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Fibroblast fiber contraction: role of C and Rho kinase in activation by thromboxane A2
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Zeitschriftentitel: | American Journal of Physiology-Cell Physiology |
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Personen und Körperschaften: | , , |
In: | American Journal of Physiology-Cell Physiology, 285, 2003, 6, S. C1411-C1419 |
Format: | E-Article |
Sprache: | Englisch |
veröffentlicht: |
American Physiological Society
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Schlagwörter: |
author_facet |
Nobe, Hiromi Nobe, Koji Paul, Richard J. Nobe, Hiromi Nobe, Koji Paul, Richard J. |
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author |
Nobe, Hiromi Nobe, Koji Paul, Richard J. |
spellingShingle |
Nobe, Hiromi Nobe, Koji Paul, Richard J. American Journal of Physiology-Cell Physiology Fibroblast fiber contraction: role of C and Rho kinase in activation by thromboxane A2 Cell Biology Physiology |
author_sort |
nobe, hiromi |
spelling |
Nobe, Hiromi Nobe, Koji Paul, Richard J. 0363-6143 1522-1563 American Physiological Society Cell Biology Physiology http://dx.doi.org/10.1152/ajpcell.00067.2003 <jats:p>We investigated the mechanisms underlying regulation of contraction with measurements of isometric force and intracellular Ca<jats:sup>2+</jats:sup>concentration ([Ca<jats:sup>2+</jats:sup>]<jats:sub>i</jats:sub>) in NIH 3T3 fibroblast reconstituted into fibers with the use of a collagen matrix. Treatment with the major phospholipids, neurotransmitters, and growth factors had little effect on baseline isometric force. However, U-46619, a thromboxane A<jats:sub>2</jats:sub>(TxA<jats:sub>2</jats:sub>) analog, increased force and [Ca<jats:sup>2+</jats:sup>]<jats:sub>i</jats:sub>; EC<jats:sub>50</jats:sub>values were 11.0 and 10.0 nM, respectively. The time courses were similar to those induced by calf serum (CS), and the maximal force was 65% of a CS-mediated contraction. The selective TxA<jats:sub>2</jats:sub>receptor antagonist SQ-29548 abolished the U-46619-induced responses. CS-induced contractions are dependent on an intracellular Ca<jats:sup>2+</jats:sup>store function; however, the U-46619 response depended not only on intracellular Ca<jats:sup>2+</jats:sup>stores, but also on Ca<jats:sup>2+</jats:sup>influx from the extracellular medium. Inhibition of Rho kinase suppressed U-46619- and CS-induced responses; in contrast, inhibition of C kinase (PKC) reduced only the U-46619 response. Moreover, addition of U-46619 to a CS contracture enhanced force and [Ca<jats:sup>2+</jats:sup>]<jats:sub>i</jats:sub>responses. These results indicate that U-46619-induced responses involve PKC and Rho kinase pathways, in contrast to activation by CS. Thus TxA<jats:sub>2</jats:sub>may have a role in not only the initial step of wound repair as an activator of blood coagulation, but also in fibroblast contractility in later stages.</jats:p> Fibroblast fiber contraction: role of C and Rho kinase in activation by thromboxane A<sub>2</sub> American Journal of Physiology-Cell Physiology |
doi_str_mv |
10.1152/ajpcell.00067.2003 |
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Biologie |
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American Physiological Society, 2003 |
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2003 |
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American Physiological Society |
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American Journal of Physiology-Cell Physiology |
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title |
Fibroblast fiber contraction: role of C and Rho kinase in activation by thromboxane A2 |
title_unstemmed |
Fibroblast fiber contraction: role of C and Rho kinase in activation by thromboxane A2 |
title_full |
