Morphologic, histologic, and immunohistochemical analyses were performed on arteries treated with the CaPO4 model and the conventional
CaCl2 model as the control. In vitro methods were performed using a mixture of CaCl2 and PBS to create CaPO4 crystals. CaPO4-induced apoptosis of primary cultured mouse vascular smooth muscle cells (VSMCs) was measured by DNA fragmentation enzyme-linked immunosorbent assay.
Results: The CaPO4 model produces AAA, defined as an increase of >= 50% in the diameter of the aorta, faster than in the CaCl2 model. The CaPO4 model showed significantly larger aneurysmal dilation at 7, 28, and 42 days, as reflected by a maximum diameter (measured in mm) fold-change of 1.69 +/- 0.07, 1.99 +/- 0.14, and 2.13 Y-27632 purchase +/- 0.09 vs 1.22 +/- 0.04, 1.48 +/- 0.07, and 1.68 +/- 0.06 in a CaCl2 model, respectively (n = 6; P < .05). A semiquantitative selleck chemical grading analysis of elastin fiber integrity at 7 days revealed a significant increase in elastin degradation in the CaPO4 model compared with the CaCl2 model (2.7 +/- 0.2 vs 1.5 +/- 0.2;
n = 6; P < .05). A significantly higher level of apoptosis occurred in the CaPO4 model (apoptosis index at 1, 2, and 3 days postsurgery: 0.26 +/- 0.14, 0.37 +/- 0.14, and 0.33 +/- 0.08 vs 0.012 +/- 0.10, 0.15 +/- 0.02, and 0.12 +/- 0.05 in the conventional CaCl2 model; n = 3; P < .05). An enhancement of macrophage infiltration and calcification was also observed at 3 and 7 days in the CaPO4 model. CaPO4 induced approximately 3.7 times more apoptosis in VSMCs than a mixture of CaCl2 (n
= 4; P < .0001) in vitro.
Conclusions: The CaPO4 model accelerates aneurysm formation with the enhancement of apoptosis, macrophage infiltration, and calcium deposition. This modified model, with its rapid and robust dilation, can be used as a new model for AAAs. (J Vasc Surg 2012;56:455-61.)”
“Neural progenitors/stem cells (NSCs) exist in neonatal mouse subventricular zone (SVZ). To explore the differentiation of the NSCs in neonatal mouse SVZ and the distribution of the progeny cells derived from these NSCs in early adulthood, the enhanced green fluorescent protein (EGFP) plasmid was transferred into the NSCs in the lateral ventricle of newborn mice (P0) by in-vivo electroporation Sitaxentan to trace these cells and their progeny cells. Thirty days after electroporation, histological sections of mouse brain were prepared for immunofluorescence with cell-specific antibodies to identify the type(s) of cells that were marked by EGFP. The results showed that EGFP-positive cells were distributed mainly in the olfactory bulb (OB), cortex, and SVZ, and double labeled with NeuN (neuron marker) in OB, glial fibrillary acidic protein (GFAP) (astrocyte marker) in the cortex, and Blbp and GFAP (astrocyte marker) in SVZ. However, there was no-EGFP-positive cell in the hippocampus.