author_facet Dahan, Diana
Ekman, Mari
Larsson-Callerfelt, Anna-Karin
Turczyńska, Karolina
Boettger, Thomas
Braun, Thomas
Swärd, Karl
Albinsson, Sebastian
Dahan, Diana
Ekman, Mari
Larsson-Callerfelt, Anna-Karin
Turczyńska, Karolina
Boettger, Thomas
Braun, Thomas
Swärd, Karl
Albinsson, Sebastian
author Dahan, Diana
Ekman, Mari
Larsson-Callerfelt, Anna-Karin
Turczyńska, Karolina
Boettger, Thomas
Braun, Thomas
Swärd, Karl
Albinsson, Sebastian
spellingShingle Dahan, Diana
Ekman, Mari
Larsson-Callerfelt, Anna-Karin
Turczyńska, Karolina
Boettger, Thomas
Braun, Thomas
Swärd, Karl
Albinsson, Sebastian
American Journal of Physiology-Cell Physiology
Induction of angiotensin-converting enzyme after miR-143/145 deletion is critical for impaired smooth muscle contractility
Cell Biology
Physiology
author_sort dahan, diana
spelling Dahan, Diana Ekman, Mari Larsson-Callerfelt, Anna-Karin Turczyńska, Karolina Boettger, Thomas Braun, Thomas Swärd, Karl Albinsson, Sebastian 0363-6143 1522-1563 American Physiological Society Cell Biology Physiology http://dx.doi.org/10.1152/ajpcell.00250.2014 <jats:p> MicroRNAs have emerged as regulators of smooth muscle cell phenotype with a role in smooth muscle-related disease. Studies have shown that miR-143 and miR-145 are the most highly expressed microRNAs in smooth muscle cells, controlling differentiation and function. The effect of miR-143/145 knockout has been established in the vasculature but not in smooth muscle from other organs. Using knockout mice we found that maximal contraction induced by either depolarization or phosphatase inhibition was reduced in vascular and airway smooth muscle but maintained in the urinary bladder. Furthermore, a reduction of media thickness and reduced expression of differentiation markers was seen in the aorta but not in the bladder. Supporting the view that phenotype switching depends on a tissue-specific target of miR-143/145, we found induction of angiotensin-converting enzyme in the aorta but not in the bladder where angiotensin-converting enzyme was expressed at a low level. Chronic treatment with angiotensin type-1 receptor antagonist restored contractility in miR-143/145-deficient aorta while leaving bladder contractility unaffected. This shows that tissue-specific targets are critical for the effects of miR-143/145 on smooth muscle differentiation and that angiotensin converting enzyme is one such target. </jats:p> Induction of angiotensin-converting enzyme after miR-143/145 deletion is critical for impaired smooth muscle contractility American Journal of Physiology-Cell Physiology
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series American Journal of Physiology-Cell Physiology
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title Induction of angiotensin-converting enzyme after miR-143/145 deletion is critical for impaired smooth muscle contractility
title_unstemmed Induction of angiotensin-converting enzyme after miR-143/145 deletion is critical for impaired smooth muscle contractility
title_full Induction of angiotensin-converting enzyme after miR-143/145 deletion is critical for impaired smooth muscle contractility
title_fullStr Induction of angiotensin-converting enzyme after miR-143/145 deletion is critical for impaired smooth muscle contractility
title_full_unstemmed Induction of angiotensin-converting enzyme after miR-143/145 deletion is critical for impaired smooth muscle contractility
title_short Induction of angiotensin-converting enzyme after miR-143/145 deletion is critical for impaired smooth muscle contractility
title_sort induction of angiotensin-converting enzyme after mir-143/145 deletion is critical for impaired smooth muscle contractility
topic Cell Biology
Physiology
url http://dx.doi.org/10.1152/ajpcell.00250.2014
publishDate 2014
physical C1093-C1101
description <jats:p> MicroRNAs have emerged as regulators of smooth muscle cell phenotype with a role in smooth muscle-related disease. Studies have shown that miR-143 and miR-145 are the most highly expressed microRNAs in smooth muscle cells, controlling differentiation and function. The effect of miR-143/145 knockout has been established in the vasculature but not in smooth muscle from other organs. Using knockout mice we found that maximal contraction induced by either depolarization or phosphatase inhibition was reduced in vascular and airway smooth muscle but maintained in the urinary bladder. Furthermore, a reduction of media thickness and reduced expression of differentiation markers was seen in the aorta but not in the bladder. Supporting the view that phenotype switching depends on a tissue-specific target of miR-143/145, we found induction of angiotensin-converting enzyme in the aorta but not in the bladder where angiotensin-converting enzyme was expressed at a low level. Chronic treatment with angiotensin type-1 receptor antagonist restored contractility in miR-143/145-deficient aorta while leaving bladder contractility unaffected. This shows that tissue-specific targets are critical for the effects of miR-143/145 on smooth muscle differentiation and that angiotensin converting enzyme is one such target. </jats:p>
