MO761THE CONTRIBUTION OF HIGH-PHOSPHORUS IN EXTRACELLULAR MATRIX ACCUMULATION OF VALVULAR CALCIFICATION IN CHRONIC KIDNEY DISEASE

2021 ◽  
Vol 36 (Supplement_1) ◽  
Author(s):  
Liting Wang ◽  
Yuxia Zhang ◽  
Yujia Wang ◽  
Rining Tang
Keyword(s):  
Chronic Kidney Disease ◽  
Extracellular Matrix ◽  
Endothelial Cells ◽  
Kidney Disease ◽  
Early Stage ◽  
Umbilical Vein ◽  
Akt Pathway ◽  
Protein Levels ◽  
Valvular Calcification ◽  
High Phosphorus

Abstract Background and Aims The characteristics of valvular calcification (VC) in early stage are extracellular matrix (ECM) accumulation and muti-cells activation. In our previous work, we found high-phosphorus (HP) diet aggravated ECM accumulation in both aortic valve and mitral valve in rats with chronic kidney disease (CKD). However, the underlying mechanism of HP contribution in ECM accumulation of CKD-induced VC is still unknown. Method canine valvular interstitial cells (VICs), valvular endothelial cells (VECs) and human umbilical vein endothelial cells (HUVECs) were used in this study. CKD mice (C57b and Tek-EGFP-PolyA) was build by 0.2% adenine-diet for 6 weeks and HP diet/NP diet for 10 weeks. Results As for VICs, HP induced qVICs transfer into aVICs, not oVICs, which was characterized with upregulated level of smoothelin and viemitin. There was no calcium accumulation was observed, suggesting that VICs do not have the ability to synthesize calcium crystals under pure HP intervention. As for VECs, aVICs activated by HP induced VECs EndMT in a transwell-assay, which was characterized with decreasing protein levels of endothelial markers (CD31, vWF, VE-cadherin) and increasing protein levels of mesenchymal makers (α-SMA, FSP1, N-cadherin). Then, IL-8 was found as the main factor releasing from VICs to induce VECs EndMT. In vitro, the concentration of IL-8 in the lower chamber could reach 2-4ng/ml. Reparixin was used to inhibit IL-8 receptor of VECs, which could relive aVICs-induced EndMT. In vivo, the expression of valve CXCL-2 (the mouse IL8 functional homolog) was increased in HP-diet compared with NP-diet, though the serum level of CXCL-2 was similar between two groups. AAV9-sm22a-CXCL-2 and Reparixin could inhibit VECs EndMT by inhibiting VICs relasing CXCL-2 and inhibiting VECs IL-8 receptor in CKD mice of Tek-EGFP-PolyA respectively. Then, IL-8 was found to induced VECs EndMT by miR-214-3p/PTEN/Akt pathway. Inhibiting EndMT by blocking IL-8/miR-214-3p could alleviate ECM accumulation. Conclusion HP could induce qVICs transfer into aVICs, and aVICs could cause VECs EndMT via IL-8/miR-214-3p/PTEN/Akt pathway. Both take part in ECM accumulation in CKD-induced VC.

scholarly journals 17β-estradiol upregulates striatin protein levels via Akt pathway in human umbilical vein endothelial cells

PLoS ONE ◽  
2018 ◽  
Vol 13 (8) ◽  
pp. e0202500 ◽  
Author(s):  
Shuhui Zheng ◽  
Peng Sun ◽  
Haimei Liu ◽  
Runmei Li ◽  
Lingli Long ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Umbilical Vein ◽  
Akt Pathway ◽  
Human Umbilical Vein ◽  
Protein Levels ◽  
17Β Estradiol ◽  
Umbilical Vein Endothelial Cells

Effect of Lipoprotein(a) and LDL on Plasminogen Binding to Extracellular Matrix and on Matrix-dependent Plasminogen Activation by Tissue Plasminogen Activator

1996 ◽  
Vol 75 (03) ◽  
pp. 497-502 ◽  
Author(s):  
Hadewijch L M Pekelharing ◽  
Henne A Kleinveld ◽  
Pieter F C.C.M Duif ◽  
Bonno N Bouma ◽  
Herman J M van Rijn
Keyword(s):  
Extracellular Matrix ◽  
Endothelial Cells ◽  
Plasminogen Activator ◽  
Binding Sites ◽  
Umbilical Vein ◽  
Single Step ◽  
Plasminogen Activation ◽  
Structural Homology ◽  
Tissue Plasminogen ◽  
Umbilical Vein Endothelial Cells

