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Phylogenetic and sequence analyses of insect transferrins suggest that only transferrin 1 has a role in iron homeostasis

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Insect Science 2021年第2期28卷 495-508页

作者： Diana G.Najera Neal T.Dittmer Jacob J.Weber Michael R.Kanost Maureen J.Gorman Department of Biochemistry and Molecular Biophysics Kansas State UniversityManhattanKansasUSA

iron is essential to life,but surprisingly little is known about how iron is managed in nonvertebrate animals.In mammals,the well-characterized transferrins bind iron and are involved in iron transport or immunity,whereas other members of the transferrin family do not have a role in iron homeostasis.In insects,the functions of transferrins are still poorly understood.The goals of this project were to identify the transferrin genes in a diverse set of insect species,resolve the evolutionary relationships among these genes,and predict which of the transferrins are likely to have a role in iron homeostasis.Our phylogenetic analysis of transferrins from 16 orders of insects and two orders of noninsect hexapods demonstrated that there are four orthologous groups of insect transferrins.Our analysis suggests that transferrin 2 arose prior to the origin of insects,and transferrins/,i,and 4 arose early in insect evolution.Primary sequence analysis of each of the insect transferrins was used to predict signal peptides,carboxyl-terminal transmembrane regions,GPI-anchors,and iron binding.Based on this analysis,we suggest that transferrins 2,and 4 are unlikely to play a major role in iron homeostasis.In contrast,the transferrin 1 orthologs are predicted to be secreted,soluble,iron-binding proteins.We conclude that transferrin 1 orthologs are the most likely to play an important role in iron homeostasis.Interestingly,it appears that the louse,aphid,and thrips lineages have lost the transferrin 1 gene and,thus,have evolved to manage iron without transferrins.

关键词： hemolymph insect iron homeostasis melanotransferrin phylogeny transferrin

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Biochemistry of mammalian ferritins in the regulation of cellular iron homeostasis and oxidative responses

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Science China(Life Sciences) 2021年第3期64卷 352-362页

作者： Jianlin Zhang Xuehui Chen Juanji Hong Aifa Tang Yang Liu Ni Xie Guohui Nie Xiyun Yan Minmin Liang Guangdong Provincial Key Laboratory of Brain Function and Disease Zhongshan School of MedicineSun Yat-sen UniversityGuangzhou 510080China Institute of Post-transcriptional Medicine Shenzhen Second People’s HospitalThe First Affiliatied Hospital of Shenzhen UniversityHealth Science CenterShenzhen 518035China CAS Engineering Laboratory for Nanozyme Key Laboratory of Protein and Peptide PharmaceuticalInstitute of BiophysicsChinese Academy of SciencesBeijing 100101China Experimental Center of Advanced Materials School of Materials Science&EngineeringBeijing Institute of TechnologyBeijing 100081China

Ferritin,an iron-storage protein,regulates cellular iron metabolism and oxidative stress.The ferritin structure is characterized as a spherical cage,inside which large amounts of iron are deposited in a safe,compact and bioavailable form.All ferritins readily catalyze Fe(II)oxidation by peroxides at the ferroxidase center to prevent free Fe(II)from participating in oxygen free radical formation via Fenton chemistry.Thus,ferritin is generally recognized as a cytoprotective stratagem against intracellular oxidative damage.The expression of cytosolic ferritins is usually regulated by iron status and oxidative stress at both the transcriptional and post-transcriptional levels.The mechanism of ferritin-mediated iron recycling is far from clarified,though nuclear receptor co-activator 4(NCOA4)was recently identified as a cargo receptor for ferritin-based lysosomal degradation.Cytosolic ferritins are heteropolymers assembled by H-and L-chains in different proportions.The mitochondrial ferritins are homopolymers and distributed in restricted tissues.They play protective roles in mitochondria where heme-and Fe/S-enzymes are synthesized and high levels of ROS are produced.Genetic ferritin disorders are mainly related to the L-chain mutations,which generally cause severe movement diseases.This review is focused on the biochemistry and function of mammalian intracellular ferritin as the major iron-storage and anti-oxidation protein.

