Toll-like receptor 7 promotes the apoptosis of THP-1-derived macrophages through the CHOP-dependent pathway.
Identifieur interne : 000E96 ( Main/Exploration ); précédent : 000E95; suivant : 000E97Toll-like receptor 7 promotes the apoptosis of THP-1-derived macrophages through the CHOP-dependent pathway.
Auteurs : Xiaochen Yu [République populaire de Chine] ; Yang Wang [République populaire de Chine] ; Wenhui Zhao [République populaire de Chine] ; Haizhou Zhou [République populaire de Chine] ; Wei Yang [République populaire de Chine] ; Xiuru Guan [République populaire de Chine]Source :
- International journal of molecular medicine [ 1791-244X ] ; 2014.
Descripteurs français
- KwdFr :
- ARN messager (génétique), ARN messager (métabolisme), Aminoquinoléines (pharmacologie), Animaux, Apoptose (), Cellules rénales canines Madin-Darby, Chiens, Dexaméthasone (pharmacologie), Facteur de transcription CHOP (métabolisme), Grippe humaine (anatomopathologie), Grippe humaine (virologie), Humains, Interleukine-6 (métabolisme), Lignée cellulaire, Lipoprotéines LDL (métabolisme), Macrophages (), Macrophages (anatomopathologie), Macrophages (métabolisme), Macrophages (virologie), Médiateurs de l'inflammation (métabolisme), Protéines du choc thermique HSP70 (métabolisme), Protéines membranaires (métabolisme), Récepteur de type Toll-7 (génétique), Récepteur de type Toll-7 (métabolisme), Régulation positive (), Stress du réticulum endoplasmique (), Virus de la grippe A (), Virus de la grippe A (physiologie).
- MESH :
- anatomopathologie : Grippe humaine, Macrophages.
- génétique : ARN messager, Récepteur de type Toll-7.
- métabolisme : ARN messager, Facteur de transcription CHOP, Interleukine-6, Lipoprotéines LDL, Macrophages, Médiateurs de l'inflammation, Protéines du choc thermique HSP70, Protéines membranaires, Récepteur de type Toll-7.
- pharmacologie : Aminoquinoléines, Dexaméthasone.
- physiologie : Virus de la grippe A.
- virologie : Grippe humaine, Macrophages.
- Animaux, Apoptose, Cellules rénales canines Madin-Darby, Chiens, Humains, Lignée cellulaire, Macrophages, Régulation positive, Stress du réticulum endoplasmique, Virus de la grippe A.
English descriptors
- KwdEn :
- Aminoquinolines (pharmacology), Animals, Apoptosis (drug effects), Cell Line, Dexamethasone (pharmacology), Dogs, Endoplasmic Reticulum Stress (drug effects), HSP70 Heat-Shock Proteins (metabolism), Humans, Imiquimod, Inflammation Mediators (metabolism), Influenza A virus (drug effects), Influenza A virus (physiology), Influenza, Human (pathology), Influenza, Human (virology), Interleukin-6 (metabolism), Lipoproteins, LDL (metabolism), Macrophages (drug effects), Macrophages (metabolism), Macrophages (pathology), Macrophages (virology), Madin Darby Canine Kidney Cells, Membrane Proteins (metabolism), RNA, Messenger (genetics), RNA, Messenger (metabolism), Toll-Like Receptor 7 (genetics), Toll-Like Receptor 7 (metabolism), Transcription Factor CHOP (metabolism), Up-Regulation (drug effects).
- MESH :
- chemical , genetics : RNA, Messenger, Toll-Like Receptor 7.
- chemical , metabolism : HSP70 Heat-Shock Proteins, Inflammation Mediators, Interleukin-6, Lipoproteins, LDL, Membrane Proteins, RNA, Messenger, Toll-Like Receptor 7, Transcription Factor CHOP.
- chemical , pharmacology : Aminoquinolines, Dexamethasone.
- drug effects : Apoptosis, Endoplasmic Reticulum Stress, Influenza A virus, Macrophages, Up-Regulation.
- metabolism : Macrophages.
- pathology : Influenza, Human, Macrophages.
- physiology : Influenza A virus.
- virology : Influenza, Human, Macrophages.
- Animals, Cell Line, Dogs, Humans, Imiquimod, Madin Darby Canine Kidney Cells.
