Induction of angiotensin converting enzyme after miR-143/145 deletion is critical for impaired smooth muscle contractility.
Dahan, Diana LU ; Ekman, Mari LU ; Larsson Callerfelt, Anna-Karin LU
; Turczynska, Karolina
LU
; Boettger, Thomas
; Braun, Thomas
; Swärd, Karl
LU
and Albinsson, Sebastian
LU
(2014)
In American Journal of Physiology: Cell Physiology
307(12).
p.1093-1101
- Abstract
- 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... (More)
- 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. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/4738574
- author
- Dahan, Diana
LU
; Ekman, Mari
LU
; Larsson Callerfelt, Anna-Karin
LU
; Turczynska, Karolina
LU
; Boettger, Thomas
; Braun, Thomas
; Swärd, Karl
LU
and Albinsson, Sebastian
LU
- organization
- publishing date
- 2014
- type
- Contribution to journal
- publication status
- published
- subject
- in
- American Journal of Physiology: Cell Physiology
- volume
- 307
- issue
- 12
- pages
- 1093 - 1101
- publisher
- American Physiological Society
- external identifiers
-
- pmid:25273883
- wos:000346473400004
- scopus:84918778428
- pmid:25273883
- ISSN
- 1522-1563
- DOI
- 10.1152/ajpcell.00250.2014
- language
- English
- LU publication?
- yes
- id
- 831feed0-c5ea-4af4-bf03-f0e4d6d77205 (old id 4738574)
- alternative location
- http://www.ncbi.nlm.nih.gov/pubmed/25273883?dopt=Abstract
- date added to LUP
- 2016-04-01 10:56:45
- date last changed
- 2022-03-27 20:59:40
@article{831feed0-c5ea-4af4-bf03-f0e4d6d77205,
abstract = {{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.}},
author = {{Dahan, Diana and Ekman, Mari and Larsson Callerfelt, Anna-Karin and Turczynska, Karolina and Boettger, Thomas and Braun, Thomas and Swärd, Karl and Albinsson, Sebastian}},
issn = {{1522-1563}},
language = {{eng}},
number = {{12}},
pages = {{1093--1101}},
publisher = {{American Physiological Society}},
series = {{American Journal of Physiology: Cell Physiology}},
title = {{Induction of angiotensin converting enzyme after miR-143/145 deletion is critical for impaired smooth muscle contractility.}},
url = {{https://lup.lub.lu.se/search/files/7280527/2260137.pdf}},
doi = {{10.1152/ajpcell.00250.2014}},
volume = {{307}},
year = {{2014}},
}