Arterial wall injury in giant cell arteritis

: Giant Cell Arteritis (GCA), or Horton’s Arteritis, is a chronic form of vasculitis of the large and medium vessels, especially involving the extracranial branches of the carotid arteries, in particular, the temporal artery, with the involvement of the axillary, femoral and iliac arteries too. Arterial wall inflammation leads to luminal occlusion and tissue ischemia, which is responsible for the clinical manifestations of the disease. : A substantial number of patients affected by GCA present head and neck symptoms, including ocular, neurological and otorhinolaryngological manifestations. : The aim of this article is to present pathogenesis, clinical aspects and treatment approaches of GCA manifestations.

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

Hypertension ◽

10.1161/01.hyp.18.4_suppl.ii47 ◽

1991 ◽

Vol 18 (4_Suppl) ◽

pp. II47-II47 ◽

Cited By ~ 11

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

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ENaC proteins contribute to VSMC migration

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.00333.2006 ◽

2006 ◽

Vol 291 (6) ◽

pp. H3076-H3086 ◽

Cited By ~ 42

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.

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