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author Dahan, Diana, Ekman, Mari, Larsson-Callerfelt, Anna-Karin, Turczyńska, Karolina, Boettger, Thomas, Braun, Thomas, Swärd, Karl, Albinsson, Sebastian
author_facet Dahan, Diana, Ekman, Mari, Larsson-Callerfelt, Anna-Karin, Turczyńska, Karolina, Boettger, Thomas, Braun, Thomas, Swärd, Karl, Albinsson, Sebastian, Dahan, Diana, Ekman, Mari, Larsson-Callerfelt, Anna-Karin, Turczyńska, Karolina, Boettger, Thomas, Braun, Thomas, Swärd, Karl, Albinsson, Sebastian
author_sort dahan, diana
container_issue 12
container_start_page 0
container_title American Journal of Physiology-Cell Physiology
container_volume 307
description <jats:p> MicroRNAs have emerged as regulators of smooth muscle cell phenotype with a role in smooth muscle-related disease. Studies have shown that miR-143 and miR-145 are the most highly expressed microRNAs in smooth muscle cells, controlling differentiation and function. The effect of miR-143/145 knockout has been established in the vasculature but not in smooth muscle from other organs. Using knockout mice we found that maximal contraction induced by either depolarization or phosphatase inhibition was reduced in vascular and airway smooth muscle but maintained in the urinary bladder. Furthermore, a reduction of media thickness and reduced expression of differentiation markers was seen in the aorta but not in the bladder. Supporting the view that phenotype switching depends on a tissue-specific target of miR-143/145, we found induction of angiotensin-converting enzyme in the aorta but not in the bladder where angiotensin-converting enzyme was expressed at a low level. Chronic treatment with angiotensin type-1 receptor antagonist restored contractility in miR-143/145-deficient aorta while leaving bladder contractility unaffected. This shows that tissue-specific targets are critical for the effects of miR-143/145 on smooth muscle differentiation and that angiotensin converting enzyme is one such target. </jats:p>
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spelling Dahan, Diana Ekman, Mari Larsson-Callerfelt, Anna-Karin Turczyńska, Karolina Boettger, Thomas Braun, Thomas Swärd, Karl Albinsson, Sebastian 0363-6143 1522-1563 American Physiological Society Cell Biology Physiology http://dx.doi.org/10.1152/ajpcell.00250.2014 <jats:p> MicroRNAs have emerged as regulators of smooth muscle cell phenotype with a role in smooth muscle-related disease. Studies have shown that miR-143 and miR-145 are the most highly expressed microRNAs in smooth muscle cells, controlling differentiation and function. The effect of miR-143/145 knockout has been established in the vasculature but not in smooth muscle from other organs. Using knockout mice we found that maximal contraction induced by either depolarization or phosphatase inhibition was reduced in vascular and airway smooth muscle but maintained in the urinary bladder. Furthermore, a reduction of media thickness and reduced expression of differentiation markers was seen in the aorta but not in the bladder. Supporting the view that phenotype switching depends on a tissue-specific target of miR-143/145, we found induction of angiotensin-converting enzyme in the aorta but not in the bladder where angiotensin-converting enzyme was expressed at a low level. Chronic treatment with angiotensin type-1 receptor antagonist restored contractility in miR-143/145-deficient aorta while leaving bladder contractility unaffected. This shows that tissue-specific targets are critical for the effects of miR-143/145 on smooth muscle differentiation and that angiotensin converting enzyme is one such target. </jats:p> Induction of angiotensin-converting enzyme after miR-143/145 deletion is critical for impaired smooth muscle contractility American Journal of Physiology-Cell Physiology
spellingShingle Dahan, Diana, Ekman, Mari, Larsson-Callerfelt, Anna-Karin, Turczyńska, Karolina, Boettger, Thomas, Braun, Thomas, Swärd, Karl, Albinsson, Sebastian, American Journal of Physiology-Cell Physiology, Induction of angiotensin-converting enzyme after miR-143/145 deletion is critical for impaired smooth muscle contractility, Cell Biology, Physiology
title Induction of angiotensin-converting enzyme after miR-143/145 deletion is critical for impaired smooth muscle contractility
title_full Induction of angiotensin-converting enzyme after miR-143/145 deletion is critical for impaired smooth muscle contractility
title_fullStr Induction of angiotensin-converting enzyme after miR-143/145 deletion is critical for impaired smooth muscle contractility
title_full_unstemmed Induction of angiotensin-converting enzyme after miR-143/145 deletion is critical for impaired smooth muscle contractility
title_short Induction of angiotensin-converting enzyme after miR-143/145 deletion is critical for impaired smooth muscle contractility
title_sort induction of angiotensin-converting enzyme after mir-143/145 deletion is critical for impaired smooth muscle contractility
title_unstemmed Induction of angiotensin-converting enzyme after miR-143/145 deletion is critical for impaired smooth muscle contractility
topic Cell Biology, Physiology
url http://dx.doi.org/10.1152/ajpcell.00250.2014