The endothelium plays an important role in maintaining vascular homeostasis, regulating vascular tone and blood flow, and preserving a non-thrombogenic blood-tissue interface, and the normal function of the vascular endothelium is essential for penile erection. In most cases, erectile dysfunction (ED) is accompanied by endothelial dysfunction, and endothelial injury is a major pathological basis of ED, which can be induced by bad lifestyles, cardiovascular diseases, reactive oxygen species, and inflammatory mediators. The vascular endothelium is capable of self-repairing, and endothelial injury results from the unbalanced factors of injury and repair. This review focuses on the mechanism and repair of endothelial injury and the relationship of endothelial injury with ED.
Endothelium, Vascular ; metabolism ; pathology ; Erectile Dysfunction ; metabolism ; pathology ; Humans ; Male

OBJECTIVE: The endothelial glycocalyx (eGC) is a dynamic and multicomponent layer of macromolecules found at the surface of vascular endothelium, which is largely underappreciated. It has recently been recognized that eGC is a major regulator of endothelial function and may have therapeutic value in organ injuries. This study aimed to explore the role of the eGC in various pathologic and physiologic conditions, by reviewing the basic research findings pertaining to the detection of the eGC and its clinical significance. We also explored different pharmacologic agents used to protect and rebuild the eGC. DATA SOURCES: An in-depth search was performed in the PubMed database, focusing on research published after 2003 with keywords including eGC, permeability, glycocalyx and injuries, and glycocalyx protection. STUDY SELECTION: Several authoritative reviews and original studies were identified and reviewed to summarize the characteristics of the eGC under physiologic and pathologic conditions as well as the detection and protection of the eGC. RESULTS: The eGC degradation is closely associated with pathophysiologic changes such as vascular permeability, edema formation, mechanotransduction, and clotting cascade, together with neutrophil and platelet adhesion in diverse injury and disease states including inflammation (sepsis and trauma), ischemia-reperfusion injury, shock, hypervolemia, hypertension, hyperglycemia, and high Na as well as diabetes and atherosclerosis. Therapeutic strategies for protecting and rebuilding the eGC should be explored through experimental test and clinical verifications. CONCLUSIONS Disturbance of the eGC usually occurs at early stages of various clinical pathophysiologies which can be partly prevented and reversed by protecting and restoring the eGC. The eGC seems to be a promising diagnostic biomarker and therapeutic target in clinical settings.
Animals ; Databases, Factual ; Endothelium, Vascular ; metabolism ; pathology ; Glycocalyx ; metabolism ; pathology ; Humans ; Shear Strength

OBJECTIVETo investigate relationship between expression of inducible nitric oxide synthase (iNOS) and proliferative potency of endothelium in hemangioma (HM).

METHODSImmunohistochemical staining was used to detect expression of iNOS and Ki-67 protein in 49 cases of HM and 29 cases of vascular malformation (VM).

RESULTSExpressive rate of iNOS and Ki-67 protein of 49 cases of HM was 38% and (10.98 +/- 7.93)%. Expressive rate of iNOS and Ki-67 protein of 29 cases of VM was respectively 3% and (0.03 +/- 0.19)%. The expressive rate of iNOS and Ki-67 protein of HM was significantly higher than that of VM (P = 0.001 and 0). The expressive rate of Ki-67 protein of HM of proliferative phase was (12.67 +/- 7.65)% , which was significantly higher than that of HM of extinctive phase, (7.27 +/- 7.49)% (P = 0.028).

CONCLUSIONSExpression of iNOS and Ki-67 protein of HM is significantly higher than that of VM, and the proliferative potency of HM is significantly higher than that of VM.

Child, Preschool ; Endothelium ; metabolism ; Endothelium, Vascular ; cytology ; Female ; Hemangioma ; metabolism ; pathology ; Humans ; Hyperplasia ; Infant ; Ki-67 Antigen ; metabolism ; Male ; Neovascularization, Pathologic ; metabolism ; Nitric Oxide Synthase Type II ; metabolism

AIMTo investigate the alleviating effect of N-acetylcysteine (NAC) on lung injury induced by lipopolysaccharides (LPS) and its mechanism.