关键词： ferritin iron homeostasis oxidative responses antioxidant Fenton reaction

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An Arabidopsis ABC Transporter Mediates Phosphate Deficiency-Induced Remodeling of Root Architecture by Modulating iron homeostasis in Roots

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Molecular Plant 2017年第2期10卷 244-259页

作者： Jinsong Dong Miguel A. PiSeros Xiaoxuan Li Haibing Yang Yu Liu Angus S. Murphy Leon V. Kochian Dong Liu Ministry of Education Key Laboratory of Bioinformatics Center for Plant Biology School of Life Sciences Tsinghua University Beijing 100084 China USDA-ARS Robert Holley Center for Agriculture and Health Cornell University ithaca NY 14580 USA Department of Horticulture Purdue University West Lafayette IN 47907-2010 USA State Key Laboratory of Plant Physiology and Biochemistry College of Life Science Zhejiang University Hangzhou 310058 China Department of Plant Science and Landscape Architecture University of Maryland College Park MD 20742 USA GIobal Institute for Food Security University of Saskatchewan Saskatoon S7N 4J8 Canada

The remodeling of root architecture is a major developmental response of plants to phosphate （Pi） deficiency and is thought to enhance a plant＇s ability to forage for the available Pi in topsoil. The underlying mechanism controlling this response, however, is poorly understood. In this study, we identified an Arabidopsis mutant, hps 10 （hypersensitive to Pi starvation 10）, which is morphologically normal under Pi sufficient condition but shows increased inhibition of primary root growth and enhanced production of lateral roots under Pi defi- ciency, hpslO is a previously identified allele （als3-3） of the ALUMINUM SENSITIVE3 （ALS3） gene, which is involved in plant tolerance to aluminum toxicity. Our results show that ALS3 and its interacting protein AtSTAR1 form an ABC transporter complex in the tonoplast. This protein complex mediates a highly electro- genic transport in Xenopus oocytes. Under Pi deficiency, als3 accumulates higher levels of Fe3＋ in its roots than the wild type does. In Arabidopsis, LPR1 （LOW PHOSPHATE ROOT1） and LPR2 encode ferroxidases, which when mutated, reduce Fe3＋ accumulation in roots and cause root growth to be insensitive to Pi defi- ciency. Here, we provide compelling evidence showing that ALS3 cooperates with LPR1/2 to regulate Pi deficiency-induced remodeling of root architecture by modulating Fe homeostasis in roots.

关键词： phosphate deficiency root architecture iron homeostasis ABC transporter ALUMINUM SENSI-TIVE3 AtS TAR1

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The correlation between iron homeostasis and telomere maintenance

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Frontiers in Biology 2014年第5期9卷 347-355页

作者： Caiguo ZHANG Department of Biochemistry and Molecular Genetics University of Colorado School of Medicine Aurora CO 80045 USA

Eukaryotic organisms require iron to sustain genome stability, cell proliferation and development. Chromosomes contain telomeres to ensure complete replications and avoid fusions. Numerous evidences reveal that iron can act directly or indirectly on telomere maintenance. In human, disruption of systemic or cellular iron homeostasis is reportedly to cause serious health problems such as iron overload （hereditary hemochromatosis）, iron deficiency anemia, carcinogenesis and acceleration of aging process. These processes commonly associate with abnormal telomere length. Additionally, cells containing mutations in iron-containing proteins such as DNA polymerases （Pola, g, and ~）, regulator of telomere length 1 （RTEL1） and the small subunit of ribonucleotide reductases （RNRs） have abnormal telomere length. This review briefly summarizes current understandings on iron homeostasis and telomere maintenance in cancer and aging process, followed by discussing their direct and indirect correlation, and the possible regulatory mechanisms.

