Vladimir Matchkov

siRNA-mediated knockdown of endogenously expressed bestrophin in smooth muscles.

Research output: Contribution to conferenceConference abstract for conferenceResearch

Standard

siRNA-mediated knockdown of endogenously expressed bestrophin in smooth muscles. / Larsen, Per; Matchkov, Vladimir; Nilsson, Holger et al.

2007. Abstract from Experimental Biology 2007, United States.

Research output: Contribution to conferenceConference abstract for conferenceResearch

Harvard

Larsen, P, Matchkov, V, Nilsson, H, Aalkjær, C & Pedersen, FS 2007, 'siRNA-mediated knockdown of endogenously expressed bestrophin in smooth muscles.', Experimental Biology 2007, United States, 27/04/2007 - 02/05/2007.

APA

Larsen, P., Matchkov, V., Nilsson, H., Aalkjær, C., & Pedersen, F. S. (2007). siRNA-mediated knockdown of endogenously expressed bestrophin in smooth muscles.. Abstract from Experimental Biology 2007, United States.

CBE

Larsen P, Matchkov V, Nilsson H, Aalkjær C, Pedersen FS. 2007. siRNA-mediated knockdown of endogenously expressed bestrophin in smooth muscles. Abstract from Experimental Biology 2007, United States.

MLA

Larsen, Per et al. siRNA-mediated knockdown of endogenously expressed bestrophin in smooth muscles.. Experimental Biology 2007, 27 Apr 2007, United States, Conference abstract for conference, 2007. 1 p.

Vancouver

Larsen P, Matchkov V, Nilsson H, Aalkjær C, Pedersen FS. siRNA-mediated knockdown of endogenously expressed bestrophin in smooth muscles.. 2007. Abstract from Experimental Biology 2007, United States.

Author

Larsen, Per ; Matchkov, Vladimir ; Nilsson, Holger et al. / siRNA-mediated knockdown of endogenously expressed bestrophin in smooth muscles. Abstract from Experimental Biology 2007, United States.1 p.

Bibtex

@conference{53fea66014eb11dcbee902004c4f4f50,
title = "siRNA-mediated knockdown of endogenously expressed bestrophin in smooth muscles.",
abstract = " We have recently characterized in smooth muscle cells a unique cGMP-dependent Ca2+-activated Cl- current (ICl(cGMP-Ca)) that co-exists with a {"}classical{"} Ca2+-activated Cl- current. We hypothesized that bestrophin-4 (a product of the VMD2-like 3 gene) could be responsible for the ICl(cGMP-Ca) based on similarities between membrane current produced by bestrophin heterologous expression and this endogenous current. This was supported by a similar distribution pattern of the ICl(cGMP-Ca) and the bestrophin expression. To test this hypothesis siRNA-mediated downregulation of gene expression was used. Cultured aortic smooth muscle cells (A7r5) were transfected with siRNA directed against bestrophin-4 and cultured for 3 days. The efficiency of transfection was demonstrated by specific perinuclear fluorescence of Cy3-labelled siRNA. The downregulation of targeted protein expression was controlled by qPCR and Western blot. The downregulation of bestrophin-4 expression (by 88% in mRNA) with siRNA was a associated with significant reduction (by 83%) of the ICl(cGMP-Ca) while the {"}classical{"} Ca2+-activated Cl- current was not affected.Our studies provide evidence that bestrophin-4 is responsible for the ICl(cGMP-Ca) in smooth muscle cells. This study presents a novel efficient technique for specific downregulation of gene expression in blood vessels, much needed in studies of vascular function.",
author = "Per Larsen and Vladimir Matchkov and Holger Nilsson and Christian Aalkj{\ae}r and Pedersen, {Finn Skou}",
year = "2007",
language = "English",
note = "null ; Conference date: 27-04-2007 Through 02-05-2007",

}

RIS

TY - ABST

T1 - siRNA-mediated knockdown of endogenously expressed bestrophin in smooth muscles.

AU - Larsen, Per

AU - Matchkov, Vladimir

AU - Nilsson, Holger

AU - Aalkjær, Christian

AU - Pedersen, Finn Skou

PY - 2007

Y1 - 2007

N2 -  We have recently characterized in smooth muscle cells a unique cGMP-dependent Ca2+-activated Cl- current (ICl(cGMP-Ca)) that co-exists with a "classical" Ca2+-activated Cl- current. We hypothesized that bestrophin-4 (a product of the VMD2-like 3 gene) could be responsible for the ICl(cGMP-Ca) based on similarities between membrane current produced by bestrophin heterologous expression and this endogenous current. This was supported by a similar distribution pattern of the ICl(cGMP-Ca) and the bestrophin expression. To test this hypothesis siRNA-mediated downregulation of gene expression was used. Cultured aortic smooth muscle cells (A7r5) were transfected with siRNA directed against bestrophin-4 and cultured for 3 days. The efficiency of transfection was demonstrated by specific perinuclear fluorescence of Cy3-labelled siRNA. The downregulation of targeted protein expression was controlled by qPCR and Western blot. The downregulation of bestrophin-4 expression (by 88% in mRNA) with siRNA was a associated with significant reduction (by 83%) of the ICl(cGMP-Ca) while the "classical" Ca2+-activated Cl- current was not affected.Our studies provide evidence that bestrophin-4 is responsible for the ICl(cGMP-Ca) in smooth muscle cells. This study presents a novel efficient technique for specific downregulation of gene expression in blood vessels, much needed in studies of vascular function.

AB -  We have recently characterized in smooth muscle cells a unique cGMP-dependent Ca2+-activated Cl- current (ICl(cGMP-Ca)) that co-exists with a "classical" Ca2+-activated Cl- current. We hypothesized that bestrophin-4 (a product of the VMD2-like 3 gene) could be responsible for the ICl(cGMP-Ca) based on similarities between membrane current produced by bestrophin heterologous expression and this endogenous current. This was supported by a similar distribution pattern of the ICl(cGMP-Ca) and the bestrophin expression. To test this hypothesis siRNA-mediated downregulation of gene expression was used. Cultured aortic smooth muscle cells (A7r5) were transfected with siRNA directed against bestrophin-4 and cultured for 3 days. The efficiency of transfection was demonstrated by specific perinuclear fluorescence of Cy3-labelled siRNA. The downregulation of targeted protein expression was controlled by qPCR and Western blot. The downregulation of bestrophin-4 expression (by 88% in mRNA) with siRNA was a associated with significant reduction (by 83%) of the ICl(cGMP-Ca) while the "classical" Ca2+-activated Cl- current was not affected.Our studies provide evidence that bestrophin-4 is responsible for the ICl(cGMP-Ca) in smooth muscle cells. This study presents a novel efficient technique for specific downregulation of gene expression in blood vessels, much needed in studies of vascular function.

M3 - Conference abstract for conference

Y2 - 27 April 2007 through 2 May 2007

ER -