Biochimica et biophysica acta. Molecular cell research最新文献

{"title":"Fe-S biogenesis by SMS and SUF pathways: A focus on the assembly step","authors":"Macha Dussouchaud ,&nbsp;Frédéric Barras ,&nbsp;Sandrine Ollagnier de Choudens","doi":"10.1016/j.bbamcr.2024.119772","DOIUrl":"10.1016/j.bbamcr.2024.119772","url":null,"abstract":"<div><p>Fe<img>S clusters are prosthetic groups present in all organisms. Proteins with Fe<img>S centers are involved in most cellular processes. ISC and SUF are machineries necessary for the formation and insertion of Fe<img>S in proteins. Recently, a phylogenetic analysis on more than 10,000 genomes of prokaryotes have uncovered two new systems, MIS and SMS, which were proposed to be ancestral to ISC and SUF. SMS is composed of SmsBC, two homologs of SufBC(D), the scaffolding complex of SUF. In this review, we will specifically focus on the current knowledge of the SUF system and on the new perspectives given by the recent discovery of its ancestor, the SMS system.</p></div>","PeriodicalId":8754,"journal":{"name":"Biochimica et biophysica acta. Molecular cell research","volume":null,"pages":null},"PeriodicalIF":4.6,"publicationDate":"2024-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0167488924001150/pdfft?md5=33bc6b5ef968b753dd8a6c051d252fdc&pid=1-s2.0-S0167488924001150-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141261504","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}

{"title":"Wnt/β-catenin signaling inhibits oxidative stress-induced ferroptosis to improve interstitial cystitis/bladder pain syndrome by reducing NF-κB","authors":"Weilin Fang ,&nbsp;Xin Song ,&nbsp;Hailong Li ,&nbsp;Fanguo Meng ,&nbsp;Tingting Lv ,&nbsp;Jin Huang ,&nbsp;Xiang Ji ,&nbsp;Jianwei Lv ,&nbsp;Zhikang Cai ,&nbsp;Zhong Wang","doi":"10.1016/j.bbamcr.2024.119766","DOIUrl":"10.1016/j.bbamcr.2024.119766","url":null,"abstract":"<div><h3>Background</h3><p>Interstitial cystitis/bladder pain syndrome (IC/BPS) is a bladder syndrome of unknown etiology. Reactive oxygen species (ROS) plays a major role in ferroptosis and bladder dysfunction of IC/BPS, while the role of ferroptosis in IC/BPS progression is still unclear. This study aims to investigate the role and mechanism of ROS-induced ferroptosis in IC/BPS using cell and rat model.</p></div><div><h3>Methods</h3><p>We collected IC/BPS patient bladder tissue samples and established a LPS-induced IC/BPS rat model (LRM). The level of oxidative stress and ferroptosis in IC/BPS patients and LRM rats was analyzed. Function and regulatory mechanism of ferroptosis in IC/BPS were explored by <em>in vitro</em> and <em>in vivo</em> experiments.</p></div><div><h3>Results</h3><p>The patients with IC/BPS showed mast cells and inflammatory cells infiltration in bladder epithelial tissues. Expression of NRF2 was up-regulated, and GPX4 was decreased in IC/BPS patients compared with normal tissues. IC model cells underwent oxidative stress, which induced ferroptosis. These above results were validated in LRM rat models, and inhibition of ferroptosis ameliorated bladder dysfunction in LRM rats. Wnt/β-catenin signaling was deactivated in IC/BPS patients and animals, and activation of Wnt/β-catenin signaling reduced cellular free radical production, thereby inhibited ferroptosis in IC model cells. Mechanistically, the Wnt/β-catenin signaling pathway inhibited oxidative stress-induced ferroptosis by down-regulating NF-κB, thus contributing to recover IC/BPS both <em>in vitro</em> and <em>in vivo</em>.</p></div><div><h3>Conclusions</h3><p>We demonstrate for the first time that oxidative stress-induced ferroptosis plays an important role in the pathology of IC/BPS. Mechanistically, the Wnt/β-catenin signaling suppressed oxidative stress-induced ferroptosis by down-regulating NF-κB to improve bladder injury in IC/BPS.</p></div>","PeriodicalId":8754,"journal":{"name":"Biochimica et biophysica acta. Molecular cell research","volume":null,"pages":null},"PeriodicalIF":4.6,"publicationDate":"2024-05-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141185997","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}

