General physiology and biophysics最新文献_第3页

Synthesis of Epimedium extract selenium nanoparticles and evaluation their efficacy against lung cancer. 淫羊藿提取物硒纳米颗粒的合成及其抗肺癌疗效评价。

IF 1.3 4区生物学

General physiology and biophysics Pub Date : 2025-03-01 DOI: 10.4149/gpb_2024046

Guangying Fu, Jin Tong

{"title":"Synthesis of Epimedium extract selenium nanoparticles and evaluation their efficacy against lung cancer.","authors":"Guangying Fu, Jin Tong","doi":"10.4149/gpb_2024046","DOIUrl":"10.4149/gpb_2024046","url":null,"abstract":"Lung cancer, the foremost cause of cancer-related mortality worldwide, necessitates the exploration for novel anti-lung cancer therapeutics to enhance efficacy and reduce adverse effects. Targeting selenium in the tumor microenvironment has become a new strategy for the treatment of lung cancer. The objective of this study was to synthesize novel selenium nanoparticles (EBM-SeNPs) using aqueous extracts derived from Epimedium brevicornum Maxim and investigate its structural characteristics and inhibitory effects against lung cancer. The physicochemical properties of EBM-SeNPs were characterized from multiple aspects using a variety of methods. The CCK-8, flow cytometry, wound healing assay, Western blot and the cell derived xenograft model were conducted to evaluate the antitumor efficacy in vivo and in vitro. EBM-SeNPs were approximately spherical and exhibited superior dispersivity and stability in water solution. And EBM-SeNPs did not display any specific cytotoxicity against human liver cells. However, they showed outstanding capability to induce apoptosis in lung cancer cells, thereby effectively suppressing their growth and migratory potential. Furthermore, EBM-SeNPs demonstrated a reduction of tumor and an increase in immune organ index of tumor-bearing mice. Collectively, the EBM-SeNPs may be an effective and safe option for the treatment of lung cancer.","PeriodicalId":12514,"journal":{"name":"General physiology and biophysics","volume":"44 2","pages":"123-138"},"PeriodicalIF":1.3,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143673802","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 effects of stress and environmental enrichment on cognitive functions and stress-related gene expressions in the brain of aged rats. 压力和丰富环境对老年大鼠大脑认知功能和压力相关基因表达的影响

IF 1.3 4区生物学

General physiology and biophysics Pub Date : 2025-03-01 DOI: 10.4149/gpb_2024044

Duygu S Oran, Evren Eraslan

{"title":"The effects of stress and environmental enrichment on cognitive functions and stress-related gene expressions in the brain of aged rats.","authors":"Duygu S Oran, Evren Eraslan","doi":"10.4149/gpb_2024044","DOIUrl":"10.4149/gpb_2024044","url":null,"abstract":"We aimed to investigate whether environmental enrichment (EE) would alter possible adverse effects of chronic unpredictable mild stress (CUMS) in elderly rats regarding corticosterone levels, stress-related gene expressions in some brain regions, and learning and memory. Wistar male rats (over 20 months) weighing 450-550 g were housed in enriched or standard cages for the duration of the study (10 weeks). After 8 weeks of CUMS application, body weight gain, adrenal weight, and corticosterone levels were measured. Morris water maze (MWM), and novel object recognition test were performed. Glucocorticoid receptor (GR), corticotropin-releasing hormone (CRH), and corticotropin-releasing hormone receptor 1 (CRHR1) expression levels were determined in the hypothalamus and hippocampus. In the stress group, body weights decreased over time. Regarding the distance swum by rats to find the platform in the MWM, while there was no significant difference between the 3rd and 4th days in the EE+CUMS group, the decrease continued until the 4th day in the standard control (SC)+CUMS group. Stress application reduced the GR and CRHR1 gene expressions in the hypothalamus. We conclude that chronic stress and EE caused brain region-specific changes, thus affecting the neurobiological and cognitive functions in the elderly. In this respect, our study will contribute to neurobiological and neurodegenerative studies on aging.","PeriodicalId":12514,"journal":{"name":"General physiology and biophysics","volume":"44 2","pages":"151-162"},"PeriodicalIF":1.3,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143673805","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