Abstract
Macrophage apoptosis is a prominent characteristic of advanced atherosclerotic plaques and leads to plaque destabilization. Certain studies have confirmed that influenza virus A (IVA) infection is related to acute myocardial infarction (AMI). However, it remains unknown as to whether this phenomenon is associated with Toll-like receptor (TLR)7, since single-stranded RNA (ssRNA) of IVA is a natural ligand of TLR7. Thus, in the present study, THP-1‑derived macrophages were infected with IVA or treated with imiquimod (IMQ) in the presence or absence of pre-treatment with oxidized low-density lipoprotein (oxLDL). The macrophages were pre-treated with oxLDL (5 µg/ml) for 24 h to mimic high lipid conditions. Cell viability and apoptosis were detected by 3-(4,5-dimethylthiazol-2-y-1)‑2,5-diphenyl-2H-tetrazolium bromide (MTT) assay and flow cytometry, respectively. Our results revealed that TLR7 played an important role in macrophage apoptosis and cytokine secretion. Both IVA infection and IMQ treatment increased TLR7 expression, as well as the secretion of pro-inflammatory cytokines [interleukin (IL)-6, monocyte chemotactic protein (MCP)-1] and apoptosis. However, this increase in cytokine secretion occurred independently of cell apoptosis. oxLDL had potential synergistic pro-apoptotic effects combined with TLR7 activation. To determine whether endoplasmic reticulum (ER) stress plays a role in cell apoptosis, the mRNA and protein expression of known markers of ER stress [glucose-regulated protein (GRP)78 and C/EBP homologous protein (CHOP)] was detected by reverse transcription PCR (RT-PCR), quantitative reverse transcription PCR (qRT-PCR) and western blot analysis. Our results revealed that apoptosis aggravated ER stress, as shown by the overexpression of the pro-apoptotic sensor, CHOP. In conclusion, our study demonstrates the converging role of oxLDL pre-treatment, IVA infection and IMQ in ER stress-induced cell apoptosis.
DOI: 10.3892/ijmm.2014.1833
PubMed: 24994112
Affiliations:
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China.</nlm:affiliation><country xml:lang="fr" wicri:curation="lc">République populaire de Chine</country><wicri:regionArea>Department of Laboratory Diagnostics, First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang 150001</wicri:regionArea><wicri:noRegion>Heilongjiang 150001</wicri:noRegion></affiliation></author><author><name sortKey="Zhou, Haizhou" sort="Zhou, Haizhou" uniqKey="Zhou H" first="Haizhou" last="Zhou">Haizhou Zhou</name><affiliation wicri:level="1"><nlm:affiliation>Department of Laboratory Diagnostics, First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang 150001, P.R. 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China.</nlm:affiliation><country xml:lang="fr" wicri:curation="lc">République populaire de Chine</country><wicri:regionArea>Department of Laboratory Diagnostics, First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang 150001</wicri:regionArea><wicri:noRegion>Heilongjiang 150001</wicri:noRegion></affiliation></author><author><name sortKey="Wang, Yang" sort="Wang, Yang" uniqKey="Wang Y" first="Yang" last="Wang">Yang Wang</name><affiliation wicri:level="1"><nlm:affiliation>Department of Laboratory Diagnostics, First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang 150001, P.R. China.</nlm:affiliation><country xml:lang="fr" wicri:curation="lc">République populaire de Chine</country><wicri:regionArea>Department of Laboratory Diagnostics, First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang 150001</wicri:regionArea><wicri:noRegion>Heilongjiang 150001</wicri:noRegion></affiliation></author><author><name sortKey="Zhao, Wenhui" sort="Zhao, Wenhui" uniqKey="Zhao W" first="Wenhui" last="Zhao">Wenhui Zhao</name><affiliation wicri:level="1"><nlm:affiliation>Department of Laboratory Diagnostics, First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang 150001, P.R. China.</nlm:affiliation><country xml:lang="fr" wicri:curation="lc">République populaire de Chine</country><wicri:regionArea>Department of Laboratory Diagnostics, First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang 150001</wicri:regionArea><wicri:noRegion>Heilongjiang 150001</wicri:noRegion></affiliation></author><author><name sortKey="Zhou, Haizhou" sort="Zhou, Haizhou" uniqKey="Zhou H" first="Haizhou" last="Zhou">Haizhou Zhou</name><affiliation wicri:level="1"><nlm:affiliation>Department of Laboratory Diagnostics, First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang 150001, P.R. China.