Fibroblast fiber contraction: role of C and Rho kinase in activation by thromboxane A2 |
title_fullStr |
Fibroblast fiber contraction: role of C and Rho kinase in activation by thromboxane A2 |
title_full_unstemmed |
Fibroblast fiber contraction: role of C and Rho kinase in activation by thromboxane A2 |
title_short |
Fibroblast fiber contraction: role of C and Rho kinase in activation by thromboxane A2 |
title_sort |
fibroblast fiber contraction: role of c and rho kinase in activation by thromboxane a<sub>2</sub> |
topic |
Cell Biology Physiology |
url |
http://dx.doi.org/10.1152/ajpcell.00067.2003 |
publishDate |
2003 |
physical |
C1411-C1419 |
description |
<jats:p>We investigated the mechanisms underlying regulation of contraction with measurements of isometric force and intracellular Ca<jats:sup>2+</jats:sup>concentration ([Ca<jats:sup>2+</jats:sup>]<jats:sub>i</jats:sub>) in NIH 3T3 fibroblast reconstituted into fibers with the use of a collagen matrix. Treatment with the major phospholipids, neurotransmitters, and growth factors had little effect on baseline isometric force. However, U-46619, a thromboxane A<jats:sub>2</jats:sub>(TxA<jats:sub>2</jats:sub>) analog, increased force and [Ca<jats:sup>2+</jats:sup>]<jats:sub>i</jats:sub>; EC<jats:sub>50</jats:sub>values were 11.0 and 10.0 nM, respectively. The time courses were similar to those induced by calf serum (CS), and the maximal force was 65% of a CS-mediated contraction. The selective TxA<jats:sub>2</jats:sub>receptor antagonist SQ-29548 abolished the U-46619-induced responses. CS-induced contractions are dependent on an intracellular Ca<jats:sup>2+</jats:sup>store function; however, the U-46619 response depended not only on intracellular Ca<jats:sup>2+</jats:sup>stores, but also on Ca<jats:sup>2+</jats:sup>influx from the extracellular medium. Inhibition of Rho kinase suppressed U-46619- and CS-induced responses; in contrast, inhibition of C kinase (PKC) reduced only the U-46619 response. Moreover, addition of U-46619 to a CS contracture enhanced force and [Ca<jats:sup>2+</jats:sup>]<jats:sub>i</jats:sub>responses. These results indicate that U-46619-induced responses involve PKC and Rho kinase pathways, in contrast to activation by CS. Thus TxA<jats:sub>2</jats:sub>may have a role in not only the initial step of wound repair as an activator of blood coagulation, but also in fibroblast contractility in later stages.</jats:p> |
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author | Nobe, Hiromi, Nobe, Koji, Paul, Richard J. |
author_facet | Nobe, Hiromi, Nobe, Koji, Paul, Richard J., Nobe, Hiromi, Nobe, Koji, Paul, Richard J. |
author_sort | nobe, hiromi |
container_issue | 6 |
container_start_page | 0 |
container_title | American Journal of Physiology-Cell Physiology |
container_volume | 285 |
description | <jats:p>We investigated the mechanisms underlying regulation of contraction with measurements of isometric force and intracellular Ca<jats:sup>2+</jats:sup>concentration ([Ca<jats:sup>2+</jats:sup>]<jats:sub>i</jats:sub>) in NIH 3T3 fibroblast reconstituted into fibers with the use of a collagen matrix. Treatment with the major phospholipids, neurotransmitters, and growth factors had little effect on baseline isometric force. However, U-46619, a thromboxane A<jats:sub>2</jats:sub>(TxA<jats:sub>2</jats:sub>) analog, increased force and [Ca<jats:sup>2+</jats:sup>]<jats:sub>i</jats:sub>; EC<jats:sub>50</jats:sub>values were 11.0 and 10.0 nM, respectively. The time courses were similar to those induced by calf serum (CS), and the maximal force was 65% of a CS-mediated contraction. The selective TxA<jats:sub>2</jats:sub>receptor antagonist SQ-29548 abolished the U-46619-induced responses. CS-induced contractions are dependent on an intracellular Ca<jats:sup>2+</jats:sup>store function; however, the U-46619 response depended not only on intracellular