Acta biochimica et biophysica Sinica最新文献

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Macrophage pyroptosis in atherosclerosis: therapeutic potential. 动脉粥样硬化中的巨噬细胞焦亡:治疗潜力。
IF 3.3 2区 生物学
Acta biochimica et biophysica Sinica Pub Date : 2025-02-14 DOI: 10.3724/abbs.2025004
Jianying Ma, Yixian Wang, Wenna Xu, Hanjing Wang, Zhengdong Wan, Jiawei Guo
{"title":"Macrophage pyroptosis in atherosclerosis: therapeutic potential.","authors":"Jianying Ma, Yixian Wang, Wenna Xu, Hanjing Wang, Zhengdong Wan, Jiawei Guo","doi":"10.3724/abbs.2025004","DOIUrl":"https://doi.org/10.3724/abbs.2025004","url":null,"abstract":"<p><p>Atherosclerosis (AS) is a chronic inflammatory disease characterized by the accumulation of lipid-rich plaques in arterial walls, leading to cardiovascular events such as myocardial infarction and stroke. Macrophage pyroptosis, a form of programmed cell death driven by the NLRP3 inflammasome and caspase-1 activation, plays a critical role in the progression and destabilization of atherosclerotic plaques. This review explores the molecular mechanisms underlying macrophage pyroptosis and their significant contributions to AS pathogenesis. Recent advancements have highlighted the therapeutic potential of targeting key components of the pyroptotic pathway, including the use of nanotechnology to increase drug delivery specificity. These strategies are promising for reducing inflammation, stabilizing plaques, and mitigating the clinical impact of AS. Future studies should focus on translating these findings into clinical applications to develop effective treatments that can halt or reverse AS progression by modulating macrophage pyroptosis.</p>","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-02-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143424539","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
MiR-133b-3p attenuates angiotensin II-induced cardiac hypertrophy through the inhibition of apoptosis by targeting CDIP1. MiR-133b-3p通过靶向CDIP1抑制细胞凋亡来减轻血管紧张素ii诱导的心肌肥厚。
IF 3.3 2区 生物学
Acta biochimica et biophysica Sinica Pub Date : 2025-02-13 DOI: 10.3724/abbs.2024181
Jiwei Gu, Zhen Li, Xinyi Li, Ziyao Yang, Xi Xu, Yanjia Wang, Xiaohan Li, Kaiyue Qin, Guizhong Li, Li Xue, Xiaoling Yang
{"title":"MiR-133b-3p attenuates angiotensin II-induced cardiac hypertrophy through the inhibition of apoptosis by targeting <i>CDIP1</i>.","authors":"Jiwei Gu, Zhen Li, Xinyi Li, Ziyao Yang, Xi Xu, Yanjia Wang, Xiaohan Li, Kaiyue Qin, Guizhong Li, Li Xue, Xiaoling Yang","doi":"10.3724/abbs.2024181","DOIUrl":"https://doi.org/10.3724/abbs.2024181","url":null,"abstract":"<p><p>MicroRNAs (miRNAs) have emerged as essential regulators that play important roles in the development of multiple systems. Recent studies have identified significant roles for miRNAs in the progression of cardiac hypertrophy. This study aims to investigate the effects of miR-133b-3p on angiotensin II (Ang II)-induced cardiac hypertrophy and apoptosis, as well as explore its underlying mechanisms. Our experimental results reveal that miR-133b-3p expression is significantly decreased in both animal and cell models of cardiac hypertrophy induced by Ang II. Overexpression of miR-133b-3p reverses the hypertrophic manifestations and apoptosis induced by Ang II. Through bioinformatics analysis and dual-luciferase reporter assays, <i>CDIP1</i> (cell death inducing p53 target 1) is identified as a direct target of miR-133b-3p, and the overexpression of miR-133b-3p reduces <i>CDIP1</i> expression. Additionally, <i>CDIP1</i> silencing suppresses cardiomyocyte hypertrophy and apoptosis induced by Ang II. In summary, these results suggest that miR-133b-3p may serve as a potential diagnostic marker for cardiac hypertrophy and that the upregulation of miR-133b-3p inhibits cardiac hypertrophy by targeting <i>CDIP1</i>.</p>","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-02-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143405124","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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
