The central nervous system and atherogenesis: role of the arterial smooth muscle cell

1990 ◽  
Vol 82 (1-2) ◽  
pp. 145-155 ◽  
Author(s):  
W GUTSTEIN
2020 ◽  
Vol 11 ◽  
Author(s):  
Sophie A. Millar ◽  
Stephen G. John ◽  
Christopher W. McIntyre ◽  
Vera Ralevic ◽  
Susan I. Anderson ◽  
...  

2001 ◽  
Vol 281 (1) ◽  
pp. L1-L12 ◽  
Author(s):  
Elizabeth A. Coppock ◽  
Jeffrey R. Martens ◽  
Michael M. Tamkun

The hypoxia-induced membrane depolarization and subsequent constriction of small resistance pulmonary arteries occurs, in part, via inhibition of vascular smooth muscle cell voltage-gated K+(KV) channels open at the resting membrane potential. Pulmonary arterial smooth muscle cell KV channel expression, antibody-based dissection of the pulmonary arterial smooth muscle cell K+ current, and the O2 sensitivity of cloned KV channels expressed in heterologous expression systems have all been examined to identify the molecular components of the pulmonary arterial O2-sensitive KV current. Likely components include Kv2.1/Kv9.3 and Kv1.2/Kv1.5 heteromeric channels and the Kv3.1b α-subunit. Although the mechanism of KV channel inhibition by hypoxia is unknown, it appears that KV α-subunits do not sense O2 directly. Rather, they are most likely inhibited through interaction with an unidentified O2 sensor and/or β-subunit. This review summarizes the role of KV channels in hypoxic pulmonary vasoconstriction, the recent progress toward the identification of KV channel subunits involved in this response, and the possible mechanisms of KV channel regulation by hypoxia.


1996 ◽  
Vol 16 (6) ◽  
pp. 815-820 ◽  
Author(s):  
Marie-Luce Bochaton-Piallat ◽  
Patricia Ropraz ◽  
Françoise Gabbiani ◽  
Giulio Gabbiani

2001 ◽  
Vol 711 ◽  
Author(s):  
Derick C. Miller ◽  
Anil Thapa ◽  
Karen M. Haberstroh ◽  
Thomas J. Webster

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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