METHODSThe effects of NAC on changes of the pulmonary arterial reactivity and the ultrastructure of pulmonary arterial endothelium induced by LPS were observed with the isolated artery ring technique and scanning electron microscope (SEM). Malondialdehyde (MDA), nitric oxide (NO) contents and superoxide dismutase (SOD) activity of pulmonary artery tissues were detected.

RESULTSThe exposure of pulmonary artery to LPS (4 microg/ml, 7 h) led to reduction of endothelium-dependent relaxation response to acetylcholine (ACh), which was reversed by the concomitant exposure to NAC (0.5 mmol/L, 7 h), whereas NAC itself had no effect on the response. Significant structural injury were observed under SEM in LPS group and alleviated the changes in LPS + NAC group. The MDA, NO contents increased but SOD activity decreased in LPS group, which were reversed by the concomitant exposure to NAC.

CONCLUSIONNAC protects pulmonary artery endothelium and enhances endothelium-dependent relaxation response of pulmonary artery by antioxidation effect, which may be one of the mechanisms of its reversing pulmonary artery hypertension and following lung injury induced by LPS.

Acetylcysteine ; pharmacology ; Animals ; Endothelium ; metabolism ; pathology ; ultrastructure ; Lipopolysaccharides ; adverse effects ; Malondialdehyde ; metabolism ; Microscopy, Electron, Scanning ; Nitric Oxide ; metabolism ; Pulmonary Artery ; metabolism ; pathology ; ultrastructure ; Rabbits ; Superoxide Dismutase ; metabolism

Atherosclerosis ; immunology ; metabolism ; pathology ; Biomarkers ; metabolism ; C-Reactive Protein ; metabolism ; Endothelium, Vascular ; metabolism ; pathology ; physiopathology ; Inflammation ; metabolism ; pathology ; Inflammation Mediators ; metabolism ; Interleukins ; metabolism ; Metabolic Syndrome ; metabolism ; pathology ; Tumor Necrosis Factor-alpha ; metabolism

OBJECTIVETo investigate the relationship between endothelial-to-mesenchymal transition (EndMT) and myocardial fibrosis in acute viral myocarditis (VMC).

METHODSTwenty-eight Balb/c mice were randomized into 3 groups: control group (n=8), VMC group(n=10) and intervention group(n=10). Mice in VMC and intervention groups were injected intraperitoneally(i.p) with single dose of coxsackievirus B3, mice in control group were injected with equal amount of viral-free vehicle. In the following day, mice in control and VMC groups were injected i.p with 0.1 ml of saline and intervention group with 0.1 ml of recombinant human bone morphogenetic protein 7(rh-BMP7) at a concentration of 300 μg/kg. The mice hearts were harvested after 7 d, cardiac collagen volume fraction (CVF) was calculated on picrosirius red-stained sections. mRNA and protein expression of TGF-β1, CD31, VE-cadherin, fibroblast special protein 1 (FSP-1) and α-smooth muscle actin (α-SMA) and collagen 1α1 in myocardiac tissues were detected by real-time RT-PCR and Western blot analysis, respectively.

RESULTSCompared to controls, overt fibrosis was presented in necrotic area of myocardium in VMC group. Meanwhile, marked increase of TGF-β1 expression accompanied with EndMT characterized by loss of endothelial phenotype (decreased expression of CD31 and VE-cadherin), gain of mesenchymal proteins (overexpression of FSP-1 and α-SMA) and increased synthesis of collagen was also demonstrated. Both EndMT and cardiac fibrosis were simultaneously reversed by TGF-β1 inhibition.

CONCLUSIONEndMT is involved in cardiac fibrosis in acute viral myocarditis, TGF-β1 might be a main mediator.

Acute Disease ; Animals ; Antigens, CD ; metabolism ; Cadherins ; metabolism ; Collagen ; metabolism ; Coxsackievirus Infections ; metabolism ; pathology ; Disease Models, Animal ; Endothelium ; pathology ; Fibrosis ; Male ; Mesoderm ; pathology ; Mice ; Mice, Inbred BALB C ; Myocarditis ; metabolism ; pathology ; virology ; Myocardium ; metabolism ; pathology ; Transforming Growth Factor beta1 ; metabolism

Diagnosis, Differential ; Endothelium, Vascular ; metabolism ; pathology ; Female ; Humans ; Hyperplasia ; Jejunal Diseases ; metabolism ; pathology ; surgery ; Jejunum ; blood supply ; pathology ; surgery ; Middle Aged ; Platelet Endothelial Cell Adhesion Molecule-1 ; metabolism

AIMTo explore the effect of hyperhomocysteinemia on vascular calcification and the underlying mechanism of it.

