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Monocyte-endothelial cell interactions in vascular and tissue remodeling
Monocytes are circulating leukocytes of innate immunity derived from the bone marrow that interact with endothelial cells under physiological or pathophysiological conditions to orchestrate inflammation, angiogenesis, or tissue remodeling. Monocytes are attracted by chemokines and specific receptors...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Frontiers Media S.A.
2023
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10360188/ https://www.ncbi.nlm.nih.gov/pubmed/37483594 http://dx.doi.org/10.3389/fimmu.2023.1196033 |
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author | Medrano-Bosch, Mireia Simón-Codina, Blanca Jiménez, Wladimiro Edelman, Elazer R. Melgar-Lesmes, Pedro |
author_facet | Medrano-Bosch, Mireia Simón-Codina, Blanca Jiménez, Wladimiro Edelman, Elazer R. Melgar-Lesmes, Pedro |
author_sort | Medrano-Bosch, Mireia |
collection | PubMed |
description | Monocytes are circulating leukocytes of innate immunity derived from the bone marrow that interact with endothelial cells under physiological or pathophysiological conditions to orchestrate inflammation, angiogenesis, or tissue remodeling. Monocytes are attracted by chemokines and specific receptors to precise areas in vessels or tissues and transdifferentiate into macrophages with tissue damage or infection. Adherent monocytes and infiltrated monocyte-derived macrophages locally release a myriad of cytokines, vasoactive agents, matrix metalloproteinases, and growth factors to induce vascular and tissue remodeling or for propagation of inflammatory responses. Infiltrated macrophages cooperate with tissue-resident macrophages during all the phases of tissue injury, repair, and regeneration. Substances released by infiltrated and resident macrophages serve not only to coordinate vessel and tissue growth but cellular interactions as well by attracting more circulating monocytes (e.g. MCP-1) and stimulating nearby endothelial cells (e.g. TNF-α) to expose monocyte adhesion molecules. Prolonged tissue accumulation and activation of infiltrated monocytes may result in alterations in extracellular matrix turnover, tissue functions, and vascular leakage. In this review, we highlight the link between interactions of infiltrating monocytes and endothelial cells to regulate vascular and tissue remodeling with a special focus on how these interactions contribute to pathophysiological conditions such as cardiovascular and chronic liver diseases. |
format | Online Article Text |
id | pubmed-10360188 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-103601882023-07-22 Monocyte-endothelial cell interactions in vascular and tissue remodeling Medrano-Bosch, Mireia Simón-Codina, Blanca Jiménez, Wladimiro Edelman, Elazer R. Melgar-Lesmes, Pedro Front Immunol Immunology Monocytes are circulating leukocytes of innate immunity derived from the bone marrow that interact with endothelial cells under physiological or pathophysiological conditions to orchestrate inflammation, angiogenesis, or tissue remodeling. Monocytes are attracted by chemokines and specific receptors to precise areas in vessels or tissues and transdifferentiate into macrophages with tissue damage or infection. Adherent monocytes and infiltrated monocyte-derived macrophages locally release a myriad of cytokines, vasoactive agents, matrix metalloproteinases, and growth factors to induce vascular and tissue remodeling or for propagation of inflammatory responses. Infiltrated macrophages cooperate with tissue-resident macrophages during all the phases of tissue injury, repair, and regeneration. Substances released by infiltrated and resident macrophages serve not only to coordinate vessel and tissue growth but cellular interactions as well by attracting more circulating monocytes (e.g. MCP-1) and stimulating nearby endothelial cells (e.g. TNF-α) to expose monocyte adhesion molecules. Prolonged tissue accumulation and activation of infiltrated monocytes may result in alterations in extracellular matrix turnover, tissue functions, and vascular leakage. In this review, we highlight the link between interactions of infiltrating monocytes and endothelial cells to regulate vascular and tissue remodeling with a special focus on how these interactions contribute to pathophysiological conditions such as cardiovascular and chronic liver diseases. Frontiers Media S.A. 2023-07-07 /pmc/articles/PMC10360188/ /pubmed/37483594 http://dx.doi.org/10.3389/fimmu.2023.1196033 Text en Copyright © 2023 Medrano-Bosch, Simón-Codina, Jiménez, Edelman and Melgar-Lesmes https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. |
spellingShingle | Immunology Medrano-Bosch, Mireia Simón-Codina, Blanca Jiménez, Wladimiro Edelman, Elazer R. Melgar-Lesmes, Pedro Monocyte-endothelial cell interactions in vascular and tissue remodeling |
title | Monocyte-endothelial cell interactions in vascular and tissue remodeling |
title_full | Monocyte-endothelial cell interactions in vascular and tissue remodeling |
title_fullStr | Monocyte-endothelial cell interactions in vascular and tissue remodeling |
title_full_unstemmed | Monocyte-endothelial cell interactions in vascular and tissue remodeling |
title_short | Monocyte-endothelial cell interactions in vascular and tissue remodeling |
title_sort | monocyte-endothelial cell interactions in vascular and tissue remodeling |
topic | Immunology |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10360188/ https://www.ncbi.nlm.nih.gov/pubmed/37483594 http://dx.doi.org/10.3389/fimmu.2023.1196033 |
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