Cell Biology International最新文献_第10页

Degradation meets development: Implications in β-cell development and diabetes 降解与发育：β细胞发育和糖尿病的影响。

IF 3.9 3区生物学

Cell Biology International Pub Date : 2024-03-18 DOI: 10.1002/cbin.12155

Akshaya Ashok, Guruprasad Kalthur, Anujith Kumar

{"title":"Degradation meets development: Implications in β-cell development and diabetes","authors":"Akshaya Ashok, Guruprasad Kalthur, Anujith Kumar","doi":"10.1002/cbin.12155","DOIUrl":"10.1002/cbin.12155","url":null,"abstract":"Pancreatic development is orchestrated by timely synthesis and degradation of stage-specific transcription factors (TFs). The transition from one stage to another stage is dependent on the precise expression of the developmentally relevant TFs. Persistent expression of particular TF would impede the exit from the progenitor stage to the matured cell type. Intracellular protein degradation-mediated protein turnover contributes to a major extent to the turnover of these TFs and thereby dictates the development of different tissues. Since even subtle changes in the crucial cellular pathways would dramatically impact pancreatic β-cell performance, it is generally acknowledged that the biological activity of these pathways is tightly regulated by protein synthesis and degradation process. Intracellular protein degradation is executed majorly by the ubiquitin proteasome system (UPS) and Lysosomal degradation pathway. As more than 90% of the TFs are targeted to proteasomal degradation, this review aims to examine the crucial role of UPS in normal pancreatic β-cell development and how dysfunction of these pathways manifests in metabolic syndromes such as diabetes. Such understanding would facilitate designing a faithful approach to obtain a therapeutic quality of β-cells from stem cells.","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":null,"pages":null},"PeriodicalIF":3.9,"publicationDate":"2024-03-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/cbin.12155","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140157643","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Silver nanoparticles stimulate 5-Fluorouracil-induced colorectal cancer cells to kill through the upregulation TRPV1-mediated calcium signaling pathways 银纳米粒子通过上调 TRPV1 介导的钙信号通路，刺激 5-氟尿嘧啶诱导的结直肠癌细胞死亡。

IF 3.9 3区生物学

Cell Biology International Pub Date : 2024-03-18 DOI: 10.1002/cbin.12141

Müge Mavioğlu Kaya

{"title":"Silver nanoparticles stimulate 5-Fluorouracil-induced colorectal cancer cells to kill through the upregulation TRPV1-mediated calcium signaling pathways","authors":"Müge Mavioğlu Kaya","doi":"10.1002/cbin.12141","DOIUrl":"10.1002/cbin.12141","url":null,"abstract":"The involvement of the TRP vanilloid 1 (TRPV1) cation channel on the 5-Fluorouracil (5-FU)-caused Ca2+ signals through the activation of the apoptotic signaling pathway and stimulating the mitochondrial Ca2+ and Zn2+ accumulation-induced reactive oxygen species (ROS) productions in several cancer cells, except the colorectal cancer (HT-29) cell line, was recently reported. I aimed to investigate the action of silver nanoparticles (SiNPs) and 5-FU incubations through the activation of TRPV1 on ROS, apoptosis, and cell death in the HT-29 cell line. The cells were divided into four groups: control, SiNP (100 µM for 48 h), 5-FU (25 μM for 24 h), and 5-FU + SiNP. SiNP treatment through TRPV1 activation (via capsaicin) stimulated the oxidant and apoptotic actions of 5-FU in the cells, whereas they were diminished in the cells by the TRPV1 antagonist (capsazepine) treatment. The apoptotic and cell death actions of 5-FU were determined by increasing the propidium iodide/Hoechst rate, caspase-3, -8, and -9 activations, mitochondrial membrane depolarization, lipid peroxidation, and ROS, but decreasing the glutathione and glutathione peroxidase. The increase of cytosolic free Ca2+ and Zn2+ into mitochondria via the stimulation of TRPV1 current density increased oxidant and apoptotic properties of 5-FU in the cells. For the therapy of HT-29 tumor cells, I found that the combination of SiNPs and 5-FU was synergistic via TRPV1 activation.","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":null,"pages":null},"PeriodicalIF":3.9,"publicationDate":"2024-03-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140157646","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

