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• W2063978768 abstract "Introduction: Vascular remodeling is a dynamic process affected by changes in the hemodynamic environment as well as direct vessel wall injury. Vascular smooth muscle cells (VSMC) undergo pathologic proliferation in response to both balloon induced injury and low flow hemodynamic states. Apoptosis, or programmed cell death, exists as a homeostatic defense mechanism to maintain cell populations in various tissues with proliferative activity, including VSMC. The purpose of this study was to assess the apoptotic response of vessels following exposure to low shear stress “τ”, balloon injury, and a combination of the two. It was hypothesized that combined low shear stress and balloon injury would result in an increased VSMC apoptotic response as compared to low shear stress or balloon injury alone. Methods: Using standard sterile techniques, the left common carotid artery (CCA) of 28 New Zealand White Rabbits was exposed. For the “low τ” group (n=7), the CCA was restricted by ligating the artery over a 0.014 guide wire distal to the cranial thyroid branch. For the “balloon injury” group (n=7), injury was created using 3 passes of a 3F balloon catheter in a 1.1:1 balloon to vessel wall diameter ratio. For the “low τ + balloon injury” group (n=7) the artery was balloon injured first then restricted as described above. For the sham group (n=7), the CCA was temporally exposed. At 3 days (n=12), the CCA was harvested. Apoptosis was assessed with TUNEL immunostaining and with caspase-3 Western Blot analysis as well as immunostaining. After 4 weeks, the remaining arteries were harvested and neointimal thickening (NIT), and wall thickness were measured and compared using One Way ANOVA with significance assigned at p<0.05. Results: All arteries were patent at sacrifice. Assessment of apoptosis at day 3 by TUNEL and caspase- 3 immunostaining revealed significantly greater apoptosis in the “low τ + balloon injury” group as compared to the sham and groups exposed to either “low τ” or “balloon injury” alone. (Fig. 1) At 4 weeks, there was a significant increase in NIT, in addition to an increase in both medial and total wall thickness in the “low τ + balloon injury” group as compared to the other groups. (Table 1, Fig. 2) Conclusions: An increase in vascular wall apoptosis via a caspase-3 dependent pathway is up-regulated in the face of combined low shear stress and balloon induced vessel wall injury. Paradoxically, this increase in apoptosis is associated with a significant increase in NIT and overall wall thickness. This paradoxical effect indicates an intensely coordinated response of cellular proliferation and cellular demise involved in vascular remodeling following balloon induced injury in the setting of low shear stress. TABLE 1 Model Neointimal thickness (μm) Medial thickness (μm) Intima:Media Wall thickness (μm) Sham 0 146 ± 18 0 146 ± 18 Low t 26 ± 3 † P < .05 compared to low t + balloon injury group. 165 ± 14 0.16 ± 0.02 † P < .05 compared to low t + balloon injury group. 191 ± 15 † P < .05 compared to low t + balloon injury group. Balloon Injury 51 ± 17 ⁎ P < .05 compared to sham. † P < .05 compared to low t + balloon injury group. 120 ± 17 † P < .05 compared to low t + balloon injury group. 0.45 ± 0.17 ⁎ P < .05 compared to sham. 171 ± 22 † P < .05 compared to low t + balloon injury group. Low t + Balloon Injury 176 ± 17 ⁎ P < .05 compared to sham. 220 ± 10 ⁎ P < .05 compared to sham. 0.80 ± 0.09 ⁎ P < .05 compared to sham. 396 ± 19 ⁎ P < .05 compared to sham. Expressed as mean ± SEM;. P < .05 compared to sham. † P < .05 compared to low t + balloon injury group. Open table in a new tab View Large Image Figure Viewer Expressed as mean ± SEM;." @default.
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• W2063978768 date "2008-02-01" @default.
• W2063978768 modified "2023-10-18" @default.
• W2063978768 title "QS358. Programmed Cell Death in Low Shear Stress and Balloon Induced Arterial Restenosis" @default.
• W2063978768 doi "https://doi.org/10.1016/j.jss.2007.12.612" @default.
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