The M2 macrophages induce autophagic vascular disorder and promote mouse sensitivity to urethane-related lung carcinogenesis.
Identifieur interne : 000D54 ( Main/Exploration ); précédent : 000D53; suivant : 000D55The M2 macrophages induce autophagic vascular disorder and promote mouse sensitivity to urethane-related lung carcinogenesis.
Auteurs : G-G Li [République populaire de Chine] ; Z-Z Guo [République populaire de Chine] ; X-F Ma [République populaire de Chine] ; N. Cao [République populaire de Chine] ; S-N Geng [République populaire de Chine] ; Y-Q Zheng [République populaire de Chine] ; M-J Meng [République populaire de Chine] ; H-H Lin [République populaire de Chine] ; G. Han [République populaire de Chine] ; G-J Du [République populaire de Chine]Source :
- Developmental and comparative immunology [ 1879-0089 ] ; 2016.
Descripteurs français
- KwdFr :
- Acide clodronique (pharmacologie), Adénocarcinome (), Adénocarcinome (immunologie), Animaux, Apoptose (immunologie), Autophagie (immunologie), Benzofuranes (pharmacologie), Carcinogenèse (), Carcinogenèse (immunologie), Carcinome pulmonaire de Lewis, Cellules endothéliales, Cellules endothéliales de la veine ombilicale humaine, Chloroquine (pharmacologie), Différenciation cellulaire, Embryon de poulet, Femelle, Humains, Lignée cellulaire tumorale, Macrophages (immunologie), Milieux de culture conditionnés (pharmacologie), Mouvement cellulaire, Néovascularisation pathologique (immunologie), Perméabilité capillaire (physiologie), Phosphoprotéines (biosynthèse), Prolifération cellulaire, Protéines associées aux microtubules (biosynthèse), Souris, Souris de lignée C57BL, Transactivateurs (biosynthèse), Tumeurs du poumon (), Tumeurs du poumon (immunologie), Uréthane (pharmacologie).
- MESH :
- biosynthèse : Phosphoprotéines, Protéines associées aux microtubules, Transactivateurs.
- immunologie : Adénocarcinome, Apoptose, Autophagie, Carcinogenèse, Macrophages, Néovascularisation pathologique, Tumeurs du poumon.
- pharmacologie : Acide clodronique, Benzofuranes, Chloroquine, Milieux de culture conditionnés, Uréthane.
- physiologie : Perméabilité capillaire.
- Adénocarcinome, Animaux, Carcinogenèse, Carcinome pulmonaire de Lewis, Cellules endothéliales, Cellules endothéliales de la veine ombilicale humaine, Différenciation cellulaire, Embryon de poulet, Femelle, Humains, Lignée cellulaire tumorale, Mouvement cellulaire, Prolifération cellulaire, Souris, Souris de lignée C57BL, Tumeurs du poumon.
English descriptors
- KwdEn :
- Adenocarcinoma (chemically induced), Adenocarcinoma (immunology), Adenocarcinoma of Lung, Animals, Apoptosis (immunology), Autophagy (immunology), Benzofurans (pharmacology), Capillary Permeability (physiology), Carcinogenesis (chemically induced), Carcinogenesis (immunology), Carcinoma, Lewis Lung, Cell Differentiation, Cell Line, Tumor, Cell Movement, Cell Proliferation, Chick Embryo, Chloroquine (pharmacology), Clodronic Acid (pharmacology), Culture Media, Conditioned (pharmacology), Endothelial Cells, Female, Human Umbilical Vein Endothelial Cells, Humans, Lung Neoplasms (chemically induced), Lung Neoplasms (immunology), Macrophages (immunology), Mice, Mice, Inbred C57BL, Microtubule-Associated Proteins (biosynthesis), Neovascularization, Pathologic (immunology), Phosphoproteins (biosynthesis), Trans-Activators (biosynthesis), Urethane (pharmacology).
- MESH :
- chemical , biosynthesis : Microtubule-Associated Proteins, Phosphoproteins, Trans-Activators.
