Activities of wild‐type and variant tissue‐type plasminogen activators retained on vascular endothelial cells

Sano, Hideto; Tomczyk, Martyna; Brzóska, Tomasz; Urano, Tetsumei

doi:10.1002/2211-5463.12057

Cited by 8 publications

(3 citation statements)

References 23 publications

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“…However, cardiovascular diseases, such as arterial stiffness, will develop when the function of endothelium is impaired. 22,23 Angiotensin II is reported to be one of the main factors that contribute to the process and development of arterial stiffness. The infiltration of inflammatory cells into the injured VECs could be induced by angiotensin II, which will be produced by inflammatory cells in turn.…”

Section: Discussionmentioning

confidence: 99%

<p>Loxoprofen Sodium Alleviates Oxidative Stress and Apoptosis Induced by Angiotensin II in Human Umbilical Vein Endothelial Cells (HUVECs)</p>

Ji¹,

Yu²,

Zhang³

et al. 2020

DDDT

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Section: Discussionmentioning

confidence: 99%

<p>Loxoprofen Sodium Alleviates Oxidative Stress and Apoptosis Induced by Angiotensin II in Human Umbilical Vein Endothelial Cells (HUVECs)</p>

Ji¹,

Yu²,

Zhang³

et al. 2020

DDDT

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“…Our analyses of the secretory dynamics of green fluorescent protein (GFP)-tagged tPA (tPA-GFP) from VECs using total internal reflection fluorescence (TIRF) microscopy revealed that tPA-GFP has unique secretory dynamics and is retained on the surface of VECs after its release from the granules [14]. This binding to VECs is dependent on the finger-domain and the kringle 2-domain of tPA, similar to its binding to fibrin [31], and also on a positively charged region consisting of K296, H297, R298, and R299 [32]. The secretion and the retention of tPA contribute to the effective activation of plg bound on the surface of VECs, and to effective fibrinolysis when fibrin is generated [15].…”

Section: Pasmentioning

confidence: 99%

Regulation of plasminogen activation on cell surfaces and fibrin

Urano

Castellino

Suzuki

2018

Journal of Thrombosis and Haemostasis

106

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SummaryThe fibrinolytic system dissolves fibrin and maintains vascular patency. Recent advances in imaging analyses allowed visualization of the spatiotemporal regulatory mechanism of fibrinolysis, as well as its regulation by other plasma hemostasis cofactors. Vascular endothelial cells (VECs) retain tissue‐type plasminogen activator (tPA) after secretion and maintain high plasminogen (plg) activation potential on their surfaces. As in plasma, the serpin, plasminogen activator inhibitor type 1 (PAI‐1), regulates fibrinolytic potential via inhibition of the VEC surface‐bound plg activator, tPA. Once fibrin is formed, plg activation by tPA is initiated and effectively amplified on the surface of fibrin, and fibrin is rapidly degraded. The specific binding of plg and tPA to lytic edges of partly degraded fibrin via newly generated C‐terminal lysine residues, which amplifies fibrin digestion, is a central aspect of this pathophysiological mechanism. Thrombomodulin (TM) plays a role in the attenuation of plg binding on fibrin and the associated fibrinolysis, which is reversed by a carboxypeptidase B inhibitor. This suggests that the plasma procarboxypeptidase B, thrombin‐activatable fibrinolysis inhibitor (TAFI), which is activated by thrombin bound to TM on VECs, is a critical aspect of the regulation of plg activation on VECs and subsequent fibrinolysis. Platelets also contain PAI‐1, TAFI, TM, and the fibrin cross‐linking enzyme, factor (F) XIIIa, and either secrete or expose these agents upon activation in order to regulate fibrinolysis. In this review, the native machinery of plg activation and fibrinolysis, as well as their spatiotemporal regulatory mechanisms, as revealed by imaging analyses, are discussed.

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“…The human EA.hy926 endothelial cell line [ 15 , 16 ] was obtained from the Cell Resource Center of Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences (Shanghai, China). S. cerevisiae BG was provided by the Institute of Modern Physics, Chinese Academy of Sciences (Lanzhou, China).…”

Section: Methodsmentioning

confidence: 99%

ß-D-Glucan promotes NF-κB activation and ameliorates high-LET carbon-ion irradiation-induced human umbilical vein endothelial cell injury

LIU,

WEI,

WANG

2023

Turkish Journal of Medical Sciences

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Background/aim Heavy-ion irradiation seriously perturbs cellular homeostasis and thus damages cells. Vascular endothelial cells (ECs) play an important role in the pathological process of radiation damage. Protecting ECs from heavy-ion radiation is of great significance in the radioprotection of normal tissues. In this study, the radioprotective effect of β-D-glucan (BG) derived from Saccharomyces cerevisiae on human umbilical vein endothelial cell (EA.hy926) cytotoxicity produced by carbon-ion irradiation was examined and the probable mechanism was established. Materials and methods EA.hy926 cells were divided into seven groups: a control group; 1, 2, or 4 Gy radiation; and 10 μg/mL BG pretreatment for 24 h before 1, 2, or 4 Gy irradiation. Cell survival was assessed by colony formation assay. Cell cycles, apoptosis, DNA damage, and reactive oxygen species (ROS) levels were measured through flow cytometry. The level of malondialdehyde and antioxidant enzyme activities were analyzed using assay kits. The activation of NF-κB was analyzed using western blotting and a transcription factor assay kit. The expression of downstream target genes was detected by western blotting. Results BG pretreatment significantly increased the survival of irradiated cells, improved cell cycle progression, and decreased DNA damage and apoptosis. The levels of ROS and malondialdehyde were also decreased by BG. Further study indicated that BG increased the antioxidant enzyme activities, activated Src, and promoted NF-κB activation, especially for the p65, p50, and RelB subunits. The activated NF-κB upregulated the expression of antioxidant protein MnSOD, DNA damage-response and repair-related proteins BRCA2 and Hsp90α, and antiapoptotic protein Bcl-2. Conclusion Our results demonstrated that BG protects EA.hy926 cells from high linear-energy-transfer carbon-ion irradiation damage through the upregulation of prosurvival signaling triggered by the interaction of BG with its receptor. This confirms that BG is a promising radioprotective agent for heavy-ion exposure.

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Activities of wild‐type and variant tissue‐type plasminogen activators retained on vascular endothelial cells

Cited by 8 publications

References 23 publications

<p>Loxoprofen Sodium Alleviates Oxidative Stress and Apoptosis Induced by Angiotensin II in Human Umbilical Vein Endothelial Cells (HUVECs)</p>

<p>Loxoprofen Sodium Alleviates Oxidative Stress and Apoptosis Induced by Angiotensin II in Human Umbilical Vein Endothelial Cells (HUVECs)</p>

Regulation of plasminogen activation on cell surfaces and fibrin

ß-D-Glucan promotes NF-κB activation and ameliorates high-LET carbon-ion irradiation-induced human umbilical vein endothelial cell injury

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