GZMA silencing inhibits JAK2/STAT1 pathway and improves allergic rhinitis. 抑制 GZMA 可抑制 JAK2/STAT1 通路并改善过敏性鼻炎。

IF 1.3 4区生物学

General physiology and biophysics Pub Date : 2025-03-01 DOI: 10.4149/gpb_2024045

Lin Li, Yuhao Zhang, Jingyuan Wang, Lixia Zhang, Ying Gao, Xiaolin Ji, Tian Wang, Fei Zhao

{"title":"GZMA silencing inhibits JAK2/STAT1 pathway and improves allergic rhinitis.","authors":"Lin Li, Yuhao Zhang, Jingyuan Wang, Lixia Zhang, Ying Gao, Xiaolin Ji, Tian Wang, Fei Zhao","doi":"10.4149/gpb_2024045","DOIUrl":"10.4149/gpb_2024045","url":null,"abstract":"Allergic rhinitis (AR) is an immunoglobulin E (IgE)-mediated inflammatory disorder. This study attempts to identify AR-related differential expressed genes (DEGs) and determine potential targets for AR. We employed bioinformatics analysis to screen for hub DEGs for AR, and their performances in distinguishing AR were assessed by receiver operating characteristic (ROC) curves. Quantitative reverse-transcription polymerase chain reaction (qRT-PCR) and Western blot was used to quantify Granzyme A (GZMA) in ovalbumin (OVA)-induced AR mice. TNF-α-induced cell model was utilized to assess the role of GZMA in AR, and the effect of GZMA silencing on the JAK2/STAT1 pathway was investigated in TNF-α-induced AR. We identified HIST1H2BD, RPS28, HIST1H1C, MAF, and GZMA as hub genes, all of which exhibited excellent performance in distinguishing between AR and controls (AUC > 0.800). GZMA was highly expressed in AR mice. Silencing GZMA reduced the levels of inflammatory cytokines (IL-6, IL-4 and IL-5), inhibited cell apoptosis and promoted cell proliferation in TNF-α-induced nasal mucosal epithelial cells (MIC-iCell-m024). Overexpression of GZMA exhibited the opposite effects by promoting inflammation and cell apoptosis but inhibiting proliferation. Mechanistically, silencing GZMA inhibited the phosphorylation of JAK2 and STAT1, indicating the suppression of JAK2/STAT1 pathway. This study might share new idea for AR management.","PeriodicalId":12514,"journal":{"name":"General physiology and biophysics","volume":"44 2","pages":"93-106"},"PeriodicalIF":1.3,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143673741","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

Pulmonary alveolar proteinosis: Clinical and morphological overview of a rare disease associated with macrophage dysfunction. 肺泡蛋白沉积症：一种与巨噬细胞功能障碍相关的罕见疾病的临床和形态学综述。

IF 1.3 4区生物学

General physiology and biophysics Pub Date : 2025-01-01 DOI: 10.4149/gpb_2024038

Brigita Javorská, Róbert Slivka, Barbora Durcová, Adela Vrbenská, Jozef Škarda, Janka Vecanová, Natália Hvizdošová, Mária Makovická, Vojtěch Kamarád, Jozef Muri