METHODSArterial calcification of Sprague-Dawley rats was induced by vitamin D3 plus nicotine. Hyperhomocysteinemia was established by feeding high methionine diet for six weeks and was assessed b y plasma total homocysteine (tHcy) level detected by HPLC method. Calcification was confirmed by von Kossa staining, measurement of calcium content, alkaline phosphatases (ALP) activity and osteocalcin (OC) concentration of vascular tissue. Lipid conjugated dienes formation were determined to reflecting the production of lipid peroxide.

RESULTSThe results showed that there were mass black granules deposited in aortic wall of the calcified rats by von Kossa staining. Calcium content, ALP activity, OC concentration in calcified rats increased by 8.09-fold, 45.57% and 2.81-fold compared with those of the control group (P < 0.01). Calcium content in calcified rats with high methionine diet increased by 34.29% compared with that of the calcified rats, while ALP activity and OC content decreased by 29.13% and 74.69% compared with that of the calcified rats. Lipid conjugated dienes formation in plasma of the rat with high methionine diet and of calcified rats with high methionine diet increased by 1.93 and 2.89-fold compared with those of the control group, respectively (P < 0.01), and in calcified rats with high methionine diet group was increased by 32.90% compared with that of high methionine diet group (P < 0.01).

CONCLUSIONHyperhomocysteinemia could promote vascular calcification, which might be mediated through the production of lipid peroxide.

Alkaline Phosphatase ; metabolism ; Animals ; Calcium ; metabolism ; Endothelium, Vascular ; Hyperhomocysteinemia ; metabolism ; pathology ; Lipid Peroxidation ; Male ; Methionine ; administration & dosage ; Osteocalcin ; analysis ; Rats ; Rats, Sprague-Dawley ; Vascular Calcification ; metabolism ; pathology

Actins ; metabolism ; Animals ; Antigens, CD ; metabolism ; Cadherins ; metabolism ; Carotid Artery Injuries ; metabolism ; pathology ; Endothelium, Vascular ; metabolism ; ultrastructure ; Fluorescent Antibody Technique ; Microscopy, Confocal ; Rats ; Troponin ; metabolism

OBJECTIVE: To observe the effect of intrauterine hypoxia on the development of rat lung after birth under ordinary pressure and normoxia, on the expression of vascular endothelial growth factor (VEGF) in the lung as the age increasing after birth, and to provide experimental basis for the treatment of intrauterine hypoxia after baby was born. METHODS: Intrauterine hypoxia models were established. The rats were divided into an air-control group (the control group) and a hypoxic 6-day group (the hypoxic group). All rats were fed under normal pressure and normoxia after they were born. At postnatal 7, 14, and 21 days, we measured the pulmonary vascular morphometry, detected the expression of VEGF protein with immunohistochemisty, the expression of VEGF mRNA with real-time PCR, and observed the alteration of capillary endothelium in the lung tissues under the electron microscope. RESULTS: The expression of VEGF protein and VEGF mRNA in the 2 groups increased as the rats grew, but the expression increased slower in the hypoxic group than that in the control group. The increase curve of the 2 groups crossed. There was no significant difference between the 2 groups in the pulmonary vascular morphometry at each experiment time point. Hyperplasia of capillary endothelium decreased with age. Cellular edema of capillary endothelium was obvious especially at the 14th day after birth under the electron microscope. CONCLUSION The expression of VEGF protein and VEGF mRNA has slower increase in the intrauterine hypoxic rats than that in the normal control rats. The expression of VEGF may influence the development of lung vessel after rats was born.
Animals ; Animals, Newborn ; Endothelium, Vascular ; pathology ; Hypoxia ; Lung ; blood supply ; metabolism ; RNA, Messenger ; Rats ; Vascular Endothelial Growth Factor A ; metabolism