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Updated: Feb 9, 2026
11:45
Generation and 3-Dimensional Quantitation of Arterial Lesions in Mice Using Optical Projection Tomography
Published on: May 26, 2015
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Notch2 and Proteomic Signatures in Mouse Neointimal Lesion Formation.
Sarah M Peterson1,2, Jacqueline E Turner1, Anne Harrington1
1From the Maine Medical Center Research Institute, Scarborough (S.M.P., J.E.T., A.H., J.D.-K., V.L., T.G., C.P.H.V., L.L.).
Arteriosclerosis, Thrombosis, and Vascular Biology
|June 2, 2018
Summary
Loss of Notch2 in smooth muscle cells does not affect neointimal lesion formation or proliferation, despite altering vascular remodeling protein profiles. Compensatory pathways likely explain the lack of increased lesion size in vascular remodeling.
Area of Science:
- Vascular Biology
- Proteomics
- Cellular Signaling
Background:
- Vascular remodeling involves complex molecular changes, with Notch2 promoting quiescence in smooth muscle cells.
- Understanding the role of Notch2 in neointimal lesion formation is crucial for vascular health.
Purpose of the Study:
- Investigate molecular signatures of neointimal lesion formation with and without Notch2.
- Test if Notch2 loss increases lesion formation due to hyperproliferation.
Main Methods:
- Utilized mass spectrometry for unbiased protein profiling of murine carotid arteries post-injury.
- Employed a tamoxifen-inducible Cre-lox system to delete Notch2 in smooth muscle cells.
- Performed morphometric analysis and immunohistochemistry to assess lesion characteristics and cell proliferation.
Main Results:
- Loss of Notch2 in smooth muscle cells altered vessel wall protein profiles during remodeling.
- No significant changes were observed in overall neointimal lesion morphology or smooth muscle cell proliferation.
- Decreased expression of enhancer of rudimentary homolog, plectin, and annexin A2 was noted in smooth muscle Notch2-deficient vessels.
Conclusions:
- Identified unique protein signatures reflecting temporal changes during neointimal lesion formation.
- Overall lesion formation was unaffected by smooth muscle Notch2 loss, suggesting compensatory mechanisms.
- Validated Notch- and injury-related targets, offering insights into conserved vascular remodeling pathways.
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