Deep Learning-Based Automated Detection of Arterial Vessel Wall and Plaque on Magnetic Resonance Vessel Wall Images.

Purpose: To develop and evaluate an automatic segmentation method of arterial vessel walls and plaques, which is beneficial for facilitating the arterial morphological quantification in magnetic resonance vessel wall imaging (MRVWI). Methods: MRVWI images acquired from 124 patients with atherosclerotic plaques were included. A convolutional neural network-based deep learning model, namely VWISegNet, was used to extract the features from MRVWI images and calculate the category of each pixel to facilitate the segmentation of vessel wall. Two-dimensional (2D) cross-sectional slices reconstructed from all plaques and 7 main arterial segments of 115 patients were used to build and optimize the deep learning model. The model performance was evaluated on the remaining nine-patient test set using the Dice similarity coefficient (DSC) and average surface distance (ASD). Results: The proposed automatic segmentation method demonstrated satisfactory agreement with the manual method, with DSCs of 93.8% for lumen contours and 86.0% for outer wall contours, which were higher than those obtained from the traditional U-Net, Attention U-Net, and Inception U-Net on the same nine-subject test set. And all the ASD values were less than 0.198 mm. The Bland-Altman plots and scatter plots also showed that there was a good agreement between the methods. All intraclass correlation coefficient values between the automatic method and manual method were greater than 0.780, and greater than that between two manual reads. Conclusion: The proposed deep learning-based automatic segmentation method achieved good consistency with the manual methods in the segmentation of arterial vessel wall and plaque and is even more accurate than manual results, hence improved the convenience of arterial morphological quantification.

OxLDL stimulates Id1 nucleocytoplasmic shuttling in endothelial cell angiogenesis via PI3K pathway.

Angiogenesis plays remarkable roles in the development of atherosclerotic rupture plaques. However, its essential mechanism remains unclear. The purpose of the study was to investigate whether inhibitor of DNA binding-1 or inhibitor of differentiation 1 (Id1) promoted angiogenesis when exposed to oxidised low-density lipoprotein (oxLDL), and to determine the molecular mechanism involved. Using aortic ring assay and tube formation assay as a model system, a low concentration of oxLDL was found to induce angiogenic sprouting and capillary lumen formation of endothelial cell. But the Id1 expression was significantly upregulated by oxLDL at low and high concentrations. The Id1 was localised in the nuclei of the human umbilical vein endothelial cells in the control group and in the high-concentration oxLDL group. Id1 was translocated to the cytoplasm at low oxLDL concentrations. The nucleocytoplasmic shuttling at low oxLDL concentration was inhibited by treatment with the nuclear export inhibitor leptomycin B. Protein kinase A (PKA) inhibitor H89 promoted nuclear export of Id1, and phosphatidylinositol-3-kinase (PI3K) inhibitor LY294002 reduced the nuclear export of Id1. PI3K inhibition blocked oxLDL-induced angiogenesis. Low concentrations of oxLDL promoted angiogenic sprouting and capillary formation. And this process depends on nuclear export of Id1, which in turn is controlled by the PI3K pathway. This report presents a new link between oxLDL and Id1 localisation, and may provide a new insight into the interactions of ox-LDL and Id1 in the context of atherosclerosis.

Id1 induces tubulogenesis by regulating endothelial cell adhesion and cytoskeletal organization through ß1-integrin and Rho-kinase signalling.

The inhibitor of differentiation 1 (Id1) protein is required for tubulogenesis, but the molecular signalling pathways remain unclear. Overexpression (Id1-t) or down-regulation (si-Id1) of Id-1 in cell lines, were used to study the function of Id1. The expression of Id1 and ß1-integrin was assessed by Western blotting. Up-regulation of Id1 in human umbilical vascular endothelial cells (HUVECs) activated the expression of ß1-integrin and promoted cell adhesion and spreading. Conversely, down-regulation of Id1 suppressed ß1-integrin expression and inhibited tubulogenesis. By using a ß1-integrin antibody to inhibit ß1-integrin function, we demonstrated that Id1-induced cell adhesion and tubulogenesis were mediated by ß1-integrin. In addition, HUVECs overexpressing Id1 were able to promote capillary tube formation through cytoskeleton reorganization and cell contraction. Finally, the Rho-kinase inhibitor Y27632 inhibited tubulo-genesis induced by Id1. Our findings provide evidence that Id1 regulates tubulogenesis in vitro through ß1-integrin and Rho-kinase signalling.