- chemical , pharmacology : Benzofurans, Chloroquine, Clodronic Acid, Culture Media, Conditioned, Urethane.
- chemically induced : Adenocarcinoma, Carcinogenesis, Lung Neoplasms.
- immunology : Adenocarcinoma, Apoptosis, Autophagy, Carcinogenesis, Lung Neoplasms, Macrophages, Neovascularization, Pathologic.
- physiology : Capillary Permeability.
- Adenocarcinoma of Lung, Animals, Carcinoma, Lewis Lung, Cell Differentiation, Cell Line, Tumor, Cell Movement, Cell Proliferation, Chick Embryo, Endothelial Cells, Female, Human Umbilical Vein Endothelial Cells, Humans, Mice, Mice, Inbred C57BL.
Abstract
Tumor vessels are known to be abnormal, with typically aberrant, leaky and disordered vessels. Here, we investigated whether polarized macrophage phenotypes are involved in tumor abnormal angiogenesis and what is its mechanism. We found that there was no difference in chemotaxis of polarized M1 and M2 macrophages to lewis lung carcinoma (LLC) cells and that either M1 or M2 macrophage-conditioned media had no effect on LLC cell proliferation. Unexpectedly, the M2 but not M1 macrophage-conditioned media promoted the proliferation of human umbilical vein endothelial cells (HUVECs) and simultaneously increased endothelial cell permeability in vitro and angiogenic index in the chick embryo chorioallantoic membrane (CAM). The treatment with M2 but not M1 macrophage-conditioned media increased autophagosomes as well as microtubule-associated protein light chain 3B (LC3-B) expression (a robust marker of autophagosomes) but decreased p62 protein expression (a selective autophagy substrate) in HUVECs, the treatment with chloroquine that blocked autophagy abrogated the abnormal angiogenic efficacy of M2 macrophage-conditioned media. These results were confirmed in urethane-induced lung carcinogenic progression. Urethane-induced lung carcinogenesis led to more M2 macrophage phenotype and increased abnormal angiogenesis concomitant with the upregulation of LC3-B and the downregulation of p62. Clodronate liposome-induced macrophage depletion, chloroquine-induced autophagic prevention or salvianolic acid B-induced vascular protection decreased abnormal angiogenesis and lung carcinogenesis. In addition, we found that the tendency of age-related M2 macrophage polarization also promoted vascular permeability and carcinogenesis in urethane carcinogenic progression. These findings indicate that the M2 macrophages induce autophagic vascular disorder to promote lung cancer progression, and the autophagy improvement represents an efficacious strategy for abnormal angiogenesis and cancer prevention.
DOI: 10.1016/j.dci.2016.01.010
PubMed: 26806760
Affiliations:
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Han</name><affiliation wicri:level="1"><nlm:affiliation>Institute of Pharmacy, Pharmacy College of Henan University, Jinming District, Kaifeng, Henan Province 475004, China. Electronic address: hang@henu.edu.cn.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Institute of Pharmacy, Pharmacy College of Henan University, Jinming District, Kaifeng, Henan Province 475004</wicri:regionArea><wicri:noRegion>Henan Province 475004</wicri:noRegion></affiliation></author><author><name sortKey="Du, G J" sort="Du, G J" uniqKey="Du G" first="G-J" last="Du">G-J Du</name><affiliation wicri:level="1"><nlm:affiliation>Institute of Pharmacy, Pharmacy College of Henan University, Jinming District, Kaifeng, Henan Province 475004, China. 