Cigarette smoke extract inhibits fibroblast-mediated collagen gel contraction
1 Dipartimento di Cardiologia, Angiologia e Pneumologia, U. O. di Pneumologia e Fisiopatologia Respiratoria, Università degli Studi di Pisa, 56214 Pisa, Italy; 2 Third Department of Internal Medicine, School of Medicine, University of Tokushima, Tokushima 770; 3 Pulmonary Medicine, Chest Disease...
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| Veröffentlicht in: | American journal of physiology. Lung cellular and molecular physiology 1998-04, Vol.274 (4), p.591-L598 |
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| container_title | American journal of physiology. Lung cellular and molecular physiology |
| container_volume | 274 |
| creator | Carnevali, S Nakamura, Y Mio, T Liu, X Takigawa, K Romberger, D. J Spurzem, J. R Rennard, S. I |
| description | 1 Dipartimento di Cardiologia,
Angiologia e Pneumologia, U. O. di Pneumologia e Fisiopatologia
Respiratoria, Università degli Studi di Pisa, 56214 Pisa, Italy;
2 Third Department of Internal
Medicine, School of Medicine, University of Tokushima, Tokushima 770;
3 Pulmonary Medicine, Chest Disease Research Institute, Kyoto University,
Kyoto 601, Japan; and 4 Pulmonary and Critical Care Medicine, University
of Nebraska Medical Center, Omaha, Nebraska 68198-5300
Cigarette smoking, the major cause of pulmonary
emphysema, is characterized by destruction of alveolar walls. Because
tissue destruction represents a balance between injury and repair, we hypothesized that cigarette smoke exposure may contribute to the development of emphysema through the inhibition of tissue contraction during the repair process. To partially evaluate this hypothesis, we
investigated the effects of cigarette smoke extract (CSE) on the
ability of cultured fibroblasts to mediate collagen gel contraction in
vitro: CSE inhibited fibroblast-mediated gel contraction in a
concentration-dependent manner ( P |
| doi_str_mv | 10.1152/ajplung.1998.274.4.l591 |
| format | Article |
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Angiologia e Pneumologia, U. O. di Pneumologia e Fisiopatologia
Respiratoria, Università degli Studi di Pisa, 56214 Pisa, Italy;
2 Third Department of Internal
Medicine, School of Medicine, University of Tokushima, Tokushima 770;
3 Pulmonary Medicine, Chest Disease Research Institute, Kyoto University,
Kyoto 601, Japan; and 4 Pulmonary and Critical Care Medicine, University
of Nebraska Medical Center, Omaha, Nebraska 68198-5300
Cigarette smoking, the major cause of pulmonary
emphysema, is characterized by destruction of alveolar walls. Because
tissue destruction represents a balance between injury and repair, we hypothesized that cigarette smoke exposure may contribute to the development of emphysema through the inhibition of tissue contraction during the repair process. To partially evaluate this hypothesis, we
investigated the effects of cigarette smoke extract (CSE) on the
ability of cultured fibroblasts to mediate collagen gel contraction in
vitro: CSE inhibited fibroblast-mediated gel contraction in a
concentration-dependent manner ( P < 0.01). Production of prostaglandin E 2 , a known inhibitor
of fibroblast contraction, was unchanged by CSE as was cell surface
integrin expression. In contrast, fibronectin production by fibroblasts
was inhibited ( P < 0.01), and
addition of exogenous fibronectin partially restored the contractile
activity, thus suggesting at least one mechanism to explain inhibition
of gel contraction by CSE. When CSE was treated to remove volatile components, it showed less inhibitory activity on fibroblast-mediated gel contraction. Therefore, we also examined the effects of acrolein and acetaldehyde, two volatile components of cigarette smoke. Inhibition of contraction was observed at 5 µM acrolein and at 0.5 mM
acetaldehyde. In conclusion, cigarette smoke inhibited fibroblast-mediated gel contraction, and this inhibition was due, at
least in part, to the volatile components of cigarette smoke and may be
mediated, at least in part, by a decrease in fibroblast fibronectin
production. By inhibition of repair, these smoke components may
contribute to the development of pulmonary emphysema.