Ageing-associated gut dysbiosis deteriorates mouse cognition. 衰老相关的肠道失调会使小鼠认知能力恶化。
IF 3.3 2区 生物学
Acta biochimica et biophysica Sinica Pub Date : 2025-02-13 DOI: 10.3724/abbs.2024217
Huihui Ju, Yile Zhou, Wanting Wei, Yan Hu, Hongwei Fang, Zhouyi Chen, Xia Sun, Yi Shi, Hao Fang
{"title":"Ageing-associated gut dysbiosis deteriorates mouse cognition.","authors":"Huihui Ju, Yile Zhou, Wanting Wei, Yan Hu, Hongwei Fang, Zhouyi Chen, Xia Sun, Yi Shi, Hao Fang","doi":"10.3724/abbs.2024217","DOIUrl":"https://doi.org/10.3724/abbs.2024217","url":null,"abstract":"<p><p>Ageing is an independent factor for cognitive dysfunction. Ageing-associated alterations in the gut microbiota also affect cognition. The present study is designed to investigate changes in the gut microbiota and their participation in ageing-associated cognitive impairment. Both 10-week-old and 18-month-old mice are used. Mouse cognition is examined by novel object recognition and T-maze tests. Mouse feces are collected for sequencing and transplantation. Protein expression in the mouse intestine and hippocampus is studied using immunohistochemistry and immunofluorescence staining. Senescent neurons are induced by hydrogen peroxide <i>in vitro</i>. The cell lysates are used for western blot analysis and adenosine triphosphate (ATP) measurement. Our results show that 18-month-old mice exhibit cognitive dysfunction compared with young mice. In aged mice, transplanting the microbiota of young mice increases the protein presence of synaptophysin in the hippocampus and partially restores cognition. The protein expressions of mucin-2 and E-cadherin in the intestine are reduced in aged mice but are increased by transplantation. Gut microbiota analyses reveal that the reduced abundance of the microbe <i>Bacilli-Lactobacillales-Lactobacillaceae-Lactobacillus</i> in aged mice is restored by transplantation. Fecal microbiota transplantation in young mice increases the serum level of acetic acid in aged mice. Hydrogen peroxide stimulation induces senescence and reduces the protein expression levels of synaptophysin and acetyl-coenzyme A synthetase member 2 (ACSS2) in primary neurons. Incubation with acetic acid upregulates the protein expressions of ACSS2 and synaptophysin and further increases ATP production in senescent neurons. In summary, gut microbiota transplantation increases the abundance of <i>Lactobacillales</i>, elevates serum acetic acid level, and improves cognitive function in aged mice. Gut microbiota transplantation has therapeutic importance for ageing-associated cognitive decline.</p>","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-02-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143405123","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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
Proline/serine-rich coiled-coil protein 1 alleviates pyroptosis in murine bone marrow-derived macrophages. 富含脯氨酸/丝氨酸的螺旋蛋白1减轻小鼠骨髓源性巨噬细胞的焦亡。
IF 3.3 2区 生物学
Acta biochimica et biophysica Sinica Pub Date : 2025-02-11 DOI: 10.3724/abbs.2025012
Qiao Wu, Qianqian Wang, Kexin Hu, Tiantian Luo, Jichen Liu, Yazhi Xue, Ling Li, Cuiqi Yang, Rongzhan Lin, Hangyu Pan, Jinhao Wang, Zhigang Guo
{"title":"Proline/serine-rich coiled-coil protein 1 alleviates pyroptosis in murine bone marrow-derived macrophages.","authors":"Qiao Wu, Qianqian Wang, Kexin Hu, Tiantian Luo, Jichen Liu, Yazhi Xue, Ling Li, Cuiqi Yang, Rongzhan Lin, Hangyu Pan, Jinhao Wang, Zhigang Guo","doi":"10.3724/abbs.2025012","DOIUrl":"https://doi.org/10.3724/abbs.2025012","url":null,"abstract":"<p><p>Pyroptosis is a regulated inflammatory cell death process that plays an essential role in various diseases. This study investigates the role of proline/serine-rich coiled-coil protein 1 (PSRC1) in pyroptosis and inflammation in macrophages. This study reports that PSRC1 expression is decreased in pyroptotic macrophages and that knockout of <i>PSRC1</i> exacerbates pyroptosis and inflammation. <i>PSRC1</i> overexpression alleviates pyroptosis and inflammation in macrophages. RNA-seq analysis reveals that PSRC1 regulates