scholarly journals Vascular endothelial cell-derived endothelin-1 mediates vascular inflammation and neointima formation following blood flow cessation

2009 ◽  
Vol 82 (1) ◽  
pp. 143-151 ◽  
Author(s):  
Dyah W. Anggrahini ◽  
Noriaki Emoto ◽  
Kazuhiko Nakayama ◽  
Bambang Widyantoro ◽  
Suko Adiarto ◽  
...  
Keyword(s):  
Blood Flow ◽  
Endothelial Cell ◽  
Vascular Inflammation ◽  
Vascular Endothelial Cell ◽  
Vascular Endothelial ◽  
Neointima Formation ◽  
Endothelin 1

scholarly journals Progesterone blunts vascular endothelial cell secretion of endothelin-1 in response to placental ischemia

2013 ◽  
Vol 209 (1) ◽  
pp. 44.e1-44.e6 ◽  
Author(s):  
Luissa V. Kiprono ◽  
Kedra Wallace ◽  
Janae Moseley ◽  
James Martin ◽  
Babbette LaMarca
Keyword(s):  
Endothelial Cell ◽  
Vascular Endothelial Cell ◽  
Vascular Endothelial ◽  
Cell Secretion ◽  
Endothelin 1 ◽  
Placental Ischemia

Analysis of blood flow velocity and structure of vascular endothelial cell by using laser light

1993 ◽  
Vol 25 (5) ◽  
pp. 328
Author(s):  
Yasuo Ogasawara ◽  
Osamu Hiramitsu ◽  
Chikako Tokuda ◽  
Katsuhiko Tsujioka ◽  
Fumihiko Kajiya
Keyword(s):  
Blood Flow ◽  
Endothelial Cell ◽  
Flow Velocity ◽  
Blood Flow Velocity ◽  
Laser Light ◽  
Vascular Endothelial Cell ◽  
Vascular Endothelial

Abstract 3556: Diabetic Cardiac and Renal Complications are attenuated in Mice with Conditional Knockout of Endothelin-1 in Vascular Endothelial Cell

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Bambang Widyantoro ◽  
Suko Adiarto ◽  
Naoko Iwasa ◽  
Kazuhiko Nakayama ◽  
Dyah W Anggrahini ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Mrna Expression ◽  
Interstitial Fibrosis ◽  
Vascular Endothelial Cell ◽  
Conditional Knockout ◽  
Vascular Endothelial ◽  
Endothelin 1 ◽  
Renal Complications ◽  
Renal Complication ◽  
Lower Expression

High plasma endothelin-1 (ET-1) level has been associated with diabetic cardiovascular and renal complications, which remained prevalent despite good glycemic control. Since endothelial dysfunction, which is characterized by enhanced ET-1 secretion, plays an important role in mediating diabetic complication, we hypothesized that disruption of ET-1 in endothelial cell will be protective against cardiac and renal complication of diabetes. To test this hypothesis, we injected streptozotocin to Vascular Endothelial cell Specific Endothelin-1 Knockout (VEETKO) mice, of which ET-1 expression in major organs including heart and kidney were reduced by 60%, and to their wild type (WT) littermates. Six months of diabetes increased systolic blood pressure (SBP) similarly in both genotypes, with DM-VEETKO mice have remained lower SBP than DM-WT mice (124±1.08 vs. 131.33±1.33 mmHg, p<0.01, n=8 each). Diabetes also exaggerated the difference in cardiac ET-1 mRNA expression between both groups. The heart of DM-VEETKO mice showed lower area of interstitial fibrosis as compared to DM-WT mice, and this is associated with lower expression of fibrotic genes (TGF-β, CTGF and Collagen-1), higher capillary density (as measured by CD-31 staining) and higher VEGF mRNA expression. Furthermore, eight months of diabetes decreased cardiac systolic function of all mice, however, the decrease is significantly attenuated in DM-VEETKO mice (fractional shortening 45.67±0.61 vs. 38.27±2.2%, p<0.01, n=4 each). Similarly, DM-VEETKO mice also preserved renal function. Diabetes caused an increase in urinary protein excretion with the values in DM-VEETKO mice being approximately one fifth of DM-WT mice (30.12±10.09 vs. 170±23.19 mg/dl, p<0.01, n=6 each) Morphologically, DM-VEETKO mice have less glomerular fibrosis which is associated with lower expression of ICAM-1, and further leads to lower glomerular macrophage recruitment. In conclusion, these findings indicate that disruption of ET-1 in endothelial cell is significantly attenuated diabetic cardiovascular and renal complication in streptozotocin-induced diabetic mice model, and may provide additional basic rationales for the use of ET-1 blockade for the prevention of cardiac and renal complication of diabetes.

