui Huang, Dawei Sang, Chizi Hao

{"title":"Mechanism of Mettl14 regulating AIM2 inflammasome activation and neuronal apoptosis and pyroptosis in spinal cord injury by mediating PPARγ m6A methylation.","authors":"Fan Wu, Liqun Li, Zhigang Li, Dabiao Zhou, Zhihui Huang, Dawei Sang, Chizi Hao","doi":"10.1007/s13105-024-01047-6","DOIUrl":"https://doi.org/10.1007/s13105-024-01047-6","url":null,"abstract":"Spinal cord injury (SCI) represents a destructive pathological and neurological state. Methyltransferase-like 14 (Mettl14)-mediated m6A modification links to spinal cord injury (SCI), and we explored its mechanism. SCI mouse models were subjected to si-Mettl14 and si-negative control treatments and mouse behavior, pathological condition and apoptosis assessments. The oxygen/glucose deprivation (OGD)-induced spinal cord neuronal cell models were processed with si-Mettl14 and si-peroxisome proliferator-activated receptor γ (PPARγ) plasmids, and pcDNA3.1-YTHDF2 or synthetic dsDNA Poly(dA: dT), followed by viability and apoptosis evaluation by MTT and flow cytometry. Levels of Mettl14, PPARγ, and YTHDF2 mRNAs and proteins, AIM2 inflammasome activation-associated and pyroptosis marker proteins, PPARγ m6A methylation and pyroptosis-related inflammatory factors were determined by RT-qPCR, Western blot, Me-RIP and ELISA, with PPARγ mRNA stability and YTHDF2-PPARγ interaction assessed. Mettl14 and PPARγ m6A modification levels rose in SCI spinal cord tissues, while PPARγ levels dropped. Mettl14 knockdown dampened m6A modification, up-regulated PPARγ levels, weakened neuronal apoptosis, and ameliorated SCI in mice. OGD down-regulated PPARγ and accelerated OGD-induced neuronal apoptosis and pyroptosis via inducing Mettl14-mediated m6A modification. Mettl14 amplified PPARγ mRNA degradation and down-regulated PPARγ by mediating m6A methylation via the YTHDF2-dependent pathway. Mettl14 silencing-mediated PPARγ m6A methylation mitigated OGD-induced neuronal apoptosis and pyroptosis by inactivating AIM2 inflammasome. Mettl14 triggered activated AIM2 inflammasomes, promoted neuronal apoptosis and pyroptosis, and worsened SCI in SCI mice via mediating PPARγ m6A methylation. Mettl14 regulates AIM2 inflammasome activation, and redounds to spinal cord neuronal apoptosis and pyroptosis in SCI by mediating m6A methylation of PPARγ.","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":" ","pages":""},"PeriodicalIF":3.7,"publicationDate":"2024-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142468315","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}

引用次数: 0

MicroRNA-enriched exosome as dazzling dancer between cancer and immune cells. 富含微RNA的外泌体是癌症细胞与免疫细胞之间的炫目舞者。

IF 3.7 3区生物学

Journal of physiology and biochemistry Pub Date : 2024-09-24 DOI: 10.1007/s13105-024-01050-x

Chou-Yi Hsu, Abdulrahman T Ahmed, Pooja Bansal, Ahmed Hjazi, Hussein Riyadh Abdul Kareem Al-Hetty, Maytham T Qasim, Ibrokhim Sapaev, Mahamedha Deorari, Yasser Fakri Mustafa, Ahmed Elawady

