Vascular smooth muscle cell apoptosis in aneurysmal, occlusive, and normal human aortas

Vincent L. Rowe, Scott Stevens, Tonya T. Reddick, Michael Freeman, Robert Donnell, Roger C. Carroll, Mitchell Goldman

Research output: Contribution to journalArticle

71 Citations (Scopus)

Abstract

Purpose: Apoptosis is a physiologic mechanism of cell death that regulates mass and architecture in many tissues. Apoptosis has been described as a feature in human vascular atherosclerosis and large vessel structural integrity. We examined the extent of vascular smooth muscle cell (VSMC) apoptosis in aneurysmal, occlusive, and normal human aortic tissue. Methods: Tissue samples of aneurysmal, occlusive, and normal human infrarenal aorta were evaluated. DNA fragmentation detection methods, immunohistochemistry, and DNA electrophoresis determined VSMC density, VSMC apoptosis, and apoptosis markers. Apoptotic cells and VSMC nuclei were counted with the use of computer-generated image analysis. Aortic subtypes were compared statistically by analysis of variance. Results: Seventeen aneurysmal, ten occlusive, and five normal human aortas were evaluated. By α1-actin immunostaining, VSMC density was least in aneurysmal aortas (271.8 ± 13.5 cells/high-power field [HPF]) compared with occlusive aorta (278.2 ± 39.4 cells/HPF) and normal aortas (291.0 ± 25.4 cells/HPF; P = not significant). Presence of apoptotic VSMCs was demonstrated by terminal deoxynucleotidyl transferase fragment end labeling and propidium iodide nuclear staining. VSMC apoptosis was greatest within aneurysmal aortas with 11.7 ± 1.5 cells/HPF compared with occlusive aortas with 3.3 ± 0.8 cells/HPF (P < .05) and normal aortas with 3.75 ± 4.6 cells/HPF (P < .05). Significant differences in apoptosis markers, p53 or bcl-2, could not be demonstrated by immunohistochemistry or DNA electrophoresis in aortic subtypes. Conclusion: Apoptosis of VSMCs is increased and VSMC density is decreased within the medial layer of aneurysmal aortic tissue. Structural degeneration of aortic tissue at the cellular level contributes to aneurysmal formation.

Original languageEnglish (US)
Pages (from-to)567-576
Number of pages10
JournalJournal of Vascular Surgery
Volume31
Issue number3
DOIs
StatePublished - Jan 1 2000

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Vascular Smooth Muscle
Smooth Muscle Myocytes
Aorta
Apoptosis
Cell Count
Electrophoresis
Immunohistochemistry
DNA Nucleotidylexotransferase
Propidium
DNA
DNA Fragmentation
Cell Nucleus
Blood Vessels
Actins
Atherosclerosis
Analysis of Variance
Cell Death
Staining and Labeling

All Science Journal Classification (ASJC) codes

  • Surgery
  • Cardiology and Cardiovascular Medicine

Cite this

Vascular smooth muscle cell apoptosis in aneurysmal, occlusive, and normal human aortas. / Rowe, Vincent L.; Stevens, Scott; Reddick, Tonya T.; Freeman, Michael; Donnell, Robert; Carroll, Roger C.; Goldman, Mitchell.

In: Journal of Vascular Surgery, Vol. 31, No. 3, 01.01.2000, p. 567-576.

Research output: Contribution to journalArticle

Rowe, Vincent L. ; Stevens, Scott ; Reddick, Tonya T. ; Freeman, Michael ; Donnell, Robert ; Carroll, Roger C. ; Goldman, Mitchell. / Vascular smooth muscle cell apoptosis in aneurysmal, occlusive, and normal human aortas. In: Journal of Vascular Surgery. 2000 ; Vol. 31, No. 3. pp. 567-576.
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T1 - Vascular smooth muscle cell apoptosis in aneurysmal, occlusive, and normal human aortas

AU - Rowe, Vincent L.

AU - Stevens, Scott

AU - Reddick, Tonya T.

