Early-Stage Dynamics in Vascular Endothelial Cells Exposed to Hydrostatic Pressure

2019 ◽  
Vol 141 (9) ◽  
Author(s):  
Daisuke Yoshino ◽  
Masaaki Sato
Keyword(s):  
Blood Pressure ◽  
Endothelial Cells ◽  
Hydrostatic Pressure ◽  
Vascular Endothelial Cells ◽  
Early Stage ◽  
Pressure Effects ◽  
Vascular Endothelial ◽  
Know How ◽  
Water Efflux ◽  
Sense And Respond

Blood pressure is an important factor both in maintaining body homeostasis and in its disruption. Vascular endothelial cells (ECs) are exposed to varying degrees of blood pressure and therefore play an important role in these physiological and pathological events. However, the effect of blood pressure on EC functions remains to be elucidated. In particular, we do not know how ECs sense and respond to changes in hydrostatic pressure even though the hydrostatic pressure is known to affect the EC functions. Here, we hypothesized that the cellular responses, leading to the reported pressure effects, occur at an early stage of pressure exposure and observed the early-stage dynamics in ECs to elucidate mechanisms through which ECs sense and respond to hydrostatic pressure. We found that exposure to hydrostatic pressure causes an early actomyosin-mediated contraction of ECs without a change in cell morphology. This response could be caused by water efflux from the ECs following exposure to hydrostatic pressure. Although only a limited study, these findings do explain a part of the mechanism through which ECs sense and respond to hydrostatic pressure.

Morphological Alterations Affecting the Microvasculature in Nasal Allergy

1983 ◽  
Vol 92 (1) ◽  
pp. 70-74 ◽  
Author(s):  
Kensuke Watanabe ◽  
Isamu Watanabe
Keyword(s):  
Endothelial Cells ◽  
Vascular Permeability ◽  
Vascular Endothelial Cells ◽  
Early Stage ◽  
Nasal Allergy ◽  
Vascular Endothelial ◽  
Gap Formation ◽  
Morphological Alterations ◽  
Vascular Dilatation ◽  
Mucosal Edema

The fine structure of human nasal blood vessels was studied in 15 nasal allergic patients. Biopsies were taken at different stages after provocation. In the early stage (two minutes after provocation), characteristic alterations of capillaries and venules were congestion, gap formation between two endothelial cells, and swollen vascular endothelial cells. Evidence of locally increased vascular permeability and congestion causing mucosal edema was found. In the late stage (20 minutes after provocation), evidence of congestion disappeared. Vascular dilatation and marked interendothelial cell gaps were observed. In both perivascular space and sometimes in intravascular space, de-granulated eosinophils were observed, suggesting that not only histamine but also lysosomal enzymes in eosinphil granules may be involved in causing increased vascular permeability.

Angiotensin II receptor blockade corrects altered expression of gap junctions in vascular endothelial cells from hypertensive rats

2004 ◽  
Vol 287 (1) ◽  
pp. H216-H224 ◽  
Author(s):  
Yasuo Kansui ◽  
Koji Fujii ◽  
Keiichiro Nakamura ◽  
Kenichi Goto ◽  
Hideyuki Oniki ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Endothelial Cells ◽  
Angiotensin Ii ◽  
Gap Junctions ◽  
Vascular Endothelial Cells ◽  
Renin Angiotensin System ◽  
Vascular Endothelial ◽  
Hypertensive Rats ◽  
Angiotensin System ◽  
Renin Angiotensin

Blockade of the renin-angiotensin system improves the impaired endothelium-dependent relaxations associated with hypertension and aging, partly through amelioration of endothelium-derived hyperpolarizing factor (EDHF)-mediated responses. Although the nature of EDHF is still controversial, recent studies have suggested the involvement of gap junctions in EDHF-mediated responses. Gap junctions consist of connexins (Cx), and we therefore tested whether the expression of Cx in vascular endothelial cells would be altered by hypertension and antihypertensive treatment. Spontaneously hypertensive rats (SHR) were treated with either the angiotensin II type 1 receptor antagonist candesartan or the combination of hydralazine and hydrochlorothiazide for 3 mo from 5 to 8 mo of age. Confocal laser scanning microscopy after immunofluorescent labeling with antibodies against Cx37, Cx40, and Cx43 revealed that the expression of Cx37 and Cx40 in endothelial cells of the mesenteric artery was significantly lower in SHR than in WKY. Treatment with candesartan, but not the combination of hydralazine and hydrochlorothiazide, significantly increased the expression of Cx37 and Cx40, although blood pressure decreased similarly. On the other hand, the expression of Cx43, though scarce and heterogeneous, was increased in SHR compared with WKY, and candesartan treatment lowered the expression of Cx43. These findings suggest that renin-angiotensin system blockade corrects the decreased expression of Cx37 and Cx40 in arterial endothelial cells of hypertensive rats, partly independently of blood pressure, whereas the expression of Cx43 changed in the opposite direction. It remains to be clarified whether these changes in Cx37 and Cx40 are related to endothelial function, particularly that attributable to EDHF.

scholarly journals Study on Damage Mechanism and Repair of Vascular Endothelial Cells Based on Ultrasound Technology