关键词： iron homeostasis telomere telomere maintenance cancer aging

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Two NPF transporters mediate iron long-distance transport and homeostasis in Arabidopsis

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Plant Communications 2021年第6期2卷 71-81页

作者： Si-Ying Chen Tian-Yu Gu Zi-Ai Qi Jing Yan Zi-Jun Fang Yu-Ting Lu Hui Li Ji-Ming Gong National Key Laboratory of Plant Molecular Genetics CAS Center for Excellence in Molecular Plant SciencesShanghai Institute of Plant Physiology and EcologyChinese Academy of SciencesShanghai 200032China University of the Chinese Academy of Sciences Beijing 100049China School of Life Science and Technology ShanghaiTech UniversityShanghai 201210China State Key Laboratory of Crop Stress Adaptation and Improvement School of Life SciencesHenan UniversityKaifeng 475004China

iron(Fe)transport and reallocation are essential to Fe homeostasis in plants,but it is unclear how Fe homeostasis is regulated,especially under stress.Here we report that NPF5.9 and its close homolog NPF5.8 redundantly regulate Fe transport and reallocation in Arabidopsis.NPF5.9 is highly upregulated in response to Fe deficiency.NPF5.9 expresses preferentially in vasculature tissues and localizes to the trans-Golgi network,and NPF5.8 showed a similar expression pattern.Long-distance Fe transport and allocation into aerial parts was significantly increased in NPF5.9-overexpressing lines.In the double mutant npf5.8 npf5.9,Fe loading in aerial parts and plant growth were decreased,which were partially rescued by Fe supplementation.Further analysis showed that expression of PYE,the negative regulator for Fe homeostasis,and its downstream target NAS4 were significantly altered in the double mutant.NPF5.9 and NPF5.8 were shown to also mediate nitrate uptake and transport,although nitrate and Fe application did not reciprocally affect each other.Our findings uncovered the novel function of NPF5.9 and NPF5.8 in long-distance Fe transport and homeostasis,and further indicated that they possibly mediate nitrate transport and Fe homeostasis independently in Arabidopsis.

关键词： NPF transporter iron homeostasis nitrate transport and allocation trans-Golgi network

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PGC-1α and HNF4α coordinately controls iron homeostasis via inhibition of hepcidin expression

PGC-1α and HNF4α coordinately controls iron homeostasis vi...

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第三届细胞结构与功能的信号基础研讨会

作者： Jinchun Qian and Chang Liu~* Jiangsu Key Laboratory for Molecular and Medical Biotechnology,College of Life Sciences,Nanjing Normal University,Nanjing 210046,China.

The small antibiotic peptide hepcidin has been shown to play a key role in iron homeostasis.When secreted into the blood,hepcidin systemically binds to and downregulates ferroportin,the basolateral iron exporter.Thus hepcidin negatively regulates the uptake of iron by transferrin,the major iron transport protein in the blood,and therefore limits erythropoiesis and is a major contributor to the anemia of chronic disease. Hepcidin expression is precisely controlled by environmental stimuli.During inflammation,the inflammatory cytokines,most notably interleukin-6,induce signaling and activation of STAT3,which binds to the promoter region of hepcidin to activate transcription.However,other factors mediating this process need to be elucidated.In the current study,we found transcriptional coactivator PGC-la and hepatocyte nuclear factor 4a(HNF4a) synergistically suppress the activity of the proximal region in hepcidin promoter.Transient cotransfection of the plasmids encoding these two genes also inhibits tunicamycin- and LPS-induced hepcidin expression in HepG2 cells.Furthermore,PGC-la is recruited to the hepcidin promoter.More importantly,we found those hepcidin agonists,such as IL-6,LPS and tunicamycin,inhibit PGC-la expression both in vitro and in vivo.These results indicate that in addition to activation of STAT3 pathway,PGC-la-HNF4a axle is inhibited during inflammation,which contributes to the elevation of hepcidin expression and iron deficiency.