{"title":"HRD1-mediated ubiquitination of HDAC2 regulates PPARα-mediated autophagy and alleviates metabolic-associated fatty liver disease","authors":"Yina Wang ,&nbsp;Yuanguo Chen ,&nbsp;Xiao Xiao ,&nbsp;Silei Deng ,&nbsp;Jingjie Kuang ,&nbsp;Yayong Li","doi":"10.1016/j.bbamcr.2024.119765","DOIUrl":"10.1016/j.bbamcr.2024.119765","url":null,"abstract":"<div><h3>Background</h3><p>Metabolic-associated fatty liver disease (MAFLD) is a leading cause of chronic liver disease worldwide. Autophagy plays a pivotal role in lipid metabolism; however, the mechanism underlying the reduced autophagic activity in MAFLD remains elusive.</p></div><div><h3>Methods</h3><p>Autophagy was monitored by TUNEL assay and immunofluorescence staining of LC3. The expression of autophagy-related proteins, PPARα, HDAC2, and HRD1 was detected by Western blot. The association between HDAC2 and PPARα promoter was assessed by chromatin immunoprecipitation (ChIP) and dual-luciferase assays, and the HRD1-mediated ubiquitin-proteasomal degradation of HDAC2 was detected by co-immunoprecipitation (co-IP). The in vitro findings were validated in a hypoxia-induced MAFLD mouse model. Histological changes, fibrosis, and apoptosis in liver tissues were detected by hematoxylin and eosin staining, Masson's trichrome staining, and TUNEL assay. The immunoreactivities of key molecules were examined by IHC analysis.</p></div><div><h3>Results</h3><p>Hypoxia-suppressed autophagy in hepatocytes. Hypoxic exposure downregulated HRD1 and PPARα, while upregulating HDAC2 in hepatocytes. Overexpression of PPARα promoted hepatic autophagy, while knocking down HDAC2 or overexpressing HRD1 reduced hypoxia-suppressed autophagy in hepatocytes. Mechanistically, HDAC2 acted as a transcriptional repressor of PPARα, and HRD1 mediated the degradation of HDAC2 through the ubiquitin-proteasome pathway. Functional studies further showed that hypoxia-suppressed hepatic autophagy via the HRD1/HDAC2/PPARα axis in vitro and in vivo.</p></div><div><h3>Conclusion</h3><p>HRD1-mediated ubiquitination of HDAC2 regulates PPARα-mediated autophagy and ameliorates hypoxia-induced MAFLD.</p></div>","PeriodicalId":8754,"journal":{"name":"Biochimica et biophysica acta. Molecular cell research","volume":null,"pages":null},"PeriodicalIF":5.1,"publicationDate":"2024-05-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141178283","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}

