Obstructive nephropathy ultimately leads to end-stage renal failure. Renovascular lesions are involved in various nephropathies, and most renal diseases have an ischemic component that underlies the resulting renal fi...Obstructive nephropathy ultimately leads to end-stage renal failure. Renovascular lesions are involved in various nephropathies, and most renal diseases have an ischemic component that underlies the resulting renal fibrosis. The aim of this study was to investigate whether morphological changes occur in the renal vasculature in hydronephrosis and the possible mechanisms involved. A model of complete unilateral ureteral obstruction（CUUO） was used. Experimental animals were divided into five groups： a normal control group（N） and groups of animals at 1st week（O1）, 2nd week（O2）, 4th week（O4） and 8th week（O8） after CUUO. Blood pressure was measured, renal arterial trees and glomeruli were assessed quantitatively, and renovascular three-dimensional reconstruction was performed on all groups. Glomerular ultrastructural changes were examined by transmission electron microscopy. The results showed that the systolic blood pressure was significantly increased in the obstructed groups（O1, O2, O4 and O8）. Three-dimensional reconstruction showed sparse arterial trees in the O8 group, and a tortuous and sometimes ruptured glomerular basement membrane was found in the O4 and O8 groups. Furthermore, epithelial media thickness and media/lumen ratio were increased, lumen diameters were decreased, and the cross-sectional area of the media was unaltered in the segmental renal artery, interlobar artery and afferent arterioles, respectively. In conclusion, renal arterial trees and glomeruli were dramatically altered following CUUO and the changes may be partially ascribed to vascular remodeling. Elucidation of the molecular mechanisms of renovascular morphological alterations will enable the development of potential therapeutic approaches for hydronephrosis.展开更多
Background This study aimed to investigate the effect of pcDNA3.1-vascular endothelial growth factor （VEGF）165 vector on vertebral cartilage endplate vascular buds and intervertebral discs. Methods Rabbits were rand...Background This study aimed to investigate the effect of pcDNA3.1-vascular endothelial growth factor （VEGF）165 vector on vertebral cartilage endplate vascular buds and intervertebral discs. Methods Rabbits were randomly assigned to the control and experimental groups with 10 in each. In the experimental group, we anesthetized the rabbits and exposed the front vertebral body. Using the mark of the longitudinal ossature of the front vertebral body of the lumbar vertebrae, we advanced a needle at the central point of the front fourth and fifth lumbar intervertebral discs and injected 20 pl pcDNA3.1-VEGF165. Similarly, in the control group, we injected 20 IJl pcDNA3.1. At 4 and 8 weeks post-injection, we examined the changes of the vertebral cartilage endplate using X-ray radiograph, histology, and scanning electron microscopy. Results The vertebral cartilage endplate calcification and degeneration in the experimental group were less than those in the control group at 8 weeks post-operation. The average number and diameter of vascular buds obviously increased in the experimental group at 4 and 8 weeks post-operation. The number of vascular buds and the diameter in the region of the inner annulus increased when compared to those in the area near the nucleus pulposus. Conclusions The pcDNA3.1-VEGF165 plasmid can increase the average number and diameter of vascular buds and decelerate intervertebral disc degeneration.展开更多
基金supported by the Natural Science Foundation of Hubei Province,China(No.2008CDA054)
文摘Obstructive nephropathy ultimately leads to end-stage renal failure. Renovascular lesions are involved in various nephropathies, and most renal diseases have an ischemic component that underlies the resulting renal fibrosis. The aim of this study was to investigate whether morphological changes occur in the renal vasculature in hydronephrosis and the possible mechanisms involved. A model of complete unilateral ureteral obstruction（CUUO） was used. Experimental animals were divided into five groups： a normal control group（N） and groups of animals at 1st week（O1）, 2nd week（O2）, 4th week（O4） and 8th week（O8） after CUUO. Blood pressure was measured, renal arterial trees and glomeruli were assessed quantitatively, and renovascular three-dimensional reconstruction was performed on all groups. Glomerular ultrastructural changes were examined by transmission electron microscopy. The results showed that the systolic blood pressure was significantly increased in the obstructed groups（O1, O2, O4 and O8）. Three-dimensional reconstruction showed sparse arterial trees in the O8 group, and a tortuous and sometimes ruptured glomerular basement membrane was found in the O4 and O8 groups. Furthermore, epithelial media thickness and media/lumen ratio were increased, lumen diameters were decreased, and the cross-sectional area of the media was unaltered in the segmental renal artery, interlobar artery and afferent arterioles, respectively. In conclusion, renal arterial trees and glomeruli were dramatically altered following CUUO and the changes may be partially ascribed to vascular remodeling. Elucidation of the molecular mechanisms of renovascular morphological alterations will enable the development of potential therapeutic approaches for hydronephrosis.
基金This study was supported by a grant from the National Natural Science Foundation of China，the Anhui Province Education Department Key Fund Project
文摘Background This study aimed to investigate the effect of pcDNA3.1-vascular endothelial growth factor （VEGF）165 vector on vertebral cartilage endplate vascular buds and intervertebral discs. Methods Rabbits were randomly assigned to the control and experimental groups with 10 in each. In the experimental group, we anesthetized the rabbits and exposed the front vertebral body. Using the mark of the longitudinal ossature of the front vertebral body of the lumbar vertebrae, we advanced a needle at the central point of the front fourth and fifth lumbar intervertebral discs and injected 20 pl pcDNA3.1-VEGF165. Similarly, in the control group, we injected 20 IJl pcDNA3.1. At 4 and 8 weeks post-injection, we examined the changes of the vertebral cartilage endplate using X-ray radiograph, histology, and scanning electron microscopy. Results The vertebral cartilage endplate calcification and degeneration in the experimental group were less than those in the control group at 8 weeks post-operation. The average number and diameter of vascular buds obviously increased in the experimental group at 4 and 8 weeks post-operation. The number of vascular buds and the diameter in the region of the inner annulus increased when compared to those in the area near the nucleus pulposus. Conclusions The pcDNA3.1-VEGF165 plasmid can increase the average number and diameter of vascular buds and decelerate intervertebral disc degeneration.
