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Published on: November 8, 2017
Mitochondrial-dependent apoptosis in experimental rodent abdominal aortic aneurysms
Indranil Sinha1, Amiya P Sinha-Hikim, Kevin K Hannawa
1Jobst Vascular Research Laboratories, Section of Vascular Surgery, Department of Surgery, University of Michigan, Ann Arbor, USA.
Surgery
|November 5, 2005
Summary
This study reveals that intrinsic, mitochondrial-dependent apoptosis, marked by caspase-9 activation, plays a role in abdominal aortic aneurysm (AAA) development. This intrinsic pathway contributes to cell death in experimental AAA formation.
Area of Science:
- Cardiovascular Biology
- Cellular Biology
- Pathology
Background:
- Extrinsic apoptosis pathways are known contributors to abdominal aortic aneurysm (AAA) pathogenesis.
- The role of intrinsic, mitochondrial-dependent apoptosis in AAA formation remains less understood.
Purpose of the Study:
- To investigate the hypothesis that intrinsic, mitochondrial-dependent apoptosis contributes to experimental AAA formation.
- To identify the specific apoptotic pathways involved in AAA development.
Main Methods:
- Rat aortas were subjected to elastase or saline perfusion and harvested after 7 days.
- Transmission electron microscopy, TUNEL assay, and immunohistochemistry for caspase-9, caspase-3, and Bid were performed.
- Quantitative analysis of apoptotic cells was conducted.
Main Results:
- Elastase perfusion significantly increased aortic diameter compared to saline controls.
- Apoptosis was observed in smooth muscle cells, macrophages, and neutrophils in aneurysmal aortas.
- Caspase-9, a key initiator of intrinsic apoptosis, was detected exclusively in elastase-perfused aortas.
Conclusions:
- Apoptosis is prevalent in multiple cell types within elastase-induced aneurysmal aortas.
- The presence of caspase-9 in aneurysmal aortas indicates activation of the intrinsic apoptotic pathway.
- Mitochondrial-dependent apoptosis is associated with the development of abdominal aortic aneurysms.