{"title":"MicroRNA-enriched exosome as dazzling dancer between cancer and immune cells.","authors":"Chou-Yi Hsu, Abdulrahman T Ahmed, Pooja Bansal, Ahmed Hjazi, Hussein Riyadh Abdul Kareem Al-Hetty, Maytham T Qasim, Ibrokhim Sapaev, Mahamedha Deorari, Yasser Fakri Mustafa, Ahmed Elawady","doi":"10.1007/s13105-024-01050-x","DOIUrl":"https://doi.org/10.1007/s13105-024-01050-x","url":null,"abstract":"Exosomes are widely recognized for their roles in numerous biological processes and as intercellular communication mediators. Human cancerous and normal cells can both produce massive amounts of exosomes. They are extensively dispersed in tumor-modeling animals' pleural effusions, ascites, and plasma from people with cancer. Tumor cells interact with host cells by releasing exosomes, which allow them to interchange various biological components. Tumor growth, invasion, metastasis, and even tumorigenesis can all be facilitated by this delicate and complex system by modifying the nearby and remote surroundings. Due to the existence of significant levels of biomolecules like microRNA, exosomes can modulate the immune system's stimulation or repression, which in turn controls tumor growth. However, the role of microRNA in exosome-mediated communication between immunological and cancer cells is still poorly understood. This study aims to get the most recent information on the \"yin and yang\" of exosomal microRNA in the regulation of tumor immunity and immunotherapy, which will aid current cancer treatment and diagnostic techniques.","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":" ","pages":""},"PeriodicalIF":3.7,"publicationDate":"2024-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142307985","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}

引用次数: 0

Increased expression of IL-1β in adipose tissue in obesity influences the development of colon cancer by promoting inflammation. 肥胖症患者脂肪组织中 IL-1β 的表达增加，通过促进炎症影响结肠癌的发展。

IF 3.7 3区生物学

Journal of physiology and biochemistry Pub Date : 2024-09-21 DOI: 10.1007/s13105-024-01048-5

Gabriela Neira, Javier Gómez-Ambrosi, Javier A Cienfuegos, Beatriz Ramírez, Sara Becerril, Amaia Rodríguez, María A Burrell, Jorge Baixauli, Amaia Mentxaka, Marcos Casado, Camilo Silva, Javier Escalada, Gema Frühbeck, Victoria Catalán

{"title":"Increased expression of IL-1β in adipose tissue in obesity influences the development of colon cancer by promoting inflammation.","authors":"Gabriela Neira, Javier Gómez-Ambrosi, Javier A Cienfuegos, Beatriz Ramírez, Sara Becerril, Amaia Rodríguez, María A Burrell, Jorge Baixauli, Amaia Mentxaka, Marcos Casado, Camilo Silva, Javier Escalada, Gema Frühbeck, Victoria Catalán","doi":"10.1007/s13105-024-01048-5","DOIUrl":"https://doi.org/10.1007/s13105-024-01048-5","url":null,"abstract":"Excess adiposity contributes to the development of colon carcinoma (CC). Interleukin (IL)-1β is a pro-inflammatory cytokine relevant in obesity-associated chronic inflammation and tumorigenic processes. We herein aimed to study how obesity and CC affects the expression of IL1B, and to determine the impact of IL-1β on the regulation of metabolic inflammation and gut barrier function in the context of obesity and CC. Samples from 71 volunteers were used in a case-control study and a rat model of diet-induced obesity (DIO). Furthermore, bariatric surgery was used to determine the effect of weight loss on the intestinal gene expression levels of Il1b. To evaluate the effect of IL-1β and obesity in CC, we treated the adenocarcinoma cell line HT-29 with IL-1β and the adipocyte-conditioned medium (ACM) from patients with obesity. We showed that obesity (P < 0.05) and CC (P < 0.01) upregulated the transcript levels of IL1B in visceral adipose tissue as well as in the colon from patients with CC (P < 0.01). The increased expression of Il1b in the ileum and colon in DIO rats decreased after weight loss achieved by either sleeve gastrectomy or caloric restriction (both P < 0.05). ACM treatment on HT-29 cells upregulated (P < 0.05) the transcripts of IL1B and CCL2, while reducing (P < 0.05) the expression of the anti-inflammatory ADIPOQ and MUC2 genes. Additionally, IL-1β upregulated (P < 0.01) the expression of CCL2 and TNF whilst downregulating (P < 0.01) the transcript levels of IL4, ADIPOQ and TJP1 in HT-29 cells. We provide evidence of the important role of IL-1β in obesity-associated CC by directly promoting inflammation.","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":" ","pages":""},"PeriodicalIF":3.7,"publicationDate":"2024-09-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142289738","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}

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