{"title":"Pulmonary alveolar proteinosis: Clinical and morphological overview of a rare disease associated with macrophage dysfunction.","authors":"Brigita Javorská, Róbert Slivka, Barbora Durcová, Adela Vrbenská, Jozef Škarda, Janka Vecanová, Natália Hvizdošová, Mária Makovická, Vojtěch Kamarád, Jozef Muri","doi":"10.4149/gpb_2024038","DOIUrl":"10.4149/gpb_2024038","url":null,"abstract":"Pulmonary alveolar proteinosis (PAP) is a rare disease characterised by excessive accumulation of surfactant components in alveolar macrophages, alveoli, and peripheral airways. The accumulation of surfactant is associated with only a minimal inflammatory response but can lead to the development of pulmonary fibrosis. Three clinical forms of PAP are distinguished - primary, secondary and congenital. In recent years, significant findings have helped to clarify the ethiology and pathogenesis of the disease. Apart from impaired surfactant protein function, a key role in the development of PAP is played by signal pathway of granulocyte and macrophage colonies stimulating growth factor (GM-CSF) which is necessary for the functioning of alveolar macrophages and for surfactant homeostasis. Surfactant is partially degraded by alveolar macrophages that are stimulated by GM-CSF. The role of GM-CSF has been shown especially in primary PAP, which is currently considered an autoimmune disease involving the development of GM-CSF neutralising autoantibodies. Clinically, the disease may be silent or manifest with dyspnoeic symptoms triggered by exertion and cough. However, there is a 10 to 15% rate of patients who develop respiratory failure. Total pulmonary lavage is regarded as the standard method of treatment. In addition, recombinant human GM-CSF has been studied as a prospective therapy for the treatment of PAP.","PeriodicalId":12514,"journal":{"name":"General physiology and biophysics","volume":"44 1","pages":"1-11"},"PeriodicalIF":1.3,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143003032","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

Senkyunolide A attenuates cerebral ischemia-reperfusion injury by inhibiting NLRP3-mediated ferroptosis in PC12 cells. 仙球内酯A通过抑制nlrp3介导的PC12细胞铁下垂减轻脑缺血再灌注损伤。

IF 1.3 4区生物学

General physiology and biophysics Pub Date : 2025-01-01 DOI: 10.4149/gpb_2024038

Qian Zhang, Yale Wang, Yihong Xiu, Zhiqiang Zhang, Tianyu Zou, Hongyan Wu, Yaping Quan

{"title":"Senkyunolide A attenuates cerebral ischemia-reperfusion injury by inhibiting NLRP3-mediated ferroptosis in PC12 cells.","authors":"Qian Zhang, Yale Wang, Yihong Xiu, Zhiqiang Zhang, Tianyu Zou, Hongyan Wu, Yaping Quan","doi":"10.4149/gpb_2024038","DOIUrl":"10.4149/gpb_2024038","url":null,"abstract":"Cerebral ischemia-reperfusion (I/R) is a serious complication in patients with ischemic stroke. Senkyunolide A (SenA) can alleviate neuronal cell damage induced by cerebral I/R; however, the exact action mechanism remains unclear. An in vitro cellular injury model was established by inducing PC-12 cells with OGD/R. The viability of SenA-treated PC-12 cells with or without OGD/R induction was detected with CCK-8 assay while the cell apoptosis was detected using TUNEL. The secretion of inflammatory cytokines, the activity of ROS, mitochondrial membrane potential and mtROS level were measured with ELISA, ROS assay kits, JC-1 staining and MitoSOX Red assay, respectively. The level of Fe2+ was detected with Fe2+ assay kits and lipid peroxidation was detected with TBARS assay. The expressions of lipid peroxides were measured using corresponding assay kits. Western blot was used to measure the expressions of NLRP3, apoptosis-, and ferroptosis-related proteins. The transfection efficiency of OV-NLRP3 was also detected using Western blot. The present study showed that SenA could attenuate viability damage, inflammatory response, oxidative stress, apoptosis and ferroptosis in OGD/R-induced PC-12 cells and it was identified that the cytoprotective effects of SenA on PC-12 cells stimulated by OGD/R may be associated with the inhibition of NLPR3. Collectively, SenA protects neuronal cells against cerebral I/R injury through the inhibition of NLRP3-mediated ferroptosis.","PeriodicalId":12514,"journal":{"name":"General physiology and biophysics","volume":"44 1","pages":"51-61"},"PeriodicalIF":1.3,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143003415","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