关键词： hepcidin iron homeostasis PGC-1α inflammation

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Ferroptosis:a critical player and potential therapeutic target in traumatic brain injury and spinal cord injury

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Neural Regeneration Research 2023年第3期18卷 506-512页

作者： Qing-Sheng Li Yan-Jie Jia Department of Neurology The First Affiliated Hospital of Zhengzhou UniversityZhengzhouHenan ProvinceChina Academy of Medical Sciences Zhengzhou UniversityZhengzhouHenan ProvinceChina

Ferroptosis,a new non-necrotizing programmed cell death(PCD),is driven by iron-dependent phospholipid peroxidation.Ferroptosis plays a key role in secondary traumatic brain injury and secondary spinal cord injury and is closely related to inflammation,immunity,and chronic injuries.The inhibitors against ferroptosis effectively improve iron homeostasis,lipid metabolism,redox stabilization,neuronal remodeling,and functional recovery after trauma.In this review,we elaborate on the latest molecular mechanisms of ferroptosis,emphasize its role in secondary central nervous trauma,and update the medicines used to suppress ferroptosis following injuries.

关键词： ferroptosis immune response inflammation iron homeostasis lipid metabolism medicine programmed cell death spinal cord injury traumatic brain injury

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Primary Non-HFE Hemochromatosis:A Review

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Journal of Clinical and Translational Hepatology 2023年第4期11卷 925-931页

作者： Alla Turshudzhyan David C.Wu George Y.Wu Department of Medicine Division of Gastroenterology-HepatologyUniversity of Connecticut Health CenterFarmingtonCTUSA

iron homeostasis is a complex process in which iron uptake and use are tightly balanced.Primary Type 1 or HFE hemochromatosis results from homozygous mutations in the gene that encodes human homeostatic iron regulator(known as human factors engineering,HFE)protein,a regulator of hepcidin,and makes up approximately 90%of all hemochromatosis cases.However,four types of hemochromatosis do not involve the HFE gene.They are non-HFE hemochromatosis type 2A(HFE2,encoding HJV),type 2B(HAMP,encoding hepcidin),type 3(TFR2,encoding transferring receptor-2),and types 4A and B(SLC40A1,encoding ferroportin.NonHFE hemochromatosis is extremely rare.Pathogenic allele frequencies have been estimated to be 74/100,000 for type 2A,20/100,000 for type 2B,30/100,000 for type 3,and 90/100,000 for type 4 hemochromatosis.Current guidelines recommend that the diagnosis be made by ruling out HFE mutations,history,physical examination,laboratory values(ferritin and transferrin saturation),magnetic resonance or other imaging,and liver biopsy if needed.While less common,non-HFE hemochromatosis can cause iron overload as severe as the HFE type.In most cases,treatment involves phlebotomy and is successful if started before irreversible damage occurs.Early diagnosis and treatment are important because it prevents chronic liver disease.This review updates the mutations and their pathogenetic consequences,the clinical picture,diagnostic guidelines,and treatment of hemochromatosis.

关键词： Non-HFE Hemochromatosis Cirrhosis iron homeostasis

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The Effects of Treatment on Serum Hepcidin and iron homeostasis in HIV-1-Infected In-dividuals

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World Journal of AIDS 2015年第3期5卷 151-160页

作者： Joel da Cunha Luciana Morganti Ferreira Maselli Jovino dos Santos Ferreira Celso Spada Sergio Paulo Bydlowski Laboratory of Genetics and Molecular Hematology(LIM31) University of Sao Paulo School of Medicine(FMUSP)Sao PauloBrazil Clinical Analysis Department Health Sciences CenterFederal University of Santa Catarina(UFSC)FlorianopolisBrazil Research Division Pro-Sangue Hemocentro de Sao Paulo FoundationSao PauloBrazil Hemotherapy Service of University Hospital Federal University of Santa Catarina(UFSC)FlorianopolisBrazil