Curcumin relieves oxaliplatin-induced neuropathic pain via reducing inflammation and activating antioxidant response 姜黄素能通过减少炎症和激活抗氧化反应缓解奥沙利铂诱发的神经性疼痛。

IF 3.9 3区生物学

Cell Biology International Pub Date : 2024-03-13 DOI: 10.1002/cbin.12153

Meng-Wei Zhang, Xu Sun, Yi-Wen Xu, Wei Meng, Qiong Tang, Hui Gao, Ling Liu, Shao-Hui Chen

{"title":"Curcumin relieves oxaliplatin-induced neuropathic pain via reducing inflammation and activating antioxidant response","authors":"Meng-Wei Zhang, Xu Sun, Yi-Wen Xu, Wei Meng, Qiong Tang, Hui Gao, Ling Liu, Shao-Hui Chen","doi":"10.1002/cbin.12153","DOIUrl":"10.1002/cbin.12153","url":null,"abstract":"Oxaliplatin (OXA) has shown high effectiveness in the treatment of cancers, but its anticancer clinical effects often induce neurotoxicity leading to neuropathic pain. Oxidative damage and NLRP3 inflammasome play important roles in neuropathic pain development. Here, neuropathic pain mouse model was constructed by continuous intraperitoneal injection of OXA. OXA administration induced mechanical pain, spontaneous pain, thermal hyperalgesia and motor disability in mice. The spinal cord tissues of OXA mice exhibited the suppressed antioxidative response, the activated NLRP3 inflammasome mediated inflammatory responses, and the increased GSK-3β activity. Next, we injected curcumin (CUR) intraperitoneally in OXA mice for seven consecutive days. CUR-treated mice showed increased mechanical pain thresholds, reduced number of spontaneous flinches, increased paw withdrawal latency, and restored latency to fall. While in the spinal cord, CUR treatment inhibited the NLRP3 inflammasome mediated inflammatory response, increased Nrf2/GPX4-mediated antioxidant responses, and decreased mitochondrial oxidative generation. Additionally, CUR combined with GSK-3β through four covalent bonds and reduced GSK-3β activity. In conclusion, our findings suggest that CUR treatment inhibits GSK-3β activation, increases Nrf2 mediated antioxidant responses, inhibits oxidative damage and inflammatory reaction, and alleviates OXA-induced neuropathic pain.","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":null,"pages":null},"PeriodicalIF":3.9,"publicationDate":"2024-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140118921","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

Paynantheine more effectively reverses multidrug resistance in malignant EPG85.257RDB and MCF7MX cells than morphine and speciociliatine 与吗啡和speciociliatine相比，Paynantheine能更有效地逆转恶性EPG85.257RDB和MCF7MX细胞的多药耐药性。

IF 3.9 3区生物学

Cell Biology International Pub Date : 2024-03-13 DOI: 10.1002/cbin.12152

Nayereh Abdali, Mohammad Nadipour Borujeni, Sayedeh Azimeh Hosseini, Rahim Malekzadeh, Marzieh Abolhasani, Seyed Abbas Mirzaei, Fatemeh Elahian

{"title":"Paynantheine more effectively reverses multidrug resistance in malignant EPG85.257RDB and MCF7MX cells than morphine and speciociliatine","authors":"Nayereh Abdali, Mohammad Nadipour Borujeni, Sayedeh Azimeh Hosseini, Rahim Malekzadeh, Marzieh Abolhasani, Seyed Abbas Mirzaei, Fatemeh Elahian","doi":"10.1002/cbin.12152","DOIUrl":"10.1002/cbin.12152","url":null,"abstract":"The possible interactions of morphine, paynantheine and speciociliatine alkaloids with ATP-binding cassette (ABC) transporters was investigated. The compounds were docked against ABCG2 and ABCB1 to predict the binding mode of alkaloids in active binding sites. The cytotoxicity of morphine, paynantheine and speciociliatine for EPG85.257RDB and MCF7MX cells was determined and ABCB1 and ABCG2 gene and protein expression were determined. The binding score of paynantheine to ABCB1 was higher in the docking studies. Paynantheine and speciociliatine had similar binding scores to ABCB1, but higher binding scores to ABCG2 than did morphine. Paynantheine and speciociliatine were more effective against MCF7MX and EPG85.257RDB cells and showed greater cyctotoxicity in the MTT assay. The effect of morphine and paynantheine on the ABCB1 gene and protein expression suggests these compounds can reduce resistance in cancer patients, but that speciociliatine may not be a suitable candidate because of its increased ABCB1 expression while speciociliatine decreased the expression of ABCG2 in MCF7MX cells. This indicates that speciociliatine is a better candidate for reducing drug resistance in this cell line. Structural modification, drug-metabolizing enzymes and differences in the binding sites could cause functional differences between these compounds.","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":null,"pages":null},"PeriodicalIF":3.9,"publicationDate":"2024-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140118922","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

