Author response: Arterial smooth muscle cell PKD2 (TRPP1) channels regulate systemic blood pressure

Systemic blood pressure is determined, in part, by arterial smooth muscle cells (myocytes). Several Transient Receptor Potential (TRP) channels are proposed to be expressed in arterial myocytes, but it is unclear if these proteins control physiological blood pressure and contribute to hypertension in vivo. We generated the first inducible, smooth muscle-specific knockout mice for a TRP channel, namely for PKD2 (TRPP1), to investigate arterial myocyte and blood pressure regulation by this protein. Using this model, we show that intravascular pressure and α1-adrenoceptors activate PKD2 channels in arterial myocytes of different systemic organs. PKD2 channel activation in arterial myocytes leads to an inward Na+ current, membrane depolarization and vasoconstriction. Inducible, smooth muscle cell-specific PKD2 knockout lowers both physiological blood pressure and hypertension and prevents pathological arterial remodeling during hypertension. Thus, arterial myocyte PKD2 controls systemic blood pressure and targeting this TRP channel reduces high blood pressure.

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Arterial smooth muscle cell PKD2 (TRPP1) channels control systemic blood pressure

10.1101/320200 ◽

2018 ◽

Author(s):

Simon Bulley ◽

Carlos Fernandez-Pena ◽

Raquibul Hasan ◽

M. Dennis Leo ◽

Padmapriya Muralidharan ◽

...

Keyword(s):

Blood Pressure ◽

Smooth Muscle ◽

Smooth Muscle Cell ◽

Muscle Cell ◽

Transient Receptor Potential ◽

Trp Channels ◽

Systemic Blood Pressure ◽

Systemic Blood ◽

Arterial Smooth Muscle

AbstractSystemic blood pressure is determined, in part, by arterial smooth muscle cells (myocytes). Several Transient Receptor Potential (TRP) channels are proposed to be expressed in arterial myocytes, but it is unclear if these proteins control physiological blood pressure and contribute to hypertension in vivo. We generated the first inducible, smooth muscle-specific knockout for a TRP channel, namely for PKD2 (TRPP1), to investigate arterial myocyte and blood pressure regulation by this protein. Using this model, we show that intravascular pressure and α1-receptors activate PKD2 channels in arterial myocytes of different systemic organs. PKD2 channel activation in arterial myocytes leads to an inward Na+ current, membrane depolarization and vasoconstriction. Inducible, smooth muscle cell-specific PKD2 knockout lowers both physiological blood pressure and hypertension and prevents pathological arterial remodeling during hypertension. In summary, we show for the first time that arterial myocyte PKD2 channels control systemic blood pressure and targeting reduces high blood pressure.

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Regulation of pulmonary arterial smooth muscle cell function in pulmonary hypertension via Paxillin

Pneumologie ◽

10.1055/s-0032-1315542 ◽

2012 ◽

Vol 66 (06) ◽

Author(s):

C Veith ◽

M Wygrecka ◽

K Rutschmann ◽

HA Ghofrani ◽

W Seeger ◽

...

Keyword(s):

Pulmonary Hypertension ◽

Smooth Muscle ◽

Smooth Muscle Cell ◽

Muscle Cell ◽

Cell Function ◽

Arterial Smooth Muscle Cell ◽

Arterial Smooth Muscle ◽

Pulmonary Arterial ◽

Pulmonary Arterial Smooth Muscle

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Phenotypic Heterogeneity of Rat Arterial Smooth Muscle Cell Clones

Arteriosclerosis Thrombosis and Vascular Biology ◽

10.1161/01.atv.16.6.815 ◽

1996 ◽

Vol 16 (6) ◽

pp. 815-820 ◽

Cited By ~ 106

Author(s):

Marie-Luce Bochaton-Piallat ◽

Patricia Ropraz ◽

Françoise Gabbiani ◽

Giulio Gabbiani

Keyword(s):

Smooth Muscle ◽

Smooth Muscle Cell ◽

Muscle Cell ◽

Phenotypic Heterogeneity ◽

Arterial Smooth Muscle Cell ◽

Arterial Smooth Muscle ◽

Cell Clones

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An In Vitro Study of Nano-fiber Polymers for Guided Vascular Regeneration

MRS Proceedings ◽

10.1557/proc-711-gg3.2.1 ◽

2001 ◽

Vol 711 ◽

Cited By ~ 4

Author(s):

Derick C. Miller ◽

Anil Thapa ◽

Karen M. Haberstroh ◽

Thomas J. Webster

Keyword(s):

Smooth Muscle ◽

Cell Adhesion ◽

Smooth Muscle Cell ◽

Muscle Cell ◽

Surrounding Tissue ◽

Arterial Smooth Muscle Cell ◽

Arterial Smooth Muscle ◽

Cell Functions ◽

Fiber Dimensions

ABSTRACTBiomaterials that successfully integrate into surrounding tissue should match not only the tissue's mechanical properties, but also the dimensions of the associated nano-structured extra-cellular matrix (ECM) components. The goal of this research was to use these ideals to develop a synthetic, nano-structured, polymeric biomaterial that has cytocompatible and mechanical behaviors similar to that of natural vascular tissue. In a novel manner, poly-lactic acid/polyglycolic acid (PLGA) (50/50 wt.% mix) and polyurethane were separately synthesized to possess a range of fiber dimensions in the micron and nanometer regime. Preliminary results indicated that decreasing fiber diameter on both PLGA and PU enhanced arterial smooth muscle cell adhesion; specifically, arterial smooth muscle cell adhesion increased 23% when PLGA fiber dimensions decreased from 500 to 50 nm and increased 76% on nano-structured, compared to conventional structured, polyurethane. However, nano-structured PLGA decreased endothelial cell adhesion by 52%, whereas adhesion of these same cells was increased by 50% on polyurethane. For these reasons, the present in vitro study provides the first evidence that polymer fiber dimensions can be used to selectively control cell functions for vascular prosthesis.

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