Senescence in neural cell lines: comparative insights from SH-SY5Y and ReNcell VM. 神经细胞系的衰老：SH-SY5Y和ReNcell VM的比较见解。

IF 1.3 4区生物学

General physiology and biophysics Pub Date : 2025-01-01 DOI: 10.4149/gpb_2024028

Kristina Macova, Diana Mjartinova, Lubica Fialova, Dalibor Nakladal, Dominika Fricova

{"title":"Senescence in neural cell lines: comparative insights from SH-SY5Y and ReNcell VM.","authors":"Kristina Macova, Diana Mjartinova, Lubica Fialova, Dalibor Nakladal, Dominika Fricova","doi":"10.4149/gpb_2024028","DOIUrl":"10.4149/gpb_2024028","url":null,"abstract":"Senescence, a crucial yet paradoxical phenomenon in cellular biology, acts as a barrier against cancer progression while simultaneously promoting aging and age-related pathologies. This duality underlines the importance of precise monitoring of senescence response, especially with regard to the proposed use of drugs selectively removing senescent cells. In particular, little is known about the role of senescence in neurons and in neurodegenerative diseases. Our study investigates the senescence response in neuroblastoma SH-SY5Y cells and human neural progenitor ReNcell VM cells exposed to doxorubicin, a chemotherapeutic agent known to induce DNA damage and subsequent senescence. Through a comprehensive analysis employing the most robust senescence markers, we characterized the senescence-associated patterns in these neural cell lines including cellular morphological changes, SA-beta-gal, γH2A.X, p21Waf1/Cip1 and p16Ink4a. Our findings indicate that ReNcell VM cells exhibit greater senescence-associated response at lower doxorubicin concentrations compared to SH-SY5Y cells. Additionally, we observed cell-type-specific differences in timing and levels of the expression of key cell cycle regulators during senescence. Our results emphasize the necessity of cell-type-specific strategies in senescence research with regard to implications as well as limitations for translation into aging and neurodegenerative disorders.","PeriodicalId":12514,"journal":{"name":"General physiology and biophysics","volume":"44 1","pages":"39-49"},"PeriodicalIF":1.3,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143003410","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

Small nucleolar RNA 42 facilitates the progression of hepatocellular carcinoma through PI3K/Akt signaling pathway. 小核仁RNA 42通过PI3K/Akt信号通路促进肝癌的进展。

IF 1.3 4区生物学

General physiology and biophysics Pub Date : 2025-01-01 DOI: 10.4149/gpb_2024042

Jing Liu, Jiuling Deng, Qing Liang, Yan Yu, Xu Yang, Guangchun Sun

{"title":"Small nucleolar RNA 42 facilitates the progression of hepatocellular carcinoma through PI3K/Akt signaling pathway.","authors":"Jing Liu, Jiuling Deng, Qing Liang, Yan Yu, Xu Yang, Guangchun Sun","doi":"10.4149/gpb_2024042","DOIUrl":"10.4149/gpb_2024042","url":null,"abstract":"Small nucleolar RNAs may serve as new potential biomarkers for the diagnosis and treatment of liver cancer. The purpose of our study was to reveal the mechanism small nucleolar RNA 42 (SNORA42) affects the proliferation and migration of liver cancer cells. Quantitative real-time PCR (qRT-PCR) was performed to detect the expression of SNORA42 and its host gene. Cell proliferation and migration were measured using the CCK-8 and Transwell assays, respectively. Western blotting was performed to measure the expression of the proteins affected by SNORA42. SNORA42 overexpression could reinforce the proliferation of hepatocellular carcinoma (HCC) cells, and promote the migration of hepatocellular carcinoma cells. In addition, SNORA42 did not affect the expression of host genes KIAA0907. SNORA42 is one of the most important components of the PI3K/Akt signaling pathway. SNORA42 augmented phospho-Akt expression, which was reversed by PI3K and Akt inhibitors. Our study displayed that SNORA42 may affect the proliferation and migration of HCC cells by interfering with the PI3K/Akt signaling pathway. Thus, SNORA42 may be a new target for detecting or treating HCC.","PeriodicalId":12514,"journal":{"name":"General physiology and biophysics","volume":"44 1","pages":"29-38"},"PeriodicalIF":1.3,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143003439","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