the expression of genes involved in the extracellular matrix (ECM). Specifically, PSRC1 downregulates the expression of periostin (POSTN), an ECM component. Knockdown of <i>POSTN</i> suppresses macrophage pyroptosis mediated by low expression of PSRC1. These findings suggest that PSRC1 can alleviate pyroptosis and inflammation in bone marrow-derived macrophages (BMDMs) by regulating the ECM and negatively regulating POSTN. This study provides insights into the role of PSRC1 in macrophage pyroptosis and identifies a potential target for the treatment of inflammatory diseases. Further research is needed to confirm these findings <i>in vivo</i> and in various disease models.</p>","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-02-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143397584","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
miR-199a-3p suppresses Vldlr expression to promote cardiomyocyte proliferation. miR-199a-3p抑制Vldlr表达,促进心肌细胞增殖。
IF 3.3 2区 生物学
Acta biochimica et biophysica Sinica Pub Date : 2025-02-11 DOI: 10.3724/abbs.2024240
Rui Jiang, Lijuan Pei, Hongjie Zhang, Fenglian He, Yuhan Min, Xinhang Li, Ke Wei
{"title":"<i>miR-199a-3p</i> suppresses <i>Vldlr</i> expression to promote cardiomyocyte proliferation.","authors":"Rui Jiang, Lijuan Pei, Hongjie Zhang, Fenglian He, Yuhan Min, Xinhang Li, Ke Wei","doi":"10.3724/abbs.2024240","DOIUrl":"https://doi.org/10.3724/abbs.2024240","url":null,"abstract":"<p><p>The proliferative capacity of cardiomyocytes is limited in adult mammals, and replacing lost tissue following acute ischemic injury is challenging. Previous studies have demonstrated that <i>miR-199a-3p</i> can promote cardiomyocyte proliferation, but the exact mechanism by which this occurs remains unclear, although multiple targets of <i>miR-199a-3p</i> have been identified. We recently showed that very-low-density-lipoprotein receptor (Vldlr) inhibits cardiomyocyte proliferation, and in this study we aim to test whether <i>Vldlr</i> is a functional target gene of <i>miR-199a-3p</i>. 3'UTR reporter assays demonstrate that <i>miR-199a-3p</i> directly binds to the 3'UTR of <i>Vldlr</i> and inhibits its translation. Overexpressing <i>Vldlr</i> blunts the pro-proliferative effect of <i>miR-199a-3p</i> on cardiomyocytes, suggesting that <i>Vldlr</i> is indeed a functional target of <i>miR-199a-3p</i>. Mechanistically, Vldlr reduces S807/811 phosphorylation of RB1, and inhibiting CDK4/6 to prevent RB1 phosphorylation can block the pro-proliferative effect of both <i>Vldlr</i> knockdown and <i>miR-199a-3p</i>, suggesting that RB1 phosphorylation is required for the cardiomyocyte proliferation induced by <i>miR-199a-3p</i> and <i>Vldlr</i> knockdown. The findings of this study reveal <i>Vldlr</i> as a novel functional target of <i>miR-199a-3p</i> in cardiomyocytes and identify RB1 as a downstream effector of cardiomyocyte proliferation. The identification of the role of the <i>miR-199a-3p</i>- <i>Vldlr</i>-RB1 axis in cardiomyocyte proliferation may provide potential therapeutic targets for cardiac regenerative medicine.</p>","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-02-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143389839","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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
Cannabidiol alleviates the inflammatory response in rats with traumatic brain injury through the PGE 2-EP2-cAMP-PKA signaling pathway. 大麻二酚通过PGE 2-EP2-cAMP-PKA信号通路减轻创伤性脑损伤大鼠的炎症反应。
IF 3.3 2区 生物学
Acta biochimica et biophysica Sinica Pub Date : 2025-02-08 DOI: 10.3724/abbs.2024183
Yan Cao, Hengxi Li, Jiali Li, Tenghan Ling, Aiping Yin, Xinyuan Luo, Ying Zhou, Jinghui Li, Hongyan Jiang, Huawei Wang, Li Yang, Haiying Wu, Ping Li
