Mechanical Stress Is Communicated between Different Cell Types to Elicit Matrix Remodeling
Tissue remodeling often reflects alterations in local mechanical conditions and manifests as an integrated response among the different cell types that share, and thus cooperatively manage, an extracellular matrix. Here we examine how two different cell types, one that undergoes the stress and the o...
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Published in | Proceedings of the National Academy of Sciences - PNAS Vol. 98; no. 11; pp. 6180 - 6185 |
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Main Authors | , , , |
Format | Journal Article |
Language | English |
Published |
United States
National Academy of Sciences
22.05.2001
National Acad Sciences The National Academy of Sciences |
Subjects | |
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Abstract | Tissue remodeling often reflects alterations in local mechanical conditions and manifests as an integrated response among the different cell types that share, and thus cooperatively manage, an extracellular matrix. Here we examine how two different cell types, one that undergoes the stress and the other that primarily remodels the matrix, might communicate a mechanical stress by using airway cells as a representative in vitro system. Normal stress is imposed on bronchial epithelial cells in the presence of unstimulated lung fibroblasts. We show that (i) mechanical stress can be communicated from stressed to unstressed cells to elicit a remodeling response, and (ii) the integrated response of two cell types to mechanical stress mimics key features of airway remodeling seen in asthma: namely, an increase in production of fibronectin, collagen types III and V, and matrix metalloproteinase type 9 (MMP-9) (relative to tissue inhibitor of metalloproteinase-1, TIMP-1). These observations provide a paradigm to use in understanding the management of mechanical forces on the tissue level. |
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AbstractList | Tissue remodeling often reflects alterations in local mechanical conditions and manifests as an integrated response among the different cell types that share, and thus cooperatively manage, an extracellular matrix. Here we examine how two different cell types, one that undergoes the stress and the other that primarily remodels the matrix, might communicate a mechanical stress by using airway cells as a representative in vitro system. Normal stress is imposed on bronchial epithelial cells in the presence of unstimulated lung fibroblasts. We show that (i) mechanical stress can be communicated from stressed to unstressed cells to elicit a remodeling response, and (ii) the integrated response of two cell types to mechanical stress mimics key features of airway remodeling seen in asthma: namely, an increase in production of fibronectin, collagen types III and V, and matrix metalloproteinase type 9 (MMP-9) (relative to tissue inhibitor of metalloproteinase-1, TIMP-1). These observations provide a paradigm to use in understanding the management of mechanical forces on the tissue level. Tissue remodeling often reflects alterations in local mechanical conditions and manifests as an integrated response among the different cell types that share, and thus cooperatively manage, an extracellular matrix. Here we examine how two different cell types, one that undergoes the stress and the other that primarily remodels the matrix, might communicate a mechanical stress by using airway cells as a representative in vitro system. Normal stress is imposed on bronchial epithelial cells in the presence of unstimulated lung fibroblasts. We show that ( i ) mechanical stress can be communicated from stressed to unstressed cells to elicit a remodeling response, and ( ii ) the integrated response of two cell types to mechanical stress mimics key features of airway remodeling seen in asthma: namely, an increase in production of fibronectin, collagen types III and V, and matrix metalloproteinase type 9 (MMP-9) (relative to tissue inhibitor of metalloproteinase-1, TIMP-1). These observations provide a paradigm to use in understanding the management of mechanical forces on the tissue level. Tissue remodeling often reflects alterations in local mechanical conditions and manifests as an integrated response among the different cell types that share, and thus cooperatively manage, an extracellular matrix. Here we examine how two different cell types, one that undergoes the stress and the other that primarily remodels the matrix, might communicate a mechanical stress by using airway cells as a representative in vitro system. Normal stress is imposed on bronchial epithelial cells in the presence of unstimulated lung fibroblasts. We show that ( i ) mechanical stress can be communicated from stressed to unstressed cells to elicit a remodeling response, and ( ii ) the integrated response of two cell types to mechanical stress mimics key features of airway remodeling seen in asthma: namely, an increase in production of fibronectin, collagen types III and V, and matrix metalloproteinase type 9 (MMP-9) (relative to tissue inhibitor of metalloproteinase-1, TIMP-1). These observations provide a paradigm to use in understanding the management of mechanical forces on the tissue level. airway wall remodeling airway epithelium asthma lung fibroblasts Tissue remodeling often reflects alterations in local mechanical conditions and manifests as an integrated response among the different cell types that share, and thus cooperatively manage, an extracellular matrix. Here we examine how two different cell types, one that undergoes the stress and the other that primarily remodels the matrix, might communicate a mechanical stress by using airway cells as a representative in vitro system. |
Author | Swartz, M. A. Kamm, R. D. Tschumperlin, D. J. Drazen, J. M. |
AuthorAffiliation | Department of Medicine, Pulmonary Division, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115; ‡ Physiology Program, Harvard School of Public Health, Boston, MA 02115; and § Department of Mechanical Engineering and Division of Bioengineering and Environmental Health, Massachusetts Institute of Technology, Cambridge, MA 02139 |
AuthorAffiliation_xml | – name: Department of Medicine, Pulmonary Division, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115; ‡ Physiology Program, Harvard School of Public Health, Boston, MA 02115; and § Department of Mechanical Engineering and Division of Bioengineering and Environmental Health, Massachusetts Institute of Technology, Cambridge, MA 02139 |
Author_xml | – sequence: 1 givenname: M. A. surname: Swartz fullname: Swartz, M. A. – sequence: 2 givenname: D. J. surname: Tschumperlin fullname: Tschumperlin, D. J. – sequence: 3 givenname: R. D. surname: Kamm fullname: Kamm, R. D. – sequence: 4 givenname: J. M. surname: Drazen fullname: Drazen, J. M. |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/11353845$$D View this record in MEDLINE/PubMed |
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Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 To whom reprint requests should be addressed. E-mail: jdrazen@rics.bwh.harvard.edu. Communicated by Yuan-Cheng B. Fung, University of California at San Diego, La Jolla, CA Present address: Departments of Biomedical and Chemical Engineering, Northwestern University, 2145 Sheridan Road, Evanston, IL 60208. |
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Snippet | Tissue remodeling often reflects alterations in local mechanical conditions and manifests as an integrated response among the different cell types that share,... Tissue remodeling often reflects alterations in local mechanical conditions and manifests as an integrated response among the different cell types that share,... |
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SubjectTerms | Asthma Biological Sciences Bronchi - cytology Cell communication Cell Communication - physiology Cell Division Cells Cells, Cultured Cellular biology Coculture techniques Coculture Techniques - methods Collagen - biosynthesis Collagens Cultured cells DNA-Binding Proteins - biosynthesis Early Growth Response Protein 1 Epithelial cells Epithelial Cells - metabolism Extracellular Matrix - metabolism Extracellular Matrix - physiology Fibroblasts Fibroblasts - cytology Fibroblasts - drug effects Fibroblasts - metabolism Fibronectins - biosynthesis Humans Immediate-Early Proteins Lung - cytology Lungs Matrix Metalloproteinase 9 - biosynthesis Mechanical stress Renovations Respiratory Mucosa - cytology Signal Transduction - physiology Space life sciences Stress, Mechanical Tissue Inhibitor of Metalloproteinase-1 - biosynthesis Transcription Factors - biosynthesis |
Title | Mechanical Stress Is Communicated between Different Cell Types to Elicit Matrix Remodeling |
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