Publications by authors named "Jessica Davis-Knowlton"
Introduction: We previously identified Notch2 in smooth muscle cells (SMC) in human atherosclerosis and found that signaling via Notch2 suppressed human SMC proliferation. Thus, we tested whether loss of Notch2 in SMC would alter atherosclerotic plaque progression using a mouse model.
Methods: Atherogenesis was examined at the brachiocephalic artery and aortic root in a vascular SMC null (inducible smooth muscle myosin heavy chain Cre) Notch2 strain on the ApoE-/- background.
Pathological Conversion of Mouse Perivascular Adipose Tissue by Notch Activation.
Arterioscler Thromb Vasc Biol
September 2020
Objective: Perivascular adipose tissue (PVAT) surrounding arteries supports healthy vascular function. During obesity, PVAT loses its vasoprotective effect. We study pathological conversion of PVAT, which involves molecular changes in protein profiles and functional changes in adipocytes.
View Article and Find Full Text PDFEnd stage kidney disease affects hundreds of thousands of patients in the United States. The therapy of choice is kidney replacement, but availability of organs is limited, and alternative sources of tissue are needed. Generation of new kidney tissue in the laboratory has been made possible through pluripotent cell reprogramming and directed differentiation.
View Article and Find Full Text PDFNotch2 and Proteomic Signatures in Mouse Neointimal Lesion Formation.
Arterioscler Thromb Vasc Biol
July 2018
Article Synopsis
- The study focuses on how the loss of Notch2, a protein that promotes cell quiescence, affects the formation of neointimal lesions in arteries after injury.
- Using mass spectrometry and other analysis techniques on mice, researchers found that while loss of Notch2 changed protein profiles in the vessel wall, it did not significantly alter overall lesion formation or smooth muscle cell proliferation.
- The research identified specific protein signatures linked to vascular remodeling, indicating that other compensatory mechanisms might take over when Notch2 is absent, highlighting the complexity of vascular responses to injury.
Article Synopsis
- - Atherosclerosis is a major cause of heart disease and stroke, and while animal models have helped us understand the disease's molecular mechanisms, insights from human tissue, particularly plaque from surgeries, are crucial for further study.
- - Researchers compared vascular smooth muscle cells (SMC) from diseased tissues (after endarterectomy) with healthy donor arteries, focusing on Notch signaling's role in SMC behavior and plaque formation.
- - They utilized advanced proteomic analysis to identify different protein expressions in diseased SMC, discovering that Notch2 signaling can influence SMC growth, but does not enhance mature muscle characteristics, indicating a complex interaction in atherosclerosis progression.