TFDP1 overexpression promotes apoptosis of nucleus pulposus cells in intervertebral disc degeneration through regulating ADAM15/MMP9 axis. TFDP1过表达通过调节ADAM15/MMP9轴促进椎间盘退变中髓核细胞凋亡。

IF 1.3 4区生物学

General physiology and biophysics Pub Date : 2025-01-01 DOI: 10.4149/gpb_2024040

Xian Tong, Lijuan Xiao, Yanxuan Xin

{"title":"TFDP1 overexpression promotes apoptosis of nucleus pulposus cells in intervertebral disc degeneration through regulating ADAM15/MMP9 axis.","authors":"Xian Tong, Lijuan Xiao, Yanxuan Xin","doi":"10.4149/gpb_2024040","DOIUrl":"10.4149/gpb_2024040","url":null,"abstract":"Intervertebral disc degeneration (IVDD) is a common contributor for low back pain, which is featured by loss of extracellular matrix and nucleus pulposus cells (NPCs). Hence, our current study is undertaken to explore the potential mechanism of NPC apoptosis during IVDD. Transcription factor Dp-1 (TFDP1) expression in degenerative and non-degenerative intervertebral disc tissues was analyzed by bioinformatics. After transfection as needed, viability and apoptosis of NPCs were evaluated by cell counting kit-8 assay and flow cytometry, respectively. Western blot or quantitative real-time reverse transcription polymerase chain reaction was applied to assess expressions of TFDP1, matrix metallopeptidase 9 (MMP9), a disintegrin and metalloproteinase 15 (ADAM15), and apoptosis-associated proteins. TFDP1 expression was upregulated in degenerative intervertebral disc tissues. TFDP1 overexpression repressed viability, promoted apoptosis, increased expressions of Bax, Cleaved caspase 3, MMP9 and ADAM15, and decreased Bcl-2 expression in NPCs, while TFDP1 silencing did conversely. ADAM15 silencing promoted viability, inhibited apoptosis, increased Bcl-2 expression, and decreased Bax, Cleaved caspase 3, and MMP9 expressions in NPCs, which were reversed by TFDP1 overexpression. TFDP1 overexpression promotes apoptosis of NPCs in IVDD through regulating ADAM15/MMP9 axis, highlighting its role as a molecular target for the treatment of low back pain.","PeriodicalId":12514,"journal":{"name":"General physiology and biophysics","volume":"44 1","pages":"63-71"},"PeriodicalIF":1.3,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143003441","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

Silencing Map3k7 suppresses pyroptosis to alleviate bronchopulmonary dysplasia through inhibiting the TGF-β1/Smad3 pathway. 沉默Map3k7可通过抑制TGF-β1/Smad3通路抑制肺焦亡，缓解支气管肺发育不良。

