Evidence for the Rapid Onset of Apoptosis in Medial Smooth Muscle Cells After Balloon Injury

Perlman, Harris; Maillard, Luc; Krasinski, Kevin; Walsh, Kenneth

doi:10.1161/01.cir.95.4.981

Cited by 267 publications

(175 citation statements)

References 19 publications

Supporting

Mentioning

152

Contrasting

Unclassified

Order By: Relevance

“…Cho et al (22) reported that reduction in blood flow in animal models resulted in reduction in VSMC number by apoptosis (22,23). Acute arterial injury is followed by rapid induction of medial cell apoptosis from 30 min to 4 h (24,25). In humans, restenosis after angioplasty has been reported to be associated with a decrease in VSMC apoptosis (21).…”

Section: Discussionmentioning

confidence: 99%

High Glucose Inhibits Apoptosis Induced by Serum Deprivation in Vascular Smooth Muscle Cells via Upregulation of Bcl-2 and Bcl-xl

Télémaque

Miller

et al. 2005

Diabetes

View full text Add to dashboard Cite

show abstract

Section: Discussionmentioning

confidence: 99%

High Glucose Inhibits Apoptosis Induced by Serum Deprivation in Vascular Smooth Muscle Cells via Upregulation of Bcl-2 and Bcl-xl

Télémaque

Miller

et al. 2005

Diabetes

View full text Add to dashboard Cite

show abstract

“…Apoptotic death of smooth muscle cells is observed as early as 30 min after arterial injury and is associated with decreased expression of the anti-apoptotic protein Bcl-x (Perlman et al, 1997). After then, a second window of apoptosis is observed and is associated with increased smooth muscle cell proliferation (Han et al, 1995).…”

Section: Apoptosis In Restenosismentioning

confidence: 99%

Apoptosis in the vasculature: mechanisms and functional importance

Mallat¹,

Tedgui²

2000

British J Pharmacology

307

214

View full text Add to dashboard Cite

Apoptotic death has now been recognized in a number of common and threatening vascular diseases, including atherosclerosis. Interest in apoptosis research relates to the fact that apoptosis, in contrast to oncosis, is a highly regulated process of cell death which raises the hope for the development of speci®c therapeutic strategies to alter disease progression. This review summarizes the mechanisms involved in vascular endothelial and smooth muscle cell survival/apoptosis, and the potential roles of apoptotic death in atherosclerosis and restenosis. The potential e ects of modulation of apoptosis in these diseases are also discussed.

show abstract

“…The oncogene c-myc is known to be upregulated during this time and is thought to be a prime contributor to SMC proliferation following injury (Ross 1993). It now appears that proliferating cells are not the only type of VSMCs found in the injured arterial wall, but that widespread VSMC apoptosis occurs following balloon catheter injury (Perlman et al 1997). In fact, within 30 min of balloon injury to rat carotid arteries, up to 70% of medial VSMCs were found to undergo apoptosis (Perlman ef af.…”

Section: Introductionmentioning

confidence: 99%

Morphologic and temporal analysis of vascular smooth muscle cell apoptosis induced by c‐Myc and E1A

1998

View full text Add to dashboard Cite

Summary: Apoptosis is a physiologic form of cell death present in many disease conditions. When the balance of mitosis versus apoptosis is altered, tumor-like growth or degeneration of tissues may ensue. This appears to occur in several diseases, including those of the cardiovascular system, where apoptosis plays a key role in atherosclerosis and restenosis following angioplasty. Since c-my is upregulated in the pathogenesis of these diseases. we chose to study the sequential morphologic features of programmed cell death in vascular smooth muscle cells induced by c-m.yc and by the adenovirus early gene E 1 A. Morphology and timed events in apoptotic cell cultures were analyzed by scanning electron microscopy, transmission electron microscopy, and time-lapse videomicroscopy. We observed that both c-mycand E 1 A-induced apoptosis (in serum-free medium) resulted in numerous, tightly packed clusters of apoptotic blebs, as well as in one or two asymmetrically larger blebs. Transmission electron microscopy analysis revealed the larger blebs contained mostly nuclear chromatin, whereas the many smaller fragments often had little or no chromatin. Timelapse studies showed that apoptosis was induced at a slower rate in cells stably transfected with c-nz.vc versus those stably transfected with EIA. The early changes of apoptosis, including cell shrinkage and intense blebbing, occurred in under 5 min in both cells. Slight alterations such as cell size and further rounding occurred up to 8 h following the initial changes of apoptosis. Rather than being a part of the apoptotic response, release from the culture floor almost entirely resulted from movement of the culture flask. These stud- Professor of Medicine Medical Microbiology and Immunology, and Biomedical Science Creighton University School of Medicine 2500 California Plaza Omaha, NE 68 178. USA E-mail: dkagr@creighton.edu ies provide a framework of timed morphologic events for future mechanistic investigation into the key aspects of mycand El A-induced apoptosis in vascular smooth muscle.

show abstract

Evidence for the Rapid Onset of Apoptosis in Medial Smooth Muscle Cells After Balloon Injury

Cited by 267 publications

References 19 publications

High Glucose Inhibits Apoptosis Induced by Serum Deprivation in Vascular Smooth Muscle Cells via Upregulation of Bcl-2 and Bcl-xl

High Glucose Inhibits Apoptosis Induced by Serum Deprivation in Vascular Smooth Muscle Cells via Upregulation of Bcl-2 and Bcl-xl

Apoptosis in the vasculature: mechanisms and functional importance

Morphologic and temporal analysis of vascular smooth muscle cell apoptosis induced by c‐Myc and E1A

Contact Info

Product

Resources

About