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Cao</name><affiliation wicri:level="1"><nlm:affiliation>Institute of Pharmacy, Pharmacy College of Henan University, Jinming District, Kaifeng, Henan Province 475004, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Institute of Pharmacy, Pharmacy College of Henan University, Jinming District, Kaifeng, Henan Province 475004</wicri:regionArea><wicri:noRegion>Henan Province 475004</wicri:noRegion></affiliation></author><author><name sortKey="Geng, S N" sort="Geng, S N" uniqKey="Geng S" first="S-N" last="Geng">S-N Geng</name><affiliation wicri:level="1"><nlm:affiliation>Institute of Pharmacy, Pharmacy College of Henan University, Jinming District, Kaifeng, Henan Province 475004, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Institute of Pharmacy, Pharmacy College of Henan University, Jinming District, Kaifeng, Henan Province 475004</wicri:regionArea><wicri:noRegion>Henan Province 475004</wicri:noRegion></affiliation></author><author><name sortKey="Zheng, Y Q" sort="Zheng, Y Q" uniqKey="Zheng Y" first="Y-Q" last="Zheng">Y-Q Zheng</name><affiliation wicri:level="1"><nlm:affiliation>Institute of Pharmacy, Pharmacy College of Henan University, Jinming District, Kaifeng, Henan Province 475004, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Institute of Pharmacy, Pharmacy College of Henan University, Jinming District, Kaifeng, Henan Province 475004</wicri:regionArea><wicri:noRegion>Henan Province 475004</wicri:noRegion></affiliation></author><author><name sortKey="Meng, M J" sort="Meng, M J" uniqKey="Meng M" first="M-J" last="Meng">M-J Meng</name><affiliation wicri:level="1"><nlm:affiliation>Institute of Pharmacy, Pharmacy College of Henan University, Jinming District, Kaifeng, Henan Province 475004, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Institute of Pharmacy, Pharmacy College of Henan University, Jinming District, Kaifeng, Henan Province 475004</wicri:regionArea><wicri:noRegion>Henan Province 475004</wicri:noRegion></affiliation></author><author><name sortKey="Lin, H H" sort="Lin, H H" uniqKey="Lin H" first="H-H" last="Lin">H-H Lin</name><affiliation wicri:level="1"><nlm:affiliation>Institute of Pharmacy, Pharmacy College of Henan University, Jinming District, Kaifeng, Henan Province 475004, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Institute of Pharmacy, Pharmacy College of Henan University, Jinming District, Kaifeng, Henan Province 475004</wicri:regionArea><wicri:noRegion>Henan Province 475004</wicri:noRegion></affiliation></author><author><name sortKey="Han, G" sort="Han, G" uniqKey="Han G" first="G" last="Han">G. Han</name><affiliation wicri:level="1"><nlm:affiliation>Institute of Pharmacy, Pharmacy College of Henan University, Jinming District, Kaifeng, Henan Province 475004, China. Electronic address: hang@henu.edu.cn.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Institute of Pharmacy, Pharmacy College of Henan University, Jinming District, Kaifeng, Henan Province 475004</wicri:regionArea><wicri:noRegion>Henan Province 475004</wicri:noRegion></affiliation></author><author><name sortKey="Du, G J" sort="Du, G J" uniqKey="Du G" first="G-J" last="Du">G-J Du</name><affiliation wicri:level="1"><nlm:affiliation>Institute of Pharmacy, Pharmacy College of Henan University, Jinming District, Kaifeng, Henan Province 475004, China. Electronic address: 724200@henu.edu.cn.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Institute of Pharmacy, Pharmacy College of Henan University, Jinming District, Kaifeng, Henan Province 475004</wicri:regionArea><wicri:noRegion>Henan Province 475004</wicri:noRegion></affiliation></author></analytic><series><title level="j">Developmental and comparative immunology</title><idno type="eISSN">1879-0089</idno><imprint><date when="2016" type="published">2016</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adenocarcinoma (chemically induced)</term><term>Adenocarcinoma (immunology)</term><term>Adenocarcinoma of Lung</term><term>Animals</term><term>Apoptosis (immunology)</term><term>Autophagy (immunology)</term><term>Benzofurans (pharmacology)</term><term>Capillary Permeability (physiology)</term><term>Carcinogenesis (chemically induced)</term><term>Carcinogenesis (immunology)</term><term>Carcinoma, Lewis Lung</term><term>Cell Differentiation</term><term>Cell Line, Tumor</term><term>Cell