{"title":"Cannabidiol alleviates the inflammatory response in rats with traumatic brain injury through the PGE <sub>2</sub>-EP2-cAMP-PKA signaling pathway.","authors":"Yan Cao, Hengxi Li, Jiali Li, Tenghan Ling, Aiping Yin, Xinyuan Luo, Ying Zhou, Jinghui Li, Hongyan Jiang, Huawei Wang, Li Yang, Haiying Wu, Ping Li","doi":"10.3724/abbs.2024183","DOIUrl":"10.3724/abbs.2024183","url":null,"abstract":"<p><p>Traumatic brain injury (TBI) is a recognized global public health problem. However, there are still limitations in the available therapeutic approaches and a lack of clinically effective drugs. Therefore, an in-depth exploration of the secondary pathological mechanism of TBI and the identification of new effective drugs are urgently needed. Cannabidiol (CBD), a component derived from the cannabis plant, has potential therapeutic effects on neurological diseases and has received increasing attention. However, few reports on CBD intervention in TBI patients exist. Here, we use the Feeney free-fall method to establish a rat TBI model. CBD significantly improves neurological deficit scores, neuronal damage and blood-brain barrier permeability in rats and significantly inhibits the expressions of the brain injury markers S-100β and NSE. Mechanistically, CBD attenuates TBI-induced astrocyte activation, reduces inflammation, and attenuates the expressions of inflammatory prostaglandin system indicators. The use of TG6-10-1 (EP2 inhibitor) and H-89 (PKA inhibitor) indicates that CBD attenuates TBI-induced neurological damage via the PGE <sub>2</sub>-EP2-cAMP-PKA signaling pathway. Overall, this research provides a novel drug candidate for the treatment of clinical brain trauma.</p>","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":"758-769"},"PeriodicalIF":3.3,"publicationDate":"2025-02-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12130728/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143373457","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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
Corrigendum to: Vitamin B6 prevents Isocarbophos-induced posterior cerebral artery injury in offspring rats through up-regulating S1P receptor expression. 更正:维生素B6通过上调S1P受体的表达来预防子代大鼠异碳磷诱导的脑后动脉损伤。
IF 3.3 2区 生物学
Acta biochimica et biophysica Sinica Pub Date : 2025-01-25 DOI: 10.3724/abbs.2025088
Yanhua Liu, Kunli Yang, Ling Wang, Jinfang Yang, Yang Wang, Hu Luo, Peng Li, Yaling Yin
{"title":"Corrigendum to: Vitamin B6 prevents Isocarbophos-induced posterior cerebral artery injury in offspring rats through up-regulating S1P receptor expression.","authors":"Yanhua Liu, Kunli Yang, Ling Wang, Jinfang Yang, Yang Wang, Hu Luo, Peng Li, Yaling Yin","doi":"10.3724/abbs.2025088","DOIUrl":"https://doi.org/10.3724/abbs.2025088","url":null,"abstract":"","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-01-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144223930","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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
Safari in the RNA world: a special issue focused on RNA biogenesis, functions, and technologies. RNA世界中的游猎:关注RNA生物发生、功能和技术的特刊。
IF 3.3 2区 生物学
Acta biochimica et biophysica Sinica Pub Date : 2025-01-25 DOI: 10.3724/abbs.2024234
Ya-Nan Chang, Hong Cheng
{"title":"Safari in the RNA world: a special issue focused on RNA biogenesis, functions, and technologies.","authors":"Ya-Nan Chang, Hong Cheng","doi":"10.3724/abbs.2024234","DOIUrl":"10.3724/abbs.2024234","url":null,"abstract":"","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":"1-2"},"PeriodicalIF":3.3,"publicationDate":"2025-01-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11879657/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142930379","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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
Melanoma-derived versican reactivates tumor-associated macrophages by upregulating pyruvate carboxylase through TLR2-MyD88-RelB axis under normoxia. 在正常缺氧条件下,黑色素瘤来源的versican通过TLR2-MyD88-RelB轴上调丙酮酸羧化酶来重新激活肿瘤相关的巨噬细胞。
IF 3.3 2区 生物学
Acta biochimica et biophysica Sinica Pub Date : 2025-01-24 DOI: 10.3724/abbs.2025011
Yuxin Shu, Linmin Zhou, Jinqin Qian, Wei-Guo Zhu
