Blood Vessels ; physiology ; Humans ; Kruppel-Like Transcription Factors ; metabolism ; physiology

Neovascularization of the adventitial vasa vasorum with extension into the intima of atherosclerotic lesions is frequently observed, but its pathophysiological significance is still subject to debate. Recently, leptin, the product of the Ob gene, was identified. Leptin, via activation of the endothelial receptor (Ob-R), generates a growth signal involving a tyrosine kinase-dependent intracellular pathway and promotes angiogenic processes. We hypothesized that a high concentration of leptin within vasa vasorum and plaque itself, may influence inflammatory and vascular neovascularization coupling with functional upregulation of the vascular endothelial growth factor (VEGF). Microscopic computerized tomography was utilized for the spatial distribution of vasa vasorum and intimal neovascularization from atherosclerotic human coronary arteries. Atherosclerotic coronary arteries showed a dense plexus of microvessels in the adventitia and plaque itself. Microscopic analysis from human atherosclerotic aortas revealed an increase in the intimal thickness with neovascularization. The immunoreactivity for Ob-R, VEGF and matrix metalloproteinase (MMP) increased in atherosclerotic plaque, predominantly in the endothelial lining of the intimal neovessel and macrophages/foam cells. Our observation of a prominent colocalization between Ob-R, VEGF and MMP supports this hypothesis and these factors participate in the neovascularization of atherosclerotic lesions. The present study is the first report on vascular tissue and it opens a promising perspective concerning future investigations of leptin-dependent modulation of atherogenesis and vascular neovascularization under pathophysiolgical conditions.
Adult ; Arteriosclerosis/physiopathology ; Arteriosclerosis/pathology ; Arteriosclerosis/metabolism* ; Blood Vessels/pathology ; Blood Vessels/metabolism ; Carrier Proteins/physiology ; Carrier Proteins/metabolism* ; Human ; Middle Age ; Neovascularization, Pathologic/physiopathology

Animals ; Blood Pressure ; Lymphatic Vessels ; physiopathology ; Male ; Norepinephrine ; metabolism ; Rats ; Rats, Wistar ; Shock, Hemorrhagic ; metabolism ; physiopathology

Humans ; Lung Neoplasms ; blood supply ; pathology ; Lymphatic Vessels ; pathology ; Neovascularization, Pathologic ; metabolism ; Vascular Endothelial Growth Factors ; chemistry ; metabolism ; physiology

p53 is an important target for studying vascular aging. However, as people gradually learned more about the miR-34s and the relationship between miR-34s and p53, new research idea emerged. This paper tries to elaborate the feature of p53, microRNA and miR-34s in-depth, analyze the regulatory action of miR-34s on p53, and offer some new prevention and treatment prospects about vascular aging in Chinese medicine.
Blood Vessels ; pathology ; Cellular Senescence ; Feedback, Physiological ; Humans ; Medicine, Chinese Traditional ; MicroRNAs ; metabolism ; Tumor Suppressor Protein p53 ; metabolism

Adult ; Aged ; Carcinoma, Hepatocellular ; blood supply ; metabolism ; pathology ; Female ; Humans ; Liver Neoplasms ; blood supply ; metabolism ; pathology ; Lymphatic Vessels ; Male ; Middle Aged ; Vascular Endothelial Growth Factor C ; metabolism