{"title":"Akkermansia muciniphila ameliorates colonic injury in mice with DSS-induced acute colitis by blocking macrophage pro-inflammatory phenotype switching via the HDAC5/DAB2 axis","authors":"Yan Miao ,&nbsp;Mian Wang ,&nbsp;Hao Sun ,&nbsp;Yujie Zhang ,&nbsp;Wei Zhou ,&nbsp;Wanli Yang ,&nbsp;Lili Duan ,&nbsp;Liaoran Niu ,&nbsp;Zhenshun Li ,&nbsp;Junfeng Chen ,&nbsp;Yiding Li ,&nbsp;Aqiang Fan ,&nbsp;Qibin Xie ,&nbsp;Siyu Wei ,&nbsp;Han Bai ,&nbsp;Chenyang Wang ,&nbsp;Qian Chen ,&nbsp;Xiangjie Wang ,&nbsp;Yunlong Li ,&nbsp;Jinqiang Liu ,&nbsp;Liu Hong","doi":"10.1016/j.bbamcr.2024.119751","DOIUrl":"10.1016/j.bbamcr.2024.119751","url":null,"abstract":"<div><p><em>Akkermansia muciniphila</em> (<em>A. muciniphila</em>), a probiotic, has been linked to macrophage phenotypic polarization in different diseases. However, the role and mechanisms of <em>A. muciniphila</em> in regulating macrophage during ulcerative colitis (UC) are not clear. This research aimed to examine the impact of <em>A. muciniphila</em> on dextran sulfate sodium (DSS)-induced acute colitis and elucidate the underlying mechanism related to macrophage phenotypic polarization. <em>A. muciniphila</em> inhibited weight loss, increased disease activity index, and ameliorated inflammatory injury in colonic tissues in mice induced with DSS. Furthermore, <em>A. muciniphila</em> reduced macrophage M1 polarization and ameliorated epithelial barrier damage in colonic tissues of DSS-induced mice through inhibition of histone deacetylase 5 (HDAC5). In contrast, the effect of <em>A. muciniphila</em> was compromised by HDAC5 overexpression. HDAC5 deacetylated H3K9ac modification of the disabled homolog 2 (DAB2) promoter, which led to repressed DAB2 expression. DAB2 overexpression blocked HDAC5-induced pro-inflammatory polarization of macrophages, whereas knockdown of DAB2 resulted in the loss of effects of <em>A. muciniphila</em> against colonic injury in DSS-induced mice. Taken together, <em>A. muciniphila</em>-induced loss of HDAC5 hampered the deacetylation of DAB2 and enhanced the expression of DAB2. Our findings propose that <em>A. muciniphila</em> may be a possible probiotic agent for alleviating DSS-induced acute colitis.</p></div>","PeriodicalId":8754,"journal":{"name":"Biochimica et biophysica acta. Molecular cell research","volume":null,"pages":null},"PeriodicalIF":5.1,"publicationDate":"2024-05-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141080423","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}

{"title":"Mitophagy at the crossroads of cancer development: Exploring the role of mitophagy in tumor progression and therapy resistance","authors":"K. Deepak ,&nbsp;Pritam Kumar Roy ,&nbsp;Chandan Kanta Das ,&nbsp;Budhaditya Mukherjee ,&nbsp;Mahitosh Mandal","doi":"10.1016/j.bbamcr.2024.119752","DOIUrl":"10.1016/j.bbamcr.2024.119752","url":null,"abstract":"<div><p>Preserving a functional mitochondrial network is crucial for cellular well-being, considering the pivotal role of mitochondria in ensuring cellular survival, especially under stressful conditions. Mitophagy, the selective removal of damaged mitochondria through autophagy, plays a pivotal role in preserving cellular homeostasis by preventing the production of harmful reactive oxygen species from dysfunctional mitochondria. While the involvement of mitophagy in neurodegenerative diseases has been thoroughly investigated, it is becoming increasingly evident that mitophagy plays a significant role in cancer biology. Perturbations in mitophagy pathways lead to suboptimal mitochondrial quality control, catalyzing various aspects of carcinogenesis, including establishing metabolic plasticity, stemness, metabolic reconfiguration of cancer-associated fibroblasts, and immunomodulation. While mitophagy performs a delicate balancing act at the intersection of cell survival and cell death, mounting evidence indicates that, particularly in the context of stress responses induced by cancer therapy, it predominantly promotes cell survival. Here, we showcase an overview of the current understanding of the role of mitophagy in cancer biology and its potential as a target for cancer therapy. Gaining a more comprehensive insight into the interaction between cancer therapy and mitophagy has the potential to reveal novel targets and pathways, paving the way for enhanced treatment strategies for therapy-resistant tumors in the near future.</p></div>","PeriodicalId":8754,"journal":{"name":"Biochimica et biophysica acta. Molecular cell research","volume":null,"pages":null},"PeriodicalIF":5.1,"publicationDate":"2024-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141080425","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}