SummaryLp(a) is an LDL-like lipoprotein plus an additional apolipoprotein apo(a). Based on the structural homology of apo(a) with plasminogen, it is hypothesized that Lp(a) interferes with fibrinolysis. Extracellular matrix (ECM) produced by human umbilical vein endothelial cells was used to study the effect of Lp(a) and LDL on plasminogen binding and activation. Both lipoproteins were isolated from the same plasma in a single step. Plasminogen bound to ECM via its lysine binding sites. Lp(a) as well as LDL were capable of competing with plasminogen binding. The degree of inhibition was dependent on the lipoprotein donor as well as the ECM donor. When Lp(a) and LDL obtained from one donor were compared, Lp(a) was always a much more potent competitor. The effect of both lipoproteins on plasminogen binding was reflected in their effect on plasminogen activation. It is speculated that Lp(a) interacts with ECM via its LDL-like lipoprotein moiety as well as via its apo(a) moiety.

Perturbation of Platelet Adhesion to Endothelial Cells by Plasminogen Activation In Vitro

1997 ◽  
Vol 78 (02) ◽  
pp. 934-938 ◽  
Author(s):  
Hsiun-ing Chen ◽  
Yueh-I Wu ◽  
Yu-Lun Hsieh ◽  
Guey-Yueh Shi ◽  
Meei-Jyh Jiang ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Endothelial Cells ◽  
Platelet Adhesion ◽  
Treatment Time ◽  
Shape Change ◽  
Umbilical Vein ◽  
Tissue Type ◽  
Apical Surface ◽  
Plasminogen Activation

SummaryTo investigate whether the endothelium-platelet interactions may be altered by plasminogen activation, cultured human umbilical vein endothelial cells (ECs) were treated with tissue-type plasminogen activator (t-PA) in the presence of plasminogen, and platelet adhesion to ECs was subsequently measured by using a tapered flow chamber. Our results demonstrated that platelets adhered more readily to t-PA treated EC monolayer than to the control monolayer at all shear stress levels tested. This phenomenon was treatment time-dependent and dose-dependent, and it could be blocked by adding plasmin inhibitors, such as e-amino caproic acid and aprotinin. Adherent platelets on t-PA treated EC monolayer underwent more severe shape change than those on the control monolayer. While the extracellular matrix directly treated with t-PA attracted less platelets than the control matrix did, platelet adhesion to the matrix that was produced by t-PA-treated ECs was unaltered. These data suggest that t-PA treatment on ECs compromised antiplatelet-adhesion capability on their apical surface without altering the reactivity of their extracellular matrix towards platelets.

Desmopressin (DDAVP) Enhances Platelet Adhesion to the Extracellular Matrix of Cultured Human Endothelial Cells through Increased Expression of Tissue Factor

1997 ◽  
Vol 77 (05) ◽  
pp. 0975-0980 ◽  
Author(s):  
Angel Gálvez ◽  
Goretti Gómez-Ortiz ◽  
Maribel Díaz-Ricart ◽  
Ginés Escolar ◽  
Rogelio González-Sarmiento ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Endothelial Cells ◽  
Tissue Factor ◽  
Platelet Adhesion ◽  
Umbilical Vein ◽  
Procoagulant Activity ◽  
Experimental Conditions ◽  
Chromogenic Assay

SummaryThe effect of desmopressin (DDAVP) on thrombogenicity, expression of tissue factor and procoagulant activity (PCA) of extracellular matrix (ECM) generated by human umbilical vein endothelial cells cultures (HUVEC), was studied under different experimental conditions. HUVEC were incubated with DDAVP (1, 5 and 30 ng/ml) and then detached from their ECM. The reactivity towards platelets of this ECM was tested in a perfusion system. Coverslips covered with DD A VP-treated ECMs were inserted in a parallel-plate chamber and exposed to normal blood anticoagulated with low molecular weight heparin (Fragmin®, 20 U/ml). Perfusions were run for 5 min at a shear rate of 800 s1. Deposition of platelets on ECMs was significantly increased with respect to control ECMs when DDAVP was used at 5 and 30 ng/ml (p <0.05 and p <0.01 respectively). The increase in platelet deposition was prevented by incubation of ECMs with an antibody against human tissue factor prior to perfusion. Immunofluorescence studies positively detected tissue factor antigen on DDAVP derived ECMs. A chromogenic assay performed under standardized conditions revealed a statistically significant increase in the procoagulant activity of the ECMs produced by ECs incubated with 30 ng/ml DDAVP (p <0.01 vs. control samples). Northern blot analysis revealed increased levels of tissue factor mRNA in extracts from ECs exposed to DDAVP. Our data indicate that DDAVP in vitro enhances platelet adhesion to the ECMs through increased expression of tissue factor. A similar increase in the expression of tissue factor might contribute to the in vivo hemostatic effect of DDAVP.