</nlm:affiliation><country xml:lang="fr" wicri:curation="lc">République populaire de Chine</country><wicri:regionArea>Department of Laboratory Diagnostics, First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang 150001</wicri:regionArea><wicri:noRegion>Heilongjiang 150001</wicri:noRegion></affiliation></author><author><name sortKey="Yang, Wei" sort="Yang, Wei" uniqKey="Yang W" first="Wei" last="Yang">Wei Yang</name><affiliation wicri:level="1"><nlm:affiliation>Department of Laboratory Diagnostics, First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang 150001, P.R. China.</nlm:affiliation><country xml:lang="fr" wicri:curation="lc">République populaire de Chine</country><wicri:regionArea>Department of Laboratory Diagnostics, First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang 150001</wicri:regionArea><wicri:noRegion>Heilongjiang 150001</wicri:noRegion></affiliation></author><author><name sortKey="Guan, Xiuru" sort="Guan, Xiuru" uniqKey="Guan X" first="Xiuru" last="Guan">Xiuru Guan</name><affiliation wicri:level="1"><nlm:affiliation>Department of Laboratory Diagnostics, First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang 150001, P.R. China.</nlm:affiliation><country xml:lang="fr" wicri:curation="lc">République populaire de Chine</country><wicri:regionArea>Department of Laboratory Diagnostics, First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang 150001</wicri:regionArea><wicri:noRegion>Heilongjiang 150001</wicri:noRegion></affiliation></author></analytic><series><title level="j">International journal of molecular medicine</title><idno type="eISSN">1791-244X</idno><imprint><date when="2014" type="published">2014</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Aminoquinolines (pharmacology)</term><term>Animals</term><term>Apoptosis (drug effects)</term><term>Cell Line</term><term>Dexamethasone (pharmacology)</term><term>Dogs</term><term>Endoplasmic Reticulum Stress (drug effects)</term><term>HSP70 Heat-Shock Proteins (metabolism)</term><term>Humans</term><term>Imiquimod</term><term>Inflammation Mediators (metabolism)</term><term>Influenza A virus (drug effects)</term><term>Influenza A virus (physiology)</term><term>Influenza, Human (pathology)</term><term>Influenza, Human (virology)</term><term>Interleukin-6 (metabolism)</term><term>Lipoproteins, LDL (metabolism)</term><term>Macrophages (drug effects)</term><term>Macrophages (metabolism)</term><term>Macrophages (pathology)</term><term>Macrophages (virology)</term><term>Madin Darby Canine Kidney Cells</term><term>Membrane Proteins (metabolism)</term><term>RNA, Messenger (genetics)</term><term>RNA, Messenger (metabolism)</term><term>Toll-Like Receptor 7 (genetics)</term><term>Toll-Like Receptor 7 (metabolism)</term><term>Transcription Factor CHOP (metabolism)</term><term>Up-Regulation (drug effects)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>ARN messager (génétique)</term><term>ARN messager (métabolisme)</term><term>Aminoquinoléines (pharmacologie)</term><term>Animaux</term><term>Apoptose ()</term><term>Cellules rénales canines Madin-Darby</term><term>Chiens</term><term>Dexaméthasone (pharmacologie)</term><term>Facteur de transcription CHOP (métabolisme)</term><term>Grippe humaine (anatomopathologie)</term><term>Grippe humaine (virologie)</term><term>Humains</term><term>Interleukine-6 (métabolisme)</term><term>Lignée cellulaire</term><term>Lipoprotéines LDL (métabolisme)</term><term>Macrophages ()</term><term>Macrophages (anatomopathologie)</term><term>Macrophages (métabolisme)</term><term>Macrophages (virologie)</term><term>Médiateurs de l'inflammation (métabolisme)</term><term>Protéines du choc thermique HSP70 (métabolisme)</term><term>Protéines membranaires (métabolisme)</term><term>Récepteur de type Toll-7 (génétique)</term><term>Récepteur de type Toll-7 (métabolisme)</term><term>Régulation positive ()</term><term>Stress du réticulum endoplasmique ()</term><term>Virus de la grippe A ()</term><term>Virus de la grippe A (physiologie)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>RNA, Messenger</term><term>Toll-Like Receptor 7</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>HSP70 Heat-Shock Proteins</term><term>Inflammation Mediators</term><term>Interleukin-6</term><term>Lipoproteins, LDL</term><term>Membrane Proteins</term><term>RNA, Messenger</term><term>Toll-Like Receptor 7</term><term>Transcription Factor CHOP</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Aminoquinolines</term><term>Dexamethasone</term></keywords><keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Grippe humaine</term><term>Macrophages</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Apoptosis</term><term>Endoplasmic Reticulum