Polyclonal 111In-IgG, 125I-LDL and 125I-endothelin-1 accumulation in experimental arterial wall injury

1993 ◽  
Vol 20 (12) ◽  
Author(s):  
L. Prat ◽  
G. Torres ◽  
I. Carri� ◽  
M. Roca ◽  
V. Riambau ◽  
...  
Keyword(s):  
Arterial Wall ◽  
Endothelin 1 ◽  
Arterial Wall Injury ◽  
Wall Injury

Effect of converting enzyme inhibition on allograft-induced arterial wall injury and response.

Hypertension ◽  
1991 ◽  
Vol 18 (4_Suppl) ◽  
pp. II47-II47 ◽  
Author(s):  
D. Plissonnier ◽  
G. Amichot ◽  
M. Duriez ◽  
J. Legagneux ◽  
B. I. Levy ◽  
...  
Keyword(s):  
Enzyme Inhibition ◽  
Arterial Wall ◽  
Converting Enzyme ◽  
Converting Enzyme Inhibition ◽  
Arterial Wall Injury ◽  
Wall Injury

ENaC proteins contribute to VSMC migration

2006 ◽  
Vol 291 (6) ◽  
pp. H3076-H3086 ◽  
Author(s):  
Samira C. Grifoni ◽  
Kimberly P. Gannon ◽  
David E. Stec ◽  
Heather A. Drummond
Keyword(s):  
Tissue Repair ◽  
Arterial Wall ◽  
Vascular Tissue ◽  
Rt Pcr ◽  
Mechanical Signaling ◽  
Signaling Mechanisms ◽  
Isolated Artery ◽  
Arterial Wall Injury ◽  
Wall Injury ◽  
Interfering Rna

Vascular smooth muscle cell (VSMC) migration plays a key role in tissue repair after arterial wall injury. VSMC migration requires integration of chemical and mechanical signaling mechanisms. Recently, we showed that epithelial Na+ channel (ENaC) proteins are expressed in VSMCs and that ENaC inhibition abolishes pressure-induced constriction in isolated artery segments. However, whether ENaC proteins play a role in VSMC migration is unknown. The goal of this study was to determine whether ENaC molecules are required for VSMC migration. Using RT-PCR, immunoblotting, and immunolabeling, we detected expression of α-, β-, and γENaC transcripts and proteins in cultured VSMCs (SV40-LT and A10 cells). Of the three proteins, βENaC was the most readily detected in both cell lines by immunolocalization and Western blotting. Inhibition of ENaC activity with 1 μM benzamil blunted VSMC migration associated with wound healing (40.3% at 8 h and 26.2% at 24 h) and in response to the chemotactic stimulant platelet-derived growth factor-BB (38.1%). Furthermore, silencing ENaC gene expression with small interfering RNA blunted VSMC migration. These data indicate that expression of ENaC proteins is required for normal VSMC migration and suggest a potential new role for ENaC proteins in vascular tissue repair.

Relationship between Platelets and Neutrophil Adhesion and Neointimal Growth after Repeated Arterial Wall Injury Induced by Angioplasty in Pigs

2001 ◽  
Vol 38 (2) ◽  
pp. 153-162 ◽  
Author(s):  
Jean-Guy Bienvenu ◽  
Jean-François Tanguay ◽  
Patrick Chauvet ◽  
Yahye Merhi
Keyword(s):  
Arterial Wall ◽  
Neutrophil Adhesion ◽  
Arterial Wall Injury ◽  
Wall Injury

The Effect of Prolonged Aspirin Therapy on Experimental Balloon-Catheter Arterial Wall Injury

1990 ◽  
Vol 3 (1) ◽  
pp. 5-10 ◽  
Author(s):  
Richard A. Yeager ◽  
Dennis R. Trune ◽  
Susamarie Jacobson ◽  
Reid S. Connell ◽  
William T. Galey ◽  
...  
Keyword(s):  
Arterial Wall ◽  
Balloon Catheter ◽  
Aspirin Therapy ◽  
Arterial Wall Injury ◽  
Wall Injury

Arterial wall injury, arterial wall healing and restenosis

1991 ◽  
Vol 6 (3) ◽  
pp. 271-279 ◽  
Author(s):  
L. Van Erven ◽  
M. J. Post ◽  
C. Borst
Keyword(s):  
Arterial Wall ◽  
Arterial Wall Injury ◽  
Wall Injury
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