{"title":"Melanoma-derived versican reactivates tumor-associated macrophages by upregulating pyruvate carboxylase through TLR2-MyD88-RelB axis under normoxia.","authors":"Yuxin Shu, Linmin Zhou, Jinqin Qian, Wei-Guo Zhu","doi":"10.3724/abbs.2025011","DOIUrl":"https://doi.org/10.3724/abbs.2025011","url":null,"abstract":"<p><p>Relieving hypoxia in the tumor microenvironment (TME) promotes innate and adaptive immunity. Our previous research demonstrated that reoxygenation of the TME promotes the phagocytosis and tumor-killing functions of tumor-associated macrophages (TAMs) by upregulating pyruvate carboxylase (PCB). However, the mechanism remains obscure. In the present study, we find that versican derived from melanoma cells binds to TLR2 and activates the downstream transcription factor RelB, which transcribes PCB under normoxia. Blocking the versican-TLR2-MyD88-RelB axis not only reverses the upregulation of PCB in TAMs but also hinders the clearance of tumor cells by TAMs. Our work suggests a pathway that modulates the functions of TAMs under normoxia, which could be harnessed for strengthening anti-tumor immunity.</p>","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-01-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143035545","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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
Continuous carbon source supply is essential for high rifamycin productivity of Amycolatopsis mediterranei in nitrate-stimulated fermentation revealed by a metabolomic study. 一项代谢组学研究显示,在硝酸盐刺激发酵中,持续的碳源供应是地中海Amycolatopsis利福霉素高产率的必要条件。
IF 3.3 2区 生物学
Acta biochimica et biophysica Sinica Pub Date : 2025-01-23 DOI: 10.3724/abbs.2024245
Qi Yan, Zhihui Shao, Chen Yang, Guoping Zhao
{"title":"Continuous carbon source supply is essential for high rifamycin productivity of <i>Amycolatopsis mediterranei</i> in nitrate-stimulated fermentation revealed by a metabolomic study.","authors":"Qi Yan, Zhihui Shao, Chen Yang, Guoping Zhao","doi":"10.3724/abbs.2024245","DOIUrl":"10.3724/abbs.2024245","url":null,"abstract":"<p><p><i>Amycolatopsis</i> <i>mediterranei</i> U32 is an industrial strain capable of producing therapeutically useful rifamycin SV. In early days of fermentation studies, nitrate was found to increase the yield of rifamycin along with globally, affecting both carbon and nitrogen metabolism in favor of antibiotic biosynthesis; thus, the <i>nitrate-stimulating effect</i> (NSE) hypothesis was proposed. Although GlnR is likely the master regulator of the pleotropic effect of NSE, the global metabolism affected by NSE has never been systematically examined. In this study, we use mass spectrometry-based metabolomics to quantitatively monitor the metabolomic responses of <i>A</i>. <i>mediterranei</i> U32 to nitrate supplementation. The concentrations of many metabolites involved in central carbon metabolism, including glucose 6-phosphate, glucose 1-phosphate, UDP-glucose, and acetyl-coenzyme A, decrease significantly after the addition of 80 mM potassium nitrate to the medium. We find that the rifamycin SV production yield could be increased by the addition of glucose during the logarithmic growth phase. Moreover, at multiple time points during glucose supplementation in the mid- and late-exponential phases, the yield of rifamycin SV further increases, reaching 354.3%. Quantitative real-time PCR assays of the key genes corresponding to the synthesis of the rifamycin SV precursor combined with data from metabolomics analysis confirm that carbon source deficiency is compensated for after glucose supplementation and that the expression of genes involved in the pathway of 3-amino-5-hydroxybenzoic acid synthesis by UDP-glucose and glutamine is significantly increased. This preliminary exploration of dynamic metabolomic profiles has the potential to increase our understanding of the NSE.</p>","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":"738-748"},"PeriodicalIF":3.3,"publicationDate":"2025-01-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12130708/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143027691","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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
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