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Angiologia e Pneumologia, U. O. di Pneumologia e Fisiopatologia
Respiratoria, Università degli Studi di Pisa, 56214 Pisa, Italy;
2 Third Department of Internal
Medicine, School of Medicine, University of Tokushima, Tokushima 770;
3 Pulmonary Medicine, Chest Disease Research Institute, Kyoto University,
Kyoto 601, Japan; and 4 Pulmonary and Critical Care Medicine, University
of Nebraska Medical Center, Omaha, Nebraska 68198-5300
Cigarette smoking, the major cause of pulmonary
emphysema, is characterized by destruction of alveolar walls. Because
tissue destruction represents a balance between injury and repair, we hypothesized that cigarette smoke exposure may contribute to the development of emphysema through the inhibition of tissue contraction during the repair process. To partially evaluate this hypothesis, we
investigated the effects of cigarette smoke extract (CSE) on the
ability of cultured fibroblasts to mediate collagen gel contraction in
vitro: CSE inhibited fibroblast-mediated gel contraction in a
concentration-dependent manner ( P < 0.01). Production of prostaglandin E 2 , a known inhibitor
of fibroblast contraction, was unchanged by CSE as was cell surface
integrin expression. In contrast, fibronectin production by fibroblasts
was inhibited ( P < 0.01), and
addition of exogenous fibronectin partially restored the contractile
activity, thus suggesting at least one mechanism to explain inhibition
of gel contraction by CSE. When CSE was treated to remove volatile components, it showed less inhibitory activity on fibroblast-mediated gel contraction. Therefore, we also examined the effects of acrolein and acetaldehyde, two volatile components of cigarette smoke. Inhibition of contraction was observed at 5 µM acrolein and at 0.5 mM
acetaldehyde. In conclusion, cigarette smoke inhibited fibroblast-mediated gel contraction, and this inhibition was due, at
least in part, to the volatile components of cigarette smoke and may be
mediated, at least in part, by a decrease in fibroblast fibronectin
production. By inhibition of repair, these smoke components may
contribute to the development of pulmonary emphysema.
fibronectin; three-dimensional gel</description><subject>Cell Survival - physiology</subject><subject>Cells, Cultured</subject><subject>Collagen - physiology</subject><subject>Dinoprostone - metabolism</subject><subject>Fibroblasts - metabolism</subject><subject>Fibroblasts - physiology</subject><subject>Fibronectins - antagonists & inhibitors</subject><subject>Fibronectins - metabolism</subject><subject>Gels</subject><subject>Humans</subject><subject>Integrins - metabolism</subject><subject>Lung - cytology</subject><subject>Lung - metabolism</subject><subject>Lung - physiology</subject><subject>Nicotiana</subject><subject>Plants, Toxic</subject><subject>Receptors, Collagen</subject><subject>Smoke</subject><issn>1040-0605</issn><issn>0002-9513</issn><issn>1522-1504</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1998</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kNFOwyAUhonRzDl9BGNfoBUolHJpFqcmM97sngClLZO1TWHRvb3MbeqNVxzy5_tzzgfAHYIZQhTfy_Xgtl2TIc7LDDOSkcxRjs7ANKY4RRSS8zhDAlNYQHoJrrxfQwgphMUETDhltGTlFLzObSNHE4JJ_KZ_N4n5DKPUIbFda5UNPqmtGnvlpA_pxlRWBlMlundONqZLGuPip_tGbN9dg4taOm9uju8MrBaPq_lzunx7epk_LFOd8yKkHBdcaVMhaWrIlFES65ywUhqqMctrjBHjSla5LJnMUUW4LguIi3gIKRjOZ4AdavXYez-aWgyj3chxJxAUez3iqEfs9YioRxCxjHoieXsgh62K1_xwRx8x54e8tU37YUcjhnbnbe_6ZicWW-dW0c-p_bdXDFUd2fR_9rTQn12-AJ5Oiks</recordid><startdate>19980401</startdate><enddate>19980401</enddate><creator>Carnevali, S</creator><creator>Nakamura, Y</creator><creator>Mio, T</creator><creator>Liu, X</creator><creator>Takigawa, K</creator><creator>Romberger, D. J</creator><creator>Spurzem, J. R</creator><creator>Rennard, S. I</creator><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope></search><sort><creationdate>19980401</creationdate><title>Cigarette smoke extract inhibits fibroblast-mediated collagen gel contraction</title><author>Carnevali, S ; Nakamura, Y ; Mio, T ; Liu, X ; Takigawa, K ; Romberger, D. J ; Spurzem, J. R ; Rennard, S. I</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c396t-9269bced1aef07beba2c3478ae5c273f22179bad3a87a31d49c8602660546723</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1998</creationdate><topic>Cell Survival - physiology</topic><topic>Cells, Cultured</topic><topic>Collagen - physiology</topic><topic>Dinoprostone - metabolism</topic><topic>Fibroblasts - metabolism</topic><topic>Fibroblasts - physiology</topic><topic>Fibronectins - antagonists & inhibitors</topic><topic>Fibronectins - metabolism</topic><topic>Gels</topic><topic>Humans</topic><topic>Integrins - metabolism</topic><topic>Lung - cytology</topic><topic>Lung - metabolism</topic><topic>Lung - physiology</topic><topic>Nicotiana</topic><topic>Plants, Toxic</topic><topic>Receptors, Collagen</topic><topic>Smoke</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Carnevali, S</creatorcontrib><creatorcontrib>Nakamura, Y</creatorcontrib><creatorcontrib>Mio, T</creatorcontrib><creatorcontrib>Liu, X</creatorcontrib><creatorcontrib>Takigawa, K</creatorcontrib><creatorcontrib>Romberger, D. J</creatorcontrib><creatorcontrib>Spurzem, J. R</creatorcontrib><creatorcontrib>Rennard, S. I</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><jtitle>American journal of physiology. Lung cellular and molecular physiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Carnevali, S</au><au>Nakamura, Y</au><au>Mio, T</au><au>Liu, X</au><au>Takigawa, K</au><au>Romberger, D. J</au><au>Spurzem, J. R</au><au>Rennard, S. I</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Cigarette smoke extract inhibits fibroblast-mediated collagen gel contraction</atitle><jtitle>American journal of physiology. Lung cellular and molecular physiology</jtitle><addtitle>Am J Physiol</addtitle><date>1998-04-01</date><risdate>1998</risdate><volume>274</volume><issue>4</issue><spage>591</spage><epage>L598</epage><pages>591-L598</pages><issn>1040-0605</issn><issn>0002-9513</issn><eissn>1522-1504</eissn><abstract>1 Dipartimento di Cardiologia,
Angiologia e Pneumologia, U. O. di Pneumologia e Fisiopatologia
Respiratoria, Università degli Studi di Pisa, 56214 Pisa, Italy;
2 Third Department of Internal
Medicine, School of Medicine, University of Tokushima, Tokushima 770;
3 Pulmonary Medicine, Chest Disease Research Institute, Kyoto University,
Kyoto 601, Japan; and 4 Pulmonary and Critical Care Medicine, University
of Nebraska Medical Center, Omaha, Nebraska 68198-5300
Cigarette smoking, the major cause of pulmonary
emphysema, is characterized by destruction of alveolar walls. Because
tissue destruction represents a balance between injury and repair, we hypothesized that cigarette smoke exposure may contribute to the development of emphysema through the inhibition of tissue contraction during the repair process. To partially evaluate this hypothesis, we
investigated the effects of cigarette smoke extract (CSE) on the
ability of cultured fibroblasts to mediate collagen gel contraction in
vitro: CSE inhibited fibroblast-mediated gel contraction in a
concentration-dependent manner ( P < 0.01). Production of prostaglandin E 2 , a known inhibitor
of fibroblast contraction, was unchanged by CSE as was cell surface
integrin expression. In contrast, fibronectin production by fibroblasts
was inhibited ( P < 0.01), and
addition of exogenous fibronectin partially restored the contractile
activity, thus suggesting at least one mechanism to explain inhibition
of gel contraction by CSE. When CSE was treated to remove volatile components, it showed less inhibitory activity on fibroblast-mediated gel contraction. Therefore, we also examined the effects of acrolein and acetaldehyde, two volatile components of cigarette smoke. Inhibition of contraction was observed at 5 µM acrolein and at 0.5 mM
acetaldehyde. In conclusion, cigarette smoke inhibited fibroblast-mediated gel contraction, and this inhibition was due, at
least in part, to the volatile components of cigarette smoke and may be
mediated, at least in part, by a decrease in fibroblast fibronectin
production. By inhibition of repair, these smoke components may
contribute to the development of pulmonary emphysema.
fibronectin; three-dimensional gel</abstract><cop>United States</cop><pmid>9575878</pmid><doi>10.1152/ajplung.1998.274.4.l591</doi></addata></record> |
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| ispartof | American journal of physiology. Lung cellular and molecular physiology, 1998-04, Vol.274 (4), p.591-L598 |
| issn | 1040-0605 0002-9513 1522-1504 |
| language | eng |
| recordid | cdi_highwire_physiology_ajplung_274_4_L591 |
| source | MEDLINE; American Physiological Society; EZB-FREE-00999 freely available EZB journals |
| subjects | Cell Survival - physiology Cells, Cultured Collagen - physiology Dinoprostone - metabolism Fibroblasts - metabolism Fibroblasts - physiology Fibronectins - antagonists & inhibitors Fibronectins - metabolism Gels Humans Integrins - metabolism Lung - cytology Lung - metabolism Lung - physiology Nicotiana Plants, Toxic Receptors, Collagen Smoke |
| title | Cigarette smoke extract inhibits fibroblast-mediated collagen gel contraction |
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