Elastin is known to occur in the lung parenchyma and pleura as well as in the pulmonary vessels, but no detailed studies of this elastin's linkage between them have been done in three dimensions. For many years we have known that there is abundant elastin in the mammalian lungs, which may be associated with etiology of causing emphysema. We have developed selective casting methods to allow us to determine the location where elastin is found morphologically. The method involves casting either the vasculature via the right ventricle, or the airways via the trachea in the air sacs. Studies of the vasculature were done with the lung inflated to 80% of the vital capacity. The casted lungs were then put in 0.1 N NaOH at 75 degrees C for 48 hours, turning them frequently. THis method removed all non-elastin tissues. The scanning electron microscopy (SEM) was used to reveal the three dimensional pictures of elastin structures from both lung parenchyma and pulmonary vessels. Elastin was seen as fenestrated sheets and some fibers in both the vessels and the airways. Elastin in the two different locations was often interconnected. Studies on 6 dogs, 8 rabbits, and 2 pigs showed no significant species difference at the level of resolution of the SEM, which was used to study the specimens after they had been freeze-dried.
Animal ; Blood Vessels/metabolism/ultrastructure ; Corrosion Casting ; Dogs ; Elastin/*ultrastructure ; Lung/blood supply/*metabolism ; Microscopy, Electron, Scanning ; Pulmonary Alveoli/metabolism/ultrastructure ; Rabbits ; Swine

Blood Vessels ; chemistry ; physiopathology ; Carcinoma, Hepatocellular ; metabolism ; physiopathology ; Elasticity ; Humans ; Liver Neoplasms ; metabolism ; physiopathology ; Rupture, Spontaneous ; metabolism ; physiopathology ; von Willebrand Factor ; metabolism

The alterations of taurine transport and the expression of taurine transporter (TAUT) mRNA in myocardium and aortic wall were investigated in spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats. It was demonstrated that plasma taurine concentration and taurine release from myocardium and aortic wall in SHR were higher than those in WKY rats, whereas taurine content, taurine uptake and TAUT mRNA in myocardium and aortic wall of SHR were lower than those of WKY rats. In SHR, the maximal velocity (V(max)) of taurine transportation in myocardium and aortic wall was lower by 24% (P<0.05) and 35% (P<0.05) than that in WKY, their michaelis constants (Km) values were higher by 16% (P<0.05) and 39% (P<0.05), respectively. The results suggest that there is dysfunction of taurine transport in myocardium and aortic wall in SHR, which may be partly resulted from the decrease of TAUT activity and affinity, and down-regulation of TAUT gene expression.
Animals ; Blood Vessels ; metabolism ; physiopathology ; Carrier Proteins ; metabolism ; Heart ; physiopathology ; In Vitro Techniques ; Male ; Myocardium ; metabolism ; Rats ; Rats, Inbred SHR ; Rats, Inbred WKY ; Taurine ; metabolism

OBJECTIVETo explore the effects and related mechanism of nifedipine on vascular inflammation induced by cuff placement.

METHODSAdult male C57BL/6J mice (10 to 12 weeks of age) were assigned to control (no cuff placement without nifedipine), cuff placement (cuff placement without nifedipine) and treatment (cuff placement with nifedipine 1 or 5 mg×kg(-1)×d(-1)) groups. Activity of NF-κB in injured artery was measured 5 days after operation. MCP-1 expression and nuclear translocation of NF-κB were examined in injured artery 7 days after operation.

RESULTSDNA-binding activity of NF-κB was significantly increased in the injured artery 5 days after cuff placement which could be downregulated by nifedipine 5 mg×kg(-1)×d(-1). MCP-1 mRNA expression in the injured arteries was increased 7 days after cuff placement and which could be significantly attenuated by nifedipine 5 mg×kg(-1)×d(-1). Cuff placement decreased the cytoplasmic level of p50, IκBα, IκBβ, and increased the nuclear level of p50. Nifedipine 5 mg×kg(-1)×d(-1) significantly attenuated these changes.

CONCLUSIONOur results suggest that high dose nifedipine could suppresses expression of MCP-1 induced by injured arteries via the inhibin NF-κB DNA binding activity, thereby attenuating vascular inflammation.

Animals ; Blood Vessels ; metabolism ; Chemokine CCL2 ; metabolism ; Inflammation ; Male ; Mice ; Mice, Inbred C57BL ; NF-kappa B ; metabolism ; Nifedipine ; pharmacology ; Vascular Diseases ; metabolism