Correction to “Autophagy regulates the apoptosis of bone marrow-derived mesenchymal stem cells under hypoxic condition via AMP-activated protein kinase/mammalian target of rapamycin pathway” 自噬通过AMP激活的蛋白激酶/哺乳动物雷帕霉素靶点通路调节缺氧条件下骨髓间充质干细胞的凋亡》的更正。

IF 3.9 3区生物学

Cell Biology International Pub Date : 2024-03-11 DOI: 10.1002/cbin.12142

{"title":"Correction to “Autophagy regulates the apoptosis of bone marrow-derived mesenchymal stem cells under hypoxic condition via AMP-activated protein kinase/mammalian target of rapamycin pathway”","authors":"","doi":"10.1002/cbin.12142","DOIUrl":"10.1002/cbin.12142","url":null,"abstract":"Zhang, Z., Yang, M., Wang, Y., Wang, L., Jin, Z., Ding, L., Zhang, L., Zhang, L., Jiang, W., Gao, G., Yang, J., Lu, B., Cao, F., & Hu, T. (2016) Autophagy regulates the apoptosis of bone marrow-derived mesenchymal stem cells under hypoxic condition via AMP-activated protein kinase/mammalian target of rapamycin pathway. Cell Biology Internationa, 40(6), 671–685. https://doi.org/10.1002/cbin.10604.In the articles, the following figures are corrected asI. Additional information/correction for Figure 5a. In the original version of our article, an oversight occurred during the assembly of figures, leading to the inadvertent inclusion of an incorrect image in the \"Hypoxia+, 3-MA-, and Rapamycin-\" group within Figure 5A. We extend our apologies for any misunderstanding this may have caused. We wish to clarify that this oversight does not impact the manuscript's quantitative analyses or conclusions. We have addressed this error and the corrected Figure 5A is presented below.II. Additional information/correction for Figure 7f. In the first publication of our paper, there was an unintended mistake in the compilation of the figures, resulting in the wrong image being used in Figure 7F. We apologize for any confusion this error may have led to. We want to assure our readers that this oversight did not influence the quantitative analysis or the findings of our study. The corrected Figure 7F has been provided. We sincerely regret any disturbance or inconvenience this mistake might have caused.","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":null,"pages":null},"PeriodicalIF":3.9,"publicationDate":"2024-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/cbin.12142","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140101096","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

OxLDL enhances procoagulant activity of endothelial cells by TMEM16F-mediated phosphatidylserine exposure OxLDL 通过 TMEM16F 介导的磷脂酰丝氨酸暴露增强内皮细胞的促凝血活性。

IF 3.9 3区生物学

Cell Biology International Pub Date : 2024-03-05 DOI: 10.1002/cbin.12150

Meishan Yan, Zelong Wang, Yao An, Zhanni Li, Yun Li, Hongyu Zhang, Caixia Li, Lifeng Wang, Li Chen, Chao Gao, Dongsheng Wang, Chunyan Gao