Movement</term><term>Cell Proliferation</term><term>Chick Embryo</term><term>Chloroquine (pharmacology)</term><term>Clodronic Acid (pharmacology)</term><term>Culture Media, Conditioned (pharmacology)</term><term>Endothelial Cells</term><term>Female</term><term>Human Umbilical Vein Endothelial Cells</term><term>Humans</term><term>Lung Neoplasms (chemically induced)</term><term>Lung Neoplasms (immunology)</term><term>Macrophages (immunology)</term><term>Mice</term><term>Mice, Inbred C57BL</term><term>Microtubule-Associated Proteins (biosynthesis)</term><term>Neovascularization, Pathologic (immunology)</term><term>Phosphoproteins (biosynthesis)</term><term>Trans-Activators (biosynthesis)</term><term>Urethane (pharmacology)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Acide clodronique (pharmacologie)</term><term>Adénocarcinome ()</term><term>Adénocarcinome (immunologie)</term><term>Animaux</term><term>Apoptose (immunologie)</term><term>Autophagie (immunologie)</term><term>Benzofuranes (pharmacologie)</term><term>Carcinogenèse ()</term><term>Carcinogenèse (immunologie)</term><term>Carcinome pulmonaire de Lewis</term><term>Cellules endothéliales</term><term>Cellules endothéliales de la veine ombilicale humaine</term><term>Chloroquine (pharmacologie)</term><term>Différenciation cellulaire</term><term>Embryon de poulet</term><term>Femelle</term><term>Humains</term><term>Lignée cellulaire tumorale</term><term>Macrophages (immunologie)</term><term>Milieux de culture conditionnés (pharmacologie)</term><term>Mouvement cellulaire</term><term>Néovascularisation pathologique (immunologie)</term><term>Perméabilité capillaire (physiologie)</term><term>Phosphoprotéines (biosynthèse)</term><term>Prolifération cellulaire</term><term>Protéines associées aux microtubules (biosynthèse)</term><term>Souris</term><term>Souris de lignée C57BL</term><term>Transactivateurs (biosynthèse)</term><term>Tumeurs du poumon ()</term><term>Tumeurs du poumon (immunologie)</term><term>Uréthane (pharmacologie)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="biosynthesis" xml:lang="en"><term>Microtubule-Associated Proteins</term><term>Phosphoproteins</term><term>Trans-Activators</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Benzofurans</term><term>Chloroquine</term><term>Clodronic Acid</term><term>Culture Media, Conditioned</term><term>Urethane</term></keywords><keywords scheme="MESH" qualifier="biosynthèse" xml:lang="fr"><term>Phosphoprotéines</term><term>Protéines associées aux microtubules</term><term>Transactivateurs</term></keywords><keywords scheme="MESH" qualifier="chemically induced" xml:lang="en"><term>Adenocarcinoma</term><term>Carcinogenesis</term><term>Lung Neoplasms</term></keywords><keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Adénocarcinome</term><term>Apoptose</term><term>Autophagie</term><term>Carcinogenèse</term><term>Macrophages</term><term>Néovascularisation pathologique</term><term>Tumeurs du poumon</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Adenocarcinoma</term><term>Apoptosis</term><term>Autophagy</term><term>Carcinogenesis</term><term>Lung Neoplasms</term><term>Macrophages</term><term>Neovascularization, Pathologic</term></keywords><keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Acide clodronique</term><term>Benzofuranes</term><term>Chloroquine</term><term>Milieux de culture conditionnés</term><term>Uréthane</term></keywords><keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Perméabilité capillaire</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Capillary Permeability</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Adenocarcinoma of Lung</term><term>Animals</term><term>Carcinoma, Lewis Lung</term><term>Cell Differentiation</term><term>Cell Line, Tumor</term><term>Cell Movement</term><term>Cell Proliferation</term><term>Chick Embryo</term><term>Endothelial Cells</term><term>Female</term><term>Human Umbilical