Ca<jats:sup>2+</jats:sup>stores, but also on Ca<jats:sup>2+</jats:sup>influx from the extracellular medium. Inhibition of Rho kinase suppressed U-46619- and CS-induced responses; in contrast, inhibition of C kinase (PKC) reduced only the U-46619 response. Moreover, addition of U-46619 to a CS contracture enhanced force and [Ca<jats:sup>2+</jats:sup>]<jats:sub>i</jats:sub>responses. These results indicate that U-46619-induced responses involve PKC and Rho kinase pathways, in contrast to activation by CS. Thus TxA<jats:sub>2</jats:sub>may have a role in not only the initial step of wound repair as an activator of blood coagulation, but also in fibroblast contractility in later stages.</jats:p> |
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spelling | Nobe, Hiromi Nobe, Koji Paul, Richard J. 0363-6143 1522-1563 American Physiological Society Cell Biology Physiology http://dx.doi.org/10.1152/ajpcell.00067.2003 <jats:p>We investigated the mechanisms underlying regulation of contraction with measurements of isometric force and intracellular Ca<jats:sup>2+</jats:sup>concentration ([Ca<jats:sup>2+</jats:sup>]<jats:sub>i</jats:sub>) in NIH 3T3 fibroblast reconstituted into fibers with the use of a collagen matrix. Treatment with the major phospholipids, neurotransmitters, and growth factors had little effect on baseline isometric force. However, U-46619, a thromboxane A<jats:sub>2</jats:sub>(TxA<jats:sub>2</jats:sub>) analog, increased force and [Ca<jats:sup>2+</jats:sup>]<jats:sub>i</jats:sub>; EC<jats:sub>50</jats:sub>values were 11.0 and 10.0 nM, respectively. The time courses were similar to those induced by calf serum (CS), and the maximal force was 65% of a CS-mediated contraction. The selective TxA<jats:sub>2</jats:sub>receptor antagonist SQ-29548 abolished the U-46619-induced responses. CS-induced contractions are dependent on an intracellular Ca<jats:sup>2+</jats:sup>store function; however, the U-46619 response depended not only on intracellular Ca<jats:sup>2+</jats:sup>stores, but also on Ca<jats:sup>2+</jats:sup>influx from the extracellular medium. Inhibition of Rho kinase suppressed U-46619- and CS-induced responses; in contrast, inhibition of C kinase (PKC) reduced only the U-46619 response. Moreover, addition of U-46619 to a CS contracture enhanced force and [Ca<jats:sup>2+</jats:sup>]<jats:sub>i</jats:sub>responses. These results indicate that U-46619-induced responses involve PKC and Rho kinase pathways, in contrast to activation by CS. Thus TxA<jats:sub>2</jats:sub>may have a role in not only the initial step of wound repair as an activator of blood coagulation, but also in fibroblast contractility in later stages.</jats:p> Fibroblast fiber contraction: role of C and Rho kinase in activation by thromboxane A<sub>2</sub> American Journal of Physiology-Cell Physiology |
spellingShingle | Nobe, Hiromi, Nobe, Koji, Paul, Richard J., American Journal of Physiology-Cell Physiology, Fibroblast fiber contraction: role of C and Rho kinase in activation by thromboxane A2, Cell Biology, Physiology |
title | Fibroblast fiber contraction: role of C and Rho kinase in activation by thromboxane A2 |
title_full | Fibroblast fiber contraction: role of C and Rho kinase in activation by thromboxane A2 |
title_fullStr | Fibroblast fiber contraction: role of C and Rho kinase in activation by thromboxane A2 |
title_full_unstemmed | Fibroblast fiber contraction: role of C and Rho kinase in activation by thromboxane A2 |
title_short | Fibroblast fiber contraction: role of C and Rho kinase in activation by thromboxane A2 |
title_sort | fibroblast fiber contraction: role of c and rho kinase in activation by thromboxane a<sub>2</sub> |
title_unstemmed | Fibroblast fiber contraction: role of C and Rho kinase in activation by thromboxane A2 |
topic | Cell Biology, Physiology |
url | http://dx.doi.org/10.1152/ajpcell.00067.2003 |