{"title":"OxLDL enhances procoagulant activity of endothelial cells by TMEM16F-mediated phosphatidylserine exposure","authors":"Meishan Yan, Zelong Wang, Yao An, Zhanni Li, Yun Li, Hongyu Zhang, Caixia Li, Lifeng Wang, Li Chen, Chao Gao, Dongsheng Wang, Chunyan Gao","doi":"10.1002/cbin.12150","DOIUrl":"10.1002/cbin.12150","url":null,"abstract":"Oxidized low-density lipoprotein (oxLDL), a key component in atherosclerosis and hyperlipidemia, is a risk factor for atherothrombosis in dyslipidemia, yet its mechanism is poorly understood. In this study, we used oxLDL-induced human aortic endothelial cells (HAECs) and high-fat diet (HFD)-fed mice as a hyperlipidemia model. Phosphatidylserine (PS) exposure, cytosolic Ca2+, reactive oxygen species (ROS), and lipid peroxidation were measured by flow cytometer. TMEM16F expression was detected by immunofluorescence, western blot, and reverse transcription polymerase chain reaction. Procoagulant activity (PCA) was measured by coagulation time, intrinsic/extrinsic factor Xase, and thrombin generation. We found that oxLDL-induced PS exposure and the corresponding PCA of HAECs were increased significantly compared with control, which could be inhibited over 90% by lactadherin. Importantly, TMEM16F expression in oxLDL-induced HAECs was upregulated by enhanced intracellular Ca2+ concentration, ROS, and lipid peroxidation, which led to PS exposure. Meanwhile, the knockdown of TMEM16F by short hairpin RNA significantly inhibited PS exposure in oxLDL-induced HAECs. Moreover, we observed that HFD-fed mice dramatically increased the progress of thrombus formation and accompanied upregulated TMEM16F expression by thromboelastography analysis, FeCl3-induced carotid artery thrombosis model, and western blot. Collectively, these results demonstrate that TMEM16F-mediated PS exposure may contribute to prothrombotic status under hyperlipidemic conditions, which may serve as a novel therapeutic target for the prevention of thrombosis in hyperlipidemia.","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":null,"pages":null},"PeriodicalIF":3.9,"publicationDate":"2024-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140038834","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

Identification and validation of m6A-associated ferroptosis genes in renal clear cell carcinoma 肾透明细胞癌中与 m6A 相关的铁凋亡基因的鉴定和验证

IF 3.9 3区生物学

Cell Biology International Pub Date : 2024-03-05 DOI: 10.1002/cbin.12146

Shuo Pang, Shuo Zhao, Yuxi Dongye, Yidong Fan, Jikai Liu

{"title":"Identification and validation of m6A-associated ferroptosis genes in renal clear cell carcinoma","authors":"Shuo Pang, Shuo Zhao, Yuxi Dongye, Yidong Fan, Jikai Liu","doi":"10.1002/cbin.12146","DOIUrl":"10.1002/cbin.12146","url":null,"abstract":"Urinary cancer is synonymous with clear cell renal cell carcinoma (ccRCC). Unfortunately, existing treatments for this illness are ineffective and unpromising. Finding novel ccRCC biomarkers is crucial to creating successful treatments.The Cancer Genome Atlas provided clear cell renal cell carcinoma transcriptome data. Functional enrichment analysis was performed on ccRCC and control samples' differentially expressed N6-methyladenosine RNA methylation and ferroptosis-related genes (DEMFRGs). Machine learning was used to find and model ccRCC patients' predicted genes. A nomogram was created for clear cell renal cell carcinoma patients. Prognostic genes were enriched. We examined patients' immune profiles by risk score. Our prognostic genes predicted ccRCC treatment drugs.We found 37 DEMFRGs by comparing 1913 differentially expressed ccRCC genes to 202 m6A RNA methylation FRGs. Functional enrichment analysis showed that hypoxia-induced cell death and metabolism pathways were the most differentially expressed methylation functional regulating genes. Five prognostic genes were found by machine learning: TRIB3, CHAC1, NNMT, EGFR, and SLC1A4. An advanced renal cell carcinoma nomogram with age and risk score accurately predicted the outcome. These five prognostic genes were linked to various cancers. Immunological cell number and checkpoint expression differed between high- and low-risk groups. The risk model successfully predicted immunotherapy outcome, showing high-risk individuals had poor results. NIACIN, TAE-684, ROCILETINIB, and others treat ccRCC. We found ccRCC prognostic genes that work. This discovery may lead to new ccRCC treatments.","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":null,"pages":null},"PeriodicalIF":3.9,"publicationDate":"2024-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140027507","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