Vein Endothelial Cells</term><term>Humans</term><term>Mice</term><term>Mice, Inbred C57BL</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Adénocarcinome</term><term>Animaux</term><term>Carcinogenèse</term><term>Carcinome pulmonaire de Lewis</term><term>Cellules endothéliales</term><term>Cellules endothéliales de la veine ombilicale humaine</term><term>Différenciation cellulaire</term><term>Embryon de poulet</term><term>Femelle</term><term>Humains</term><term>Lignée cellulaire tumorale</term><term>Mouvement cellulaire</term><term>Prolifération cellulaire</term><term>Souris</term><term>Souris de lignée C57BL</term><term>Tumeurs du poumon</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Tumor vessels are known to be abnormal, with typically aberrant, leaky and disordered vessels. Here, we investigated whether polarized macrophage phenotypes are involved in tumor abnormal angiogenesis and what is its mechanism. We found that there was no difference in chemotaxis of polarized M1 and M2 macrophages to lewis lung carcinoma (LLC) cells and that either M1 or M2 macrophage-conditioned media had no effect on LLC cell proliferation. Unexpectedly, the M2 but not M1 macrophage-conditioned media promoted the proliferation of human umbilical vein endothelial cells (HUVECs) and simultaneously increased endothelial cell permeability in vitro and angiogenic index in the chick embryo chorioallantoic membrane (CAM). The treatment with M2 but not M1 macrophage-conditioned media increased autophagosomes as well as microtubule-associated protein light chain 3B (LC3-B) expression (a robust marker of autophagosomes) but decreased p62 protein expression (a selective autophagy substrate) in HUVECs, the treatment with chloroquine that blocked autophagy abrogated the abnormal angiogenic efficacy of M2 macrophage-conditioned media. These results were confirmed in urethane-induced lung carcinogenic progression. Urethane-induced lung carcinogenesis led to more M2 macrophage phenotype and increased abnormal angiogenesis concomitant with the upregulation of LC3-B and the downregulation of p62. Clodronate liposome-induced macrophage depletion, chloroquine-induced autophagic prevention or salvianolic acid B-induced vascular protection decreased abnormal angiogenesis and lung carcinogenesis. In addition, we found that the tendency of age-related M2 macrophage polarization also promoted vascular permeability and carcinogenesis in urethane carcinogenic progression. These findings indicate that the M2 macrophages induce autophagic vascular disorder to promote lung cancer progression, and the autophagy improvement represents an efficacious strategy for abnormal angiogenesis and cancer prevention.</div></front></TEI><affiliations><list><country><li>République populaire de Chine</li></country></list><tree><country name="République populaire de Chine"><noRegion><name sortKey="Li, G G" sort="Li, G G" uniqKey="Li G" first="G-G" last="Li">G-G Li</name></noRegion><name sortKey="Cao, N" sort="Cao, N" uniqKey="Cao N" first="N" last="Cao">N. Cao</name><name sortKey="Du, G J" sort="Du, G J" uniqKey="Du G" first="G-J" last="Du">G-J Du</name><name sortKey="Geng, S N" sort="Geng, S N" uniqKey="Geng S" first="S-N" last="Geng">S-N Geng</name><name sortKey="Guo, Z Z" sort="Guo, Z Z" uniqKey="Guo Z" first="Z-Z" last="Guo">Z-Z Guo</name><name sortKey="Han, G" sort="Han, G" uniqKey="Han G" first="G" last="Han">G. Han</name><name sortKey="Lin, H H" sort="Lin, H H" uniqKey="Lin H" first="H-H" last="Lin">H-H Lin</name><name sortKey="Ma, X F" sort="Ma, X F" uniqKey="Ma X" first="X-F" last="Ma">X-F Ma</name><name sortKey="Meng, M J" sort="Meng, M J" uniqKey="Meng M" first="M-J" last="Meng">M-J Meng</name><name sortKey="Zheng, Y Q" sort="Zheng, Y Q" uniqKey="Zheng Y" first="Y-Q" last="Zheng">Y-Q Zheng</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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