Background: Hepcidin is the principal regulator of iron absorption and its tissue distribution. Its correlation with iron homeostasis in individuals infected with human immunodeficiency virus type-1 (HIV-1) treated with different regimens of highly active antiretroviral therapy (HAART) was investigated. Methods: Serum hepcidin levels were determined in 448 volunteers. Of these, 372 were HIV-1-infected individuals, and 93 did not receive HAART (ART-naïve) while 279 received HAART consisting of a non-nucleoside reverse transcriptase inhibitor (NNRTI-based) and protease inhibitors (PI-based);both were used in association with a nucleoside reverse transcriptase inhibitor (NRTI). Seventy-six additional HIV-1 seronegative individuals were enrolled in the study. The following parameters were quantified: hematological parameters, iron biomarkers and markers of infection (CD4+ and CD8+ T-cells), and HIV-1 RNA (viral load). Results: Serum hepcidin, iron and ferritin levels, as well as the marker of infection, CD4+ T-cells, were significantly lower in the ART-naïve group compared with other groups. Additionally, transferrin saturation, iron binding capacity, hemoglobin level and erythrocyte level were not significantly different, and anemia was not observed in the different groups. Conclusions: HIV-1 infection affected serum hepcidin, iron and ferritin levels in the ART-naïve group, and the different HAART regimens restored the levels of hepcidin and iron homeostasis in HIV-1-infected individuals who have undetectable HIV-1 RNA levels.

关键词： Hepcidin iron homeostasis HIV-1 HAART ART-Naive CD4+ T-Cells

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Sorting nexin 3 exacerbates doxorubicin-induced cardiomyopathy via regulation of TFRC-dependent ferroptosis

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Acta Pharmaceutica Sinica B 2023年第12期13卷 4875-4892页

作者： Wenjing Yu Yuehuai Hu Zhiping Liu Kaiteng Guo Dinghu Ma Mingxia Peng Yuemei Wang Jing Zhang Xiaolei Zhang Panxia Wang Jiguo Zhang Peiqing Liu Jing Lu National and Local United Engineering Lab of Druggability and New Drugs Evaluation School of Pharmaceutical SciencesSun Yat-sen UniversityGuangzhou 510006China Guangdong Provincial Key Laboratory of New Drug Design and Evaluation Guangdong Province Engineering Laboratory for Druggability and New Drug EvaluationSchool of Pharmaceutical SciencesSun Yat-sen UniversityGuangzhou 510006China School of Pharmacy Jinan UniversityGuangzhou 510632China School of Pharmaceutical Sciences Shandong First Medical University&Shangdong Academy of Medical SciencesTaian 271016China

The clinical utilization of doxorubicin(Dox)in various malignancies is restrained by its major adverse effect:irreversible cardiomyopathy.Extensive studies have been done to explore the prevention of Dox cardiomyopathy.Currently,ferroptosis has been shown to participate in the incidence and development of Dox cardiomyopathy.Sorting Nexin 3(SNX3),the retromer-associated cargo binding protein with important physiological functions,was identified as a potent therapeutic target for cardiac hypertrophy in our previous study.However,few study has shown whether SNX3 plays a critical role in Dox-induced cardiomyopathy.In this study,a decreased level of SNX3 in Dox-induced cardiomyopathy was observed.Cardiac-specific Snx3 knockout(Snx3-cKO)significantly alleviated cardiomyopathy by downregulating Dox-induced ferroptosis significantly.SNX3 was further demonstrated to exacerbate Dox-induced cardiomyopathy via induction of ferroptosis in vivo and in vitro,and cardiac-specific Snx3 transgenic(Snx3-cTg)mice were more susceptible to Dox-induced feroptosis and cardiomyopathy.Mechanistically,SNX3 facilitated the recycling of transferrin 1 receptor(TFRC)via direct interaction,disrupting iron homeostasis,increasing the accumulation of iron,triggering ferroptosis,and eventually exacerbating Dox-induced cardiomyopathy.Overall,these findings established a direct SNX3-TFRC-ferroptosis positive regulatory axis in Dox-induced cardiomyopathy and suggested that targeting SNX3 provided a new effective therapeutic strategy for Dox-induced cardiomyopathy through TFRCdependentferroptosis.

关键词： SNX3 Ferroptosis TFRC Cardiomyopathy Doxorubicin iron homeostasis Cell death Mitochondria

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