{"title":"UKLF/PCBP2 axis governs the colorectal cancer development by transcriptionally activating SLC39A4","authors":"Yunze Li,&nbsp;Lina Liu","doi":"10.1016/j.bbamcr.2024.119755","DOIUrl":"10.1016/j.bbamcr.2024.119755","url":null,"abstract":"<div><p>Colorectal cancer (CRC) is one of the most prevalent malignant tumors with limited treatment options. Therefore, there is an urgent need to investigate new therapeutic targets against CRC. Ubiquitous Kruppel-like factor (UKLF) is involved in various cancer processes, but its effect and detailed molecular mechanism in CRC are not yet fully understood. Here, this study aimed to investigate the function and mechanism of UKLF in the development of CRC. The results showed that UKLF was highly expressed in CRC tissues from clinical patients and its high expression was related to poor prognosis. UKLF promoted cell proliferation, migration and invasion, and inhibited cell apoptosis. The promotion effect of UKLF on tumor growth was further confirmed in vivo. As far as the mechanism was concerned, poly (C) binding protein 2 (PCBP2) was verified to bind to the 3′-UTR of UKLF mRNA and enhance its mRNA stability. Moreover, UKLF modulated the expression of solute carrier family 39 member 4 (SLC39A4) at the transcriptional level. Taken together, these findings elucidated the regulatory mechanism of UKLF and uncovered the importance of the PCBP2/UKLF/SLC39A4 pathway. The targeting of UKLF may be a novel direction for molecular-targeted CRC therapy.</p></div>","PeriodicalId":8754,"journal":{"name":"Biochimica et biophysica acta. Molecular cell research","volume":null,"pages":null},"PeriodicalIF":5.1,"publicationDate":"2024-05-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141070055","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}

{"title":"Autophagy and metabolic aging: Current understanding and future applications","authors":"Sana Raza","doi":"10.1016/j.bbamcr.2024.119753","DOIUrl":"10.1016/j.bbamcr.2024.119753","url":null,"abstract":"<div><p>“Metabolic aging” refers to the gradual decline in cellular metabolic function across various tissues due to defective hormonal signaling, impaired nutrient sensing, mitochondrial dysfunction, replicative stress, and cellular senescence. While this process usually corresponds with chronological aging, the recent increase in metabolic diseases and cancers occurring at younger ages in humans suggests the premature onset of cellular fatigue and metabolic aging. Autophagy, a cellular housekeeping process facilitated by lysosomes, plays a crucial role in maintaining tissue rejuvenation and health. However, various environmental toxins, hormones, lifestyle changes, and nutrient imbalances can disrupt autophagy in humans. In this review, we explore the connection between autophagy and cellular metabolism, its regulation by extrinsic factors and its modulation to prevent the early onset of metabolic aging.</p></div>","PeriodicalId":8754,"journal":{"name":"Biochimica et biophysica acta. Molecular cell research","volume":null,"pages":null},"PeriodicalIF":5.1,"publicationDate":"2024-05-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141065364","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}