Dihydroartemisinin eliminates senescent cells by promoting autophagy-dependent ferroptosis via AMPK/mTOR signaling pathway 双氢青蒿素通过 AMPK/mTOR 信号通路促进自噬依赖性铁凋亡，从而消除衰老细胞。

IF 3.9 3区生物学

Cell Biology International Pub Date : 2024-03-04 DOI: 10.1002/cbin.12143

Xing Wan, Can Li, Yue Hao Tan, Shi Qi Zuo, Feng Mei Deng, Jing Sun, Yi Lun Liu

{"title":"Dihydroartemisinin eliminates senescent cells by promoting autophagy-dependent ferroptosis via AMPK/mTOR signaling pathway","authors":"Xing Wan, Can Li, Yue Hao Tan, Shi Qi Zuo, Feng Mei Deng, Jing Sun, Yi Lun Liu","doi":"10.1002/cbin.12143","DOIUrl":"10.1002/cbin.12143","url":null,"abstract":"Cellular senescence is an irreversible cell-cycle arrest in response to a variety of cellular stresses, which contribute to the pathogenesis of a variety of age-related degenerative diseases. However, effective antisenescence strategies are still lacking. Drugs that selectively target senescent cells represent an intriguing therapeutic strategy to delay aging and age-related diseases. Thus, we thought to investigate the effects of dihydroartemisinin (DHA) on senescent cells and elucidated its mechanisms underlying aging. Stress-induced premature senescence (SIPS) model was built in NIH3T3 cells using H2O2 and evaluated by β-galactosidase staining. Cells were exposed to DHA and subjected to cellular activity assays including viability, ferroptosis, and autophagy. The number of microtubule-associated protein light-chain 3 puncta was detected by immunofluorescence staining. The iron content was assessed by spectrophotometer and intracellular reactive oxygen species (ROS) was measured by fluorescent probe dichlorodihydrofluorescein diacetate. We found that DHA triggered senescent cell death via ferroptosis. DHA accelerated ferritin degradation via promoting autophagy, increasing the iron contents, promoting ROS accumulation, thus leading to ferroptotic cell death in SIPS cells. In addition, autophagy inhibitor BafA1 preconditioning inhibited ferroptosis induced by DHA. Moreover, Atg5 silencing and autophagy inhibitor BafA1 preconditioning inhibited ferroptosis induced by DHA. We also revealed that the expression of p-AMP-activated protein kinase (AMPK) and p-mammalian target of rapamycin (mTOR) in senescent cells was downregulated. These results suggested that DHA may be a promising drug candidate for clearing senescent cells by inducing autophagy-dependent ferroptosis via AMPK/mTOR signaling pathway.","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":null,"pages":null},"PeriodicalIF":3.9,"publicationDate":"2024-03-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140027506","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

Protective autophagy enhances antistress ability through AMPK/ULK1 signaling pathway in human immortalized keratinocytes 保护性自噬通过 AMPK/ULK1 信号通路增强人类永生角质形成细胞的抗应激能力。

IF 3.9 3区生物学

Cell Biology International Pub Date : 2024-03-04 DOI: 10.1002/cbin.12149

Zhinan Shi, Jing Wang, Min Li, Li Gu, Zhiyi Xu, Xiaoyu Zhai, Shu Zhou, Jingting Zhao, Liqun Gu, Lin Chen, Linling Ju, Bingrong Zhou, Hui Hua