IF 1.3 4区生物学

General physiology and biophysics Pub Date : 2025-01-01 DOI: 10.4149/gpb_2024043

Hong Zhen, Qiaozhen Wei, Bingmei Wei, Qingmei Huang, Ruishan Li

{"title":"Silencing Map3k7 suppresses pyroptosis to alleviate bronchopulmonary dysplasia through inhibiting the TGF-β1/Smad3 pathway.","authors":"Hong Zhen, Qiaozhen Wei, Bingmei Wei, Qingmei Huang, Ruishan Li","doi":"10.4149/gpb_2024043","DOIUrl":"10.4149/gpb_2024043","url":null,"abstract":"Bronchopulmonary dysplasia (BPD) is a serious complication in premature infants. This study aimed to investigate the mechanism of mitogen-activated protein 3 kinase 7 (Map3k7) affecting BPD by regulating caspase-1 mediated pyroptosis. The morphology of the lung tissue was observed using hematoxylin-eosin staining. TUNEL staining was performed to detect tissue apoptosis. RNA-seq and protein-protein interaction (PPI) network were performed to identify hub genes. Cell viability and apoptosis was analyzed using the CCK-8 assay and flow cytometry, respectively. Pyroptosis-related factors, inflammatory factors, oxidative stress indicators, and pathway-related proteins were detected using ELISA, qRT-PCR, and Western blotting. Hyperoxia-induced neonatal rats showed alveolar simplification with increased alveolar lumen, and decreased density of secondary alveolar cristae, demonstrating the successful BPD model. Map3k7 was identified as the crucial gene that was upregulated in BPD. Silencing Map3k7 promoted cell proliferation and suppressed apoptosis, inflammation, oxidative stress, and pyroptosis in hyperoxia-induced AEC-II, and alleviated BPD progression in hyperoxia-induced rats. Furthermore, silencing Map3k7 inhibited the TGF-β1/Smad3 pathway, and SRI-011381, the TGF-β pathway activator, weakened the inhibitory effects of silencing Map3k7 on hyperoxia-induced AEC-II. Silencing Map3k7 suppressed pyroptosis to alleviate BPD through inhibiting the TGF-β1/Smad3 pathway, providing a direction for the treatment of BPD in premature infants.","PeriodicalId":12514,"journal":{"name":"General physiology and biophysics","volume":"44 1","pages":"13-27"},"PeriodicalIF":1.3,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143003417","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

Transcription factor Yy1 modulates Trem1 to control LPS-triggered neuroinflammation and oxidative stress in mouse astrocytes via the NF-κB pathway. 转录因子Yy1通过NF-κB途径调节Trem1控制lps引发的小鼠星形胶质细胞神经炎症和氧化应激。

IF 1.3 4区生物学

General physiology and biophysics Pub Date : 2025-01-01 DOI: 10.4149/gpb_2024037

Wei Ke, Zhuofan Ye, Yiyun Huang, Shineng Ye

{"title":"Transcription factor Yy1 modulates Trem1 to control LPS-triggered neuroinflammation and oxidative stress in mouse astrocytes via the NF-κB pathway.","authors":"Wei Ke, Zhuofan Ye, Yiyun Huang, Shineng Ye","doi":"10.4149/gpb_2024037","DOIUrl":"10.4149/gpb_2024037","url":null,"abstract":"Dysfunction of astrocytes has a crucial role in the pathology of depression. Here, we aimed to define the exact action of the ubiquitous transcription factor (TF) Yin Yang-1 (Yy1) in depression pathogenesis and astrocytic dysfunction. A chronic unpredictable mild stress (CUMS) mouse model was generated. Primary mouse astrocytes were exposed to lipopolysaccharide (LPS). Cell growth was determined by CCK-8 and EdU assays. The direct interaction of Yy1 and the Trem1 promoter was validated by chromatin immunoprecipitation (ChIP) and luciferase assays. In CUMS mice, the levels of Yy1 and inflammatory cytokines were augmented and oxidative stress was enhanced. Functionally, disruption of Yy1 or triggering receptor expressed on myeloid cell 1 (Trem1) relieved LPS-triggered pro-growth, pro-inflammation, and pro-oxidative stress effects in mouse astrocytes. Mechanistically, Yy1 directly promoted the transcription and expression of Trem1 by binding to the Trem1 promoter. Yy1 disruption exerted regulatory impacts in LPS-induced mouse astrocytes via down-regulation of Trem1. Additionally, the Yy1/Trem1 cascade could modulate the activation of the NF-κB signaling in mouse astrocytes. Our study defines that Yy1 disruption relieves LPS-triggered neuroinflammation and oxidative stress in mouse astrocytes via the NF-κB pathway by down-regulating Trem1, providing possible strategies for depression treatment.","PeriodicalId":12514,"journal":{"name":"General physiology and biophysics","volume":"44 1","pages":"81-92"},"PeriodicalIF":1.3,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143003442","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