{"title":"Fe-S cluster homeostasis and beyond: The multifaceted roles of IscR","authors":"Erin L. Mettert,&nbsp;Patricia J. Kiley","doi":"10.1016/j.bbamcr.2024.119749","DOIUrl":"10.1016/j.bbamcr.2024.119749","url":null,"abstract":"<div><p>The role of IscR in regulating the transcription of genes involved in Fe-S cluster homeostasis has been well established for the model organism <em>Escherichia coli</em> K12. In this bacterium, IscR coordinates expression of the Isc and Suf Fe-S cluster assembly pathways to meet cellular Fe-S cluster demands shaped by a variety of environmental cues. However, since its initial discovery nearly 25 years ago, there has been growing evidence that IscR function extends well beyond Fe-S cluster homeostasis, not only in <em>E. coli</em>, but in bacteria of diverse lifestyles. Notably, pathogenic bacteria have exploited the ability of IscR to respond to changes in oxygen tension, oxidative and nitrosative stress, and iron availability to navigate their trajectory in their respective hosts as changes in these cues are frequently encountered during host infection. In this review, we highlight these broader roles of IscR in different cellular processes and, in particular, discuss the importance of IscR as a virulence factor for many bacterial pathogens.</p></div>","PeriodicalId":8754,"journal":{"name":"Biochimica et biophysica acta. Molecular cell research","volume":null,"pages":null},"PeriodicalIF":5.1,"publicationDate":"2024-05-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141046649","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}

{"title":"On the path to [Fe-S] protein maturation: A personal perspective","authors":"Dennis R. Dean","doi":"10.1016/j.bbamcr.2024.119750","DOIUrl":"10.1016/j.bbamcr.2024.119750","url":null,"abstract":"<div><p><em>Azotobacter vinelandii</em> is a genetically tractable Gram-negative proteobacterium able to fix nitrogen (N2) under aerobic growth conditions. This narrative describes how biochemical-genetic approaches using <em>A. vinelandii</em> to study nitrogen fixation led to the formulation of the “scaffold hypothesis” for the assembly of both simple and complex [Fe-S] clusters associated with biological nitrogen fixation. These studies also led to the discovery of a parallel, but genetically distinct, pathway for maturation of [Fe-S] proteins that support central metabolic processes.</p></div>","PeriodicalId":8754,"journal":{"name":"Biochimica et biophysica acta. Molecular cell research","volume":null,"pages":null},"PeriodicalIF":5.1,"publicationDate":"2024-05-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140955556","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}

{"title":"Overexpression of PEX14 results in mistargeting to mitochondria, accompanied by organelle fragmentation and clustering in human embryonic kidney cells","authors":"Renate L.M. Jansen ,&nbsp;Rinse de Boer ,&nbsp;Eline M.F. de Lange ,&nbsp;Janet Koster ,&nbsp;Rifka Vlijm ,&nbsp;Hans R. Waterham ,&nbsp;Ida J. van der Klei","doi":"10.1016/j.bbamcr.2024.119754","DOIUrl":"10.1016/j.bbamcr.2024.119754","url":null,"abstract":"<div><p>Peroxisome biogenesis disorders are caused by pathogenic variants in genes involved in biogenesis and maintenance of peroxisomes. However, mitochondria are also often affected in these diseases. Peroxisomal membrane proteins, including PEX14, have been found to mislocalise to mitochondria in cells lacking peroxisomes. Recent studies indicated that this mislocalisation contributes to mitochondrial abnormalities in PEX3-deficient patient fibroblasts cells. Here, we studied whether mitochondrial morphology is also affected in PEX3-deficient HEK293 cells and whether PEX14 mislocalises to mitochondria in these cells. Using high-resolution imaging techniques, we show that although endogenous PEX14 mislocalises to mitochondria, mitochondrial morphology was normal in PEX3-KO HEK293 cells. However, we discovered that overexpression of tagged PEX14 in wild-type HEK293 cells resulted in its mitochondrial localisation, accompanied by altered mitochondrial morphology. Our data indicate that overexpression of tagged PEX14 alone directly or indirectly cause mitochondrial abnormalities in cells containing peroxisomes.</p></div>","PeriodicalId":8754,"journal":{"name":"Biochimica et biophysica acta. Molecular cell research","volume":null,"pages":null},"PeriodicalIF":5.1,"publicationDate":"2024-05-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0167488924000971/pdfft?md5=2e64559a7f7cdf9e47022af4093cfc24&pid=1-s2.0-S0167488924000971-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140955496","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}