Stress</term><term>Influenza A virus</term><term>Macrophages</term><term>Up-Regulation</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>ARN messager</term><term>Récepteur de type Toll-7</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Macrophages</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>ARN messager</term><term>Facteur de transcription CHOP</term><term>Interleukine-6</term><term>Lipoprotéines LDL</term><term>Macrophages</term><term>Médiateurs de l'inflammation</term><term>Protéines du choc thermique HSP70</term><term>Protéines membranaires</term><term>Récepteur de type Toll-7</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Influenza, Human</term><term>Macrophages</term></keywords><keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Aminoquinoléines</term><term>Dexaméthasone</term></keywords><keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Virus de la grippe A</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Influenza A virus</term></keywords><keywords scheme="MESH" qualifier="virologie" xml:lang="fr"><term>Grippe humaine</term><term>Macrophages</term></keywords><keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>Influenza, Human</term><term>Macrophages</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Cell Line</term><term>Dogs</term><term>Humans</term><term>Imiquimod</term><term>Madin Darby Canine Kidney Cells</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Apoptose</term><term>Cellules rénales canines Madin-Darby</term><term>Chiens</term><term>Humains</term><term>Lignée cellulaire</term><term>Macrophages</term><term>Régulation positive</term><term>Stress du réticulum endoplasmique</term><term>Virus de la grippe A</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Macrophage apoptosis is a prominent characteristic of advanced atherosclerotic plaques and leads to plaque destabilization. Certain studies have confirmed that influenza virus A (IVA) infection is related to acute myocardial infarction (AMI). However, it remains unknown as to whether this phenomenon is associated with Toll-like receptor (TLR)7, since single-stranded RNA (ssRNA) of IVA is a natural ligand of TLR7. Thus, in the present study, THP-1‑derived macrophages were infected with IVA or treated with imiquimod (IMQ) in the presence or absence of pre-treatment with oxidized low-density lipoprotein (oxLDL). The macrophages were pre-treated with oxLDL (5 µg/ml) for 24 h to mimic high lipid conditions. Cell viability and apoptosis were detected by 3-(4,5-dimethylthiazol-2-y-1)‑2,5-diphenyl-2H-tetrazolium bromide (MTT) assay and flow cytometry, respectively. Our results revealed that TLR7 played an important role in macrophage apoptosis and cytokine secretion. Both IVA infection and IMQ treatment increased TLR7 expression, as well as the secretion of pro-inflammatory cytokines [interleukin (IL)-6, monocyte chemotactic protein (MCP)-1] and apoptosis. However, this increase in cytokine secretion occurred independently of cell apoptosis. oxLDL had potential synergistic pro-apoptotic effects combined with TLR7 activation. To determine whether endoplasmic reticulum (ER) stress plays a role in cell apoptosis, the mRNA and protein expression of known markers of ER stress [glucose-regulated protein (GRP)78 and C/EBP homologous protein (CHOP)] was detected by reverse transcription PCR (RT-PCR), quantitative reverse transcription PCR (qRT-PCR) and western blot analysis. Our results revealed that apoptosis aggravated ER stress, as shown by the overexpression of the pro-apoptotic sensor, CHOP. In conclusion, our study demonstrates the converging role of oxLDL pre-treatment, IVA infection and IMQ in ER stress-induced cell apoptosis. </div></front></TEI><affiliations><list><country><li>République populaire de Chine</li></country></list><tree><country name="République populaire de Chine"><noRegion><name sortKey="Yu, Xiaochen" sort="Yu, Xiaochen" uniqKey="Yu X" first="Xiaochen" last="Yu">Xiaochen Yu</name></noRegion><name sortKey="Guan, Xiuru" sort="Guan, Xiuru" uniqKey="Guan X" first="Xiuru" last="Guan">Xiuru Guan</name><name sortKey="Wang, Yang" sort="Wang, Yang" uniqKey="Wang Y" first="Yang" last="Wang">Yang Wang</name><name sortKey="Yang, Wei" sort="Yang, Wei" uniqKey="Yang W" first="Wei" last="Yang">Wei Yang</name><name sortKey="Zhao, Wenhui" sort="Zhao, Wenhui" uniqKey="Zhao W" first="Wenhui" last="Zhao">Wenhui Zhao</name><name sortKey="Zhou, Haizhou" sort="Zhou, Haizhou" uniqKey="Zhou H" first="Haizhou" last="Zhou">Haizhou Zhou</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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