{"title":"Protective autophagy enhances antistress ability through AMPK/ULK1 signaling pathway in human immortalized keratinocytes","authors":"Zhinan Shi, Jing Wang, Min Li, Li Gu, Zhiyi Xu, Xiaoyu Zhai, Shu Zhou, Jingting Zhao, Liqun Gu, Lin Chen, Linling Ju, Bingrong Zhou, Hui Hua","doi":"10.1002/cbin.12149","DOIUrl":"10.1002/cbin.12149","url":null,"abstract":"Keratinocytes, located in the outermost layer of human skin, are pivotal cells to resist environmental damage. Cellular autophagy plays a critical role in eliminating damaged organelles and maintaining skin cell homeostasis. Low-dose 5-Aminolevulinic acid photodynamic therapy (ALA-PDT) has been demonstrated to enhance skin's antistress ability; however, the regulatory mechanisms of autophagy in keratinocytes remain unclear. In this study, we treated immortalized human keratinocytes (HaCaT cells) with low-dose ALA-PDT (0.5 mmol/L, 3 J/cm2). Through RNA-sequencing analysis, we identified that low-dose ALA-PDT modulated autophagy-related pathways in keratinocytes and pinpointed Unc-51-like kinase 1 (ULK1) as a key gene involved. Western blot results revealed that low-dose ALA-PDT treatment upregulated the expression of autophagy-related proteins Beclin-1 and LC3-II/LC3-I ratio. Notably, low-dose ALA-PDT regulated autophagy by inducing an appropriate level of reactive oxygen species (ROS), transiently reducing mitochondrial membrane potential, and decreasing adenosine triphosphate production; all these processes functioned on the AMP-activated protein kinase (AMPK)/ULK1 pathway to activate autophagy. Finally, we simulated external environmental damage using ultraviolet B (UVB) at a dose of 60 mJ/cm2 and observed that low-dose ALA-PDT mitigated UVB-induced cell apoptosis; however, this protective effect was reversed when using the autophagy inhibitor 3-methyladenine. Overall, these findings highlight how low-dose ALA-PDT enhances antistress ability in HaCaT cells through controlling ROS generation and activating the AMPK/ULK1 pathway to arouse cellular autophagy.","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":null,"pages":null},"PeriodicalIF":3.9,"publicationDate":"2024-03-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140021010","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

Follistatin-like 1 protects against doxorubicin-induced cardiotoxicity by preventing mitochondrial dysfunction through the SIRT6/Nrf2 signaling pathway Follistatin-like 1通过SIRT6/Nrf2信号通路防止线粒体功能障碍，从而防止多柔比星诱发的心脏毒性。

IF 3.9 3区生物学

Cell Biology International Pub Date : 2024-03-04 DOI: 10.1002/cbin.12147

Haijun Xu, Hong Guo, Zhigang Tang, Ruijun Hao, Shaowei Wang, Ping Jin

{"title":"Follistatin-like 1 protects against doxorubicin-induced cardiotoxicity by preventing mitochondrial dysfunction through the SIRT6/Nrf2 signaling pathway","authors":"Haijun Xu, Hong Guo, Zhigang Tang, Ruijun Hao, Shaowei Wang, Ping Jin","doi":"10.1002/cbin.12147","DOIUrl":"10.1002/cbin.12147","url":null,"abstract":"Mitochondrial dysfunction and myocardial remodeling have been reported to be the main underlying molecular mechanisms of doxorubicin-induced cardiotoxicity. SIRT6 is a nicotinamide adenine dinucleotide-dependent enzyme that plays a vital role in cardiac protection against various stresses. Moreover, previous studies have demonstrated that FSTL1 could alleviate doxorubicin-induced cardiotoxicity by inhibiting autophagy. The present study investigated the probable mechanisms of FSTL1 on doxorubicin-induced cardiotoxicity in vivo and in vitro. We confirmed that FSTL1 exerted a pivotal protective role on cardiac tissue in vivo and on doxorubicin-induced cell injury in vitro. Furthermore, FSTL1 can alleviate doxorubicin-induced mitochondrial dysfunction by inhibiting autophagy and apoptosis. Further studies demonstrated that FSTL1 can activate SIRT6 signaling by restoring the SIRT6 protein expression in doxorubicin-induced myocardial injury. SIRT6 activation elevated the protein expression of Nrf2 in doxorubicin-induced H9C2 injury. Treatment with the Nrf2 inhibitor ML385 partially antagonized the cardioprotective role of SIRT6 on doxorubicin-induced autophagy or apoptosis. These results suggested that the protective mechanism of FSTL1 on doxorubicin-induced cardiotoxicity may be related with the inhibition of autophagy and apoptosis, partly through the activation of SIRT6/Nrf2.","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":null,"pages":null},"PeriodicalIF":3.9,"publicationDate":"2024-03-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140021009","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