A relationship between apoptosis and flow during programmed capillary regression is revealed by vital analysis

Development ◽  
1996 ◽  
Vol 122 (12) ◽  
pp. 3929-3938 ◽  
Author(s):  
A. Meeson ◽  
M. Palmer ◽  
M. Calfon ◽  
R. Lang
Keyword(s):  
Blood Flow ◽  
Endothelial Cell ◽  
Quantitative Analysis ◽  
Plasma Flow ◽  
Cell Apoptosis ◽  
Vascular Endothelial Cell ◽  
Reciprocal Relationship ◽  
Vascular Endothelial ◽  
Endothelial Cell Apoptosis

Previous analyses of developmentally programmed capillary regression suggested two distinct causes of vascular endothelial cell (VEC) death. The first appeared to be macrophage-dependent (Lang, R. A. and Bishop, M. J. (1993) Cell 74, 453–462) while the second was proposed to result from cessation of blood flow (Lang, R. A., Lustig, M., Francois, F., Sellinger, M. and Plesken, H. (1994). Development 120, 3395–3403). Combined, these analyses suggested a model in which initial, macrophage-mediated endothelial cell apoptosis blocked blood flow within a capillary segment and, as a consequence, caused apoptosis of all remaining cells in the affected segment. In the current study, we have tested this model using a new method that combines vital and histological analyses as a means of determining the fate of whole capillary segments and individual cells in vivo. This technique revealed that one of the first events in regression was the apoptosis of a single VEC in otherwise normal, flowing capillary segments (initiating apoptosis). These isolated, dying VECs projected into and restricted the capillary lumen, imposing either a temporary or permanent block to blood flow. Following cessation of flow, synchronous apoptosis of VECs occurred (secondary apoptosis). In addition, a quantitative analysis revealed a reciprocal relationship between plasma flow and VEC apoptosis. These observations are consistent with a model for capillary regression in which macrophages induce apoptosis in a limited number of VECs and, as a consequence of a block to blood flow, also cause apoptosis in those remaining.

Effect of angiotensin(1-7) on the expression of E-selectin induced by angiotensinII and its mechanism in vascular endothelial cell

2010 ◽  
Vol 34 (8) ◽  
pp. S71-S71
Author(s):  
Xiaohui Shen ◽  
Zhi‑Bin Wen ◽  
Na Li ◽  
Qingmei Cheng ◽  
Xiaofan He ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Vascular Endothelial Cell ◽  
Vascular Endothelial

Alterations in Vascular Endothelial Cell-related Plasma Proteins In Thalassaemic Patients and their Correlation with Clinical Symptoms

1995 ◽  
Vol 74 (04) ◽  
pp. 1045-1049 ◽  
Author(s):  
P Butthep ◽  
A Bunyaratvej ◽  
Y Funahara ◽  
H Kitaguchi ◽  
S Fucharoen ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Immunosorbent Assay ◽  
Plasma Proteins ◽  
Clinical Symptoms ◽  
Vascular Endothelial Cells ◽  
Vascular Endothelial Cell ◽  
Enzyme Linked Immunosorbent Assay ◽  
Vascular Endothelial ◽  
Leg Ulcers

SummaryAn increased level of plasma thrombomodulin (TM) in α- and β- thalassaemia was demonstrated using an enzyme-linked immunosorbent assay (ELISA). Nonsplenectomized patients with β-thalassaemia/ haemoglobin E (BE) had higher levels of TM than splenectomized cases (BE-S). Patients with leg ulcers (BE-LU) were found to have the highest increase in TM level. Appearance of larger platelets in all types of thalassaemic blood was observed indicating an increase in the number of younger platelets. These data indicate that injury of vascular endothelial cells is present in thalassaemic patients.

scholarly journals Uric acid promotes oxidative stress and enhances vascular endothelial cell apoptosis in rats with middle cerebral artery occlusion

2018 ◽  
Vol 38 (3) ◽  
Author(s):  
Chengfu Song ◽  
Xiangdong Zhao
Keyword(s):  
Oxidative Stress ◽  
Uric Acid ◽  
Endothelial Cell ◽  
Cell Apoptosis ◽  
Vascular Endothelial Cell ◽  
Artery Occlusion ◽  
Vascular Endothelial ◽  
Endothelial Cell Apoptosis ◽  
Related Factors ◽  
Cerebral Artery Occlusion

In patients with cerebral infarction (CI), elevated serum uric acid (UA) level may exacerbate the occurrence and development of carotid atherosclerosis (AS). Our study intended to explore the underlying mechanism. We enrolled 86 patients with CI, and divided them into four groups: Non-AS, AS-mild, AS-moderate, and AS-severe groups; the levels of UA and oxidative stress-related factors in serum were detected. The middle cerebral artery occlusion (MCAO) model was used to stimulate CI in rats, and different doses of UA were administrated. The levels of oxidative stress-related factors in serum were detected. Hematoxylin & eosin (H&E) staining was used to observe the morphological alterations, and the apoptotic cell death detection kit was used to detect apoptotic cells. Increased UA concentration and enhanced oxidative stress were found in AS patients. H&E staining results showed that UA treatment exacerbated morphological damage in rats with MCAO, promoted oxidative stress, and enhanced vascular endothelial cell apoptosis in rats with MCAO.

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