ASSESSMENT OF KIDNEY FUNCTIONAL RESERVE ON THE BACKGROUND OF ANTI-AGGREGATE THERAPY IN CHRONIC KIDNEY DISEASE II-III STAGE

2020 ◽  
Vol 6 (1) ◽  
pp. 49-54
Author(s):  
Khabib Barnoev ◽  
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Comparative Study ◽  
Early Stage ◽  
Raw Material ◽  
Functional Reserve ◽  
Functional Reserves ◽  
Term Administration ◽  
Antiaggregant Therapy

The article presents the results of a study to assess the functional reserve of the kidneys against the background of a comparative study of antiaggregant therapy dipyridamole and allthrombosepin in 50 patients with a relatively early stage of chronic kidney disease. Studies have shown that long-term administration of allthrombosepin to patients has resulted in better maintenance of kidney functional reserves. Therefore, our research has once again confirmed that diphtheridamol, which is widely used as an antiaggregant drug in chronic kidney disease, does not lag behind the domestic raw material allthrombosepin

scholarly journals An Update on Hepatocellular Carcinoma in Chronic Kidney Disease

Cancers ◽  
2021 ◽  
Vol 13 (14) ◽  
pp. 3617
Author(s):  
Fabrizio Fabrizi ◽  
Roberta Cerutti ◽  
Carlo M. Alfieri ◽  
Ezequiel Ridruejo
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Early Stage ◽  
Survival Rates ◽  
International Study ◽  
Public Health Issue ◽  
Advanced Chronic Kidney Disease ◽  
Ablative Techniques ◽  
Risk Of Cancer

Chronic kidney disease is a major public health issue globally and the risk of cancer (including HCC) is greater in patients on long-term dialysis and kidney transplant compared with the general population. According to an international study on 831,804 patients on long-term dialysis, the standardized incidence ratio for liver cancer was 1.2 (95% CI, 1.0–1.4) and 1.5 (95% CI, 1.3–1.7) in European and USA cohorts, respectively. It appears that important predictors of HCC in dialysis population are hepatotropic viruses (HBV and HCV) and cirrhosis. 1-, 3-, and 5-year survival rates are lower in HCC patients on long-term dialysis than those with HCC and intact kidneys. NAFLD is a metabolic disease with increasing prevalence worldwide and recent evidence shows that it is an important cause of liver-related and extra liver-related diseases (including HCC and CKD, respectively). Some longitudinal studies have shown that patients with chronic hepatitis B are aging and the frequency of comorbidities (such as HCC and CKD) is increasing over time in these patients; it has been suggested to connect these patients to an appropriate care earlier. Antiviral therapy of HBV and HCV plays a pivotal role in the management of HCC in CKD and some combinations of DAAs (elbasvir/grazoprevir, glecaprevir/pibrentasvir, sofosbuvir-based regimens) are now available for HCV positive patients and advanced chronic kidney disease. The interventional management of HCC includes liver resection. Some ablative techniques have been suggested for HCC in CKD patients who are not appropriate candidates to surgery. Transcatheter arterial chemoembolization has been proposed for HCC in patients who are not candidates to liver surgery due to comorbidities. The gold standard for early-stage HCC in patients with chronic liver disease and/or cirrhosis is still liver transplant.

scholarly journals Risk Factors for Progression in Patients with Early-stage Chronic Kidney Disease in the Japanese Population

2008 ◽  
Vol 47 (21) ◽  
pp. 1859-1864 ◽  
Author(s):  
Takumi Yoshida ◽  
Takashi Takei ◽  
Satsuki Shirota ◽  
Misao Tsukada ◽  
Hidekazu Sugiura ◽  
...  
Keyword(s):  
Risk Factors ◽  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Japanese Population ◽  
Early Stage
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