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Orthotopic Aortic Transplantation in Mice for the Study of Vascular Disease
Published on: November 28, 2012
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AKT2 Promotes Bone Marrow Cell-Mediated Aortic Protection in Mice
Sili Zou1, Pingping Ren2, Lin Zhang2
1Division of Cardiothoracic Surgery, Michael E. DeBakey Department of Surgery, Baylor College of Medicine, Houston, Texas; Department of Cardiovascular Surgery, Texas Heart Institute, Houston, Texas; Department of Vascular Surgery, Changzheng Hospital, Second Military Medical University, Shanghai, China.
The Annals of Thoracic Surgery
|April 20, 2016
Summary
Bone marrow cells (BMCs) protect the aorta from aneurysms and dissections (AAD). AKT2 in BMCs is crucial for this protection, as its absence leads to severe aortic damage and AAD development.
Area of Science:
- Cardiovascular Biology
- Vascular Biology
- Regenerative Medicine
Background:
- Aortic aneurysms and dissections (AAD) develop due to insufficient aortic protection and repair.
- Mechanisms underlying aortic protection and repair are not fully understood.
- The multifunctional kinase AKT2 is known to protect the aortic wall.
Purpose of the Study:
- To investigate if AKT2 promotes bone marrow cell (BMC)-mediated aortic protection against AAD.
- To elucidate the role of AKT2 in BMC function during aortic injury.
Main Methods:
- Wild-type mice received BMCs from wild-type or Akt2(-/-) donors and were infused with angiotensin II.
- BMC recruitment, aortic destruction, and AAD development were compared between groups.
- Direct effects of wild-type and Akt2(-/-) BMCs on smooth muscle cell survival were assessed in coculture.
Main Results:
- Akt2(-/-) BMC recipients showed significantly higher rates of AAD (64%) and aortic destruction compared to wild-type BMC recipients (0%).
- Aortas from Akt2(-/-) BMC recipients had reduced BMC recruitment, progenitor/fibroblast activation, and increased apoptosis/inflammation.
- Wild-type BMCs, but not Akt2(-/-) BMCs, protected smooth muscle cells from apoptosis in vitro.
Conclusions:
- BMCs are recruited to the aorta post-challenge, activating progenitors and fibroblasts to promote aortic cell survival and protection.
- AKT2 is essential for these protective BMC functions.
- Defects in AKT2 signaling within BMCs may drive aortic degeneration and AAD progression.