2021 ◽  
Vol 2021 ◽  
pp. 1-9
Author(s):  
Shuhao Deng ◽  
Quan Jiang ◽  
Xin Lu ◽  
Yuan Zhang
Keyword(s):  
Endothelial Cells ◽  
Endothelial Function ◽  
Relaxation Function ◽  
Vascular Endothelial Cells ◽  
Early Stage ◽  
Gradient Centrifugation ◽  
Control Group ◽  
Dependent Manner ◽  
Vascular Endothelial ◽  
Vascular Endothelial Function

Objective. To detect the endothelial function of external iliac artery in rats with different stages of atherosclerosis by high-resolution ultrasound, so as to provide experimental methodological basis for evaluating the function of vascular endothelial cells by ultrasound. Methods. The animals were randomly divided into the control group ( n = 6 ) and the atherosclerosis model group ( n = 15 ). The atherosclerosis group was further divided into 4-week group, 8-week group, and 12-week group, with 5 animals in each group. After separating and grinding rat spleen, the obtained cells were cultured by density gradient centrifugation. After the cells adhered, the morphology of the cells was observed under a microscope and identified by DiI-Ac-LDL and FITC-UEA-I double staining. The activities of LDH and SOD, the contents of MDA and GSH, and the contents of NO in plasma were detected by biochemical methods. Results. The protective effect of rosanilin on brain injury in rats with acute hypobaric hypoxia and its regulation on the expression of pAkt protein; ox-LDL inhibited the proliferation activity of EPCs in a concentration-dependent manner. The expression of KLF2 and S1PR1 in HAEC can be knocked down by small interfering RNA, and knocking down KLF2 can not only downregulate the expression of S1PR1 but also downregulate HAVEN. With the development of atherosclerosis, the endothelium-dependent relaxation function and endothelium-independent relaxation function of the control group and the atherosclerosis model at 4, 8, and 12 weeks were damaged in different degrees and gradually aggravated. Conclusion. Atherosclerosis is a disease with both morphological and functional damage, and vascular endothelial function is damaged in the early stage with corresponding pathological changes. Ultrasound is an effective method to evaluate vascular endothelial function.

scholarly journals Osteostat/Tumor Necrosis Factor Superfamily 18 Inhibits Osteoclastogenesis and Is Selectively Expressed by Vascular Endothelial Cells

Endocrinology ◽  
2006 ◽  
Vol 147 (1) ◽  
pp. 70-78 ◽  
Author(s):  
Bernardetta Nardelli ◽  
Liubov Zaritskaya ◽  
William McAuliffe ◽  
Yansong Ni ◽  
Clint Lincoln ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Vascular Endothelial Cells ◽  
Early Stage ◽  
Osteoclast Differentiation ◽  
Precursor Cells ◽  
In Vitro Assays ◽  
Vascular Endothelial ◽  
Tnf Superfamily ◽  
And Function

Vascular endothelial cells (EC) participate in the process of bone formation through the production of factors regulating osteoclast differentiation and function. In this study, we report the selective expression in primary human microvascular EC of Osteostat/TNF superfamily 18, a ligand of the TNF superfamily. Osteostat protein is detectable in human microvascular EC and is highly up-regulated by IFN-α and IFN-β. Moreover, an anti-Osteostat antibody strongly binds to the vascular endothelium in human tissues, demonstrating that the protein is present in the EC layers surrounding blood vessels. Functional in vitro assays were used to define Osteostat involvement in osteoclastogenesis. Both recombinant and membrane-bound Osteostat inhibit differentiation of osteoclasts from monocytic precursor cells. Osteostat suppresses the early stage of osteoclastogenesis via inhibition of macrophage colony-stimulating factor-induced receptor activator of NF-κB (RANK) expression in the osteoclast precursor cells. This effect appears to be specific for the differentiation pathway of the osteoclast lineage, because Osteostat does not inhibit lipopolysaccharide-induced RANK expression in monocytes and dendritic cells, or activation-induced RANK expression in T cells. These findings demonstrate that Osteostat is a novel regulator of osteoclast generation and substantiate the major role played by the endothelium in bone physiology.

The Effects of Ginseng Radix Rubra on Human Vascular Endothelial Cells

1998 ◽  
Vol 26 (03n04) ◽  
pp. 365-373 ◽  
Author(s):  
Shigekatsu Nakajima ◽  
Yasuhiko Uchiyama ◽  
Kazuo Yoshida ◽  
Hiromi Mizukawa ◽  
Eiichi Haruki
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Endothelial Cells ◽  
Human Body ◽  
Vascular Endothelial Cells ◽  
Plasminogen Activators ◽  
Vascular Endothelial ◽  
Red Ginseng ◽  
Tissue Plasminogen ◽  
Coagulation And Fibrinolysis

The effect of Ginseng Radix Rubra (Red ginseng) on human vascular endothelial cells was examined. Red ginseng was found to promote the proliferation of vascular endothelial cells, inhibit the production but promote the decomposition of endothelin, which is known to constrict blood vessels and raise blood pressure as well as accelerate the synthesis of nitric oxide. which is known to have an angio-tonic effect. Furthermore, Red ginseng was observed to increase the production of Interleukin 1ß, which is known to play important roles in the homeostatic activities of the human body such as immunity and inflammation as well as increasing the production of tissue plasminogen activators, which suppress the formation of thrombin in the blood coagulation and fibrinolysis mechanisms. It is suggested that Red ginseng has the effect of accelerating endothelial cells proliferation and of promoting physiological activities.

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