AU - Freeman, Michael

AU - Donnell, Robert

AU - Carroll, Roger C.

AU - Goldman, Mitchell

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N2 - Purpose: Apoptosis is a physiologic mechanism of cell death that regulates mass and architecture in many tissues. Apoptosis has been described as a feature in human vascular atherosclerosis and large vessel structural integrity. We examined the extent of vascular smooth muscle cell (VSMC) apoptosis in aneurysmal, occlusive, and normal human aortic tissue. Methods: Tissue samples of aneurysmal, occlusive, and normal human infrarenal aorta were evaluated. DNA fragmentation detection methods, immunohistochemistry, and DNA electrophoresis determined VSMC density, VSMC apoptosis, and apoptosis markers. Apoptotic cells and VSMC nuclei were counted with the use of computer-generated image analysis. Aortic subtypes were compared statistically by analysis of variance. Results: Seventeen aneurysmal, ten occlusive, and five normal human aortas were evaluated. By α1-actin immunostaining, VSMC density was least in aneurysmal aortas (271.8 ± 13.5 cells/high-power field [HPF]) compared with occlusive aorta (278.2 ± 39.4 cells/HPF) and normal aortas (291.0 ± 25.4 cells/HPF; P = not significant). Presence of apoptotic VSMCs was demonstrated by terminal deoxynucleotidyl transferase fragment end labeling and propidium iodide nuclear staining. VSMC apoptosis was greatest within aneurysmal aortas with 11.7 ± 1.5 cells/HPF compared with occlusive aortas with 3.3 ± 0.8 cells/HPF (P < .05) and normal aortas with 3.75 ± 4.6 cells/HPF (P < .05). Significant differences in apoptosis markers, p53 or bcl-2, could not be demonstrated by immunohistochemistry or DNA electrophoresis in aortic subtypes. Conclusion: Apoptosis of VSMCs is increased and VSMC density is decreased within the medial layer of aneurysmal aortic tissue. Structural degeneration of aortic tissue at the cellular level contributes to aneurysmal formation.

AB - Purpose: Apoptosis is a physiologic mechanism of cell death that regulates mass and architecture in many tissues. Apoptosis has been described as a feature in human vascular atherosclerosis and large vessel structural integrity. We examined the extent of vascular smooth muscle cell (VSMC) apoptosis in aneurysmal, occlusive, and normal human aortic tissue. Methods: Tissue samples of aneurysmal, occlusive, and normal human infrarenal aorta were evaluated. DNA fragmentation detection methods, immunohistochemistry, and DNA electrophoresis determined VSMC density, VSMC apoptosis, and apoptosis markers. Apoptotic cells and VSMC nuclei were counted with the use of computer-generated image analysis. Aortic subtypes were compared statistically by analysis of variance. Results: Seventeen aneurysmal, ten occlusive, and five normal human aortas were evaluated. By α1-actin immunostaining, VSMC density was least in aneurysmal aortas (271.8 ± 13.5 cells/high-power field [HPF]) compared with occlusive aorta (278.2 ± 39.4 cells/HPF) and normal aortas (291.0 ± 25.4 cells/HPF; P = not significant). Presence of apoptotic VSMCs was demonstrated by terminal deoxynucleotidyl transferase fragment end labeling and propidium iodide nuclear staining. VSMC apoptosis was greatest within aneurysmal aortas with 11.7 ± 1.5 cells/HPF compared with occlusive aortas with 3.3 ± 0.8 cells/HPF (P < .05) and normal aortas with 3.75 ± 4.6 cells/HPF (P < .05). Significant differences in apoptosis markers, p53 or bcl-2, could not be demonstrated by immunohistochemistry or DNA electrophoresis in aortic subtypes. Conclusion: Apoptosis of VSMCs is increased and VSMC density is decreased within the medial layer of aneurysmal aortic tissue. Structural degeneration of aortic tissue at the cellular level contributes to aneurysmal formation.

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