The associations of endothelial and podocyte injury in proliferative lupus nephritis: from observational analysis to in vitro study

Lupus ◽  
2019 ◽  
Vol 28 (3) ◽  
pp. 347-358 ◽  
Author(s):  
M Yuan ◽  
Y Tan ◽  
Y Wang ◽  
S X Wang ◽  
F Yu ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Cell Injury ◽  
In Vitro Study ◽  
Glomerular Endothelial Cell ◽  
Endothelial Cell Injury ◽  
Endothelin 1 ◽  
Glomerular Endothelial Cells ◽  
Proliferative Lupus Nephritis

Our study aims to evaluate the endothelial cell-podocyte crosstalk in proliferative lupus nephritis (LN). The semi-quantification scores of glomerular endothelial cell injury and the foot process width (FPW) were processed in 110 proliferative LN patients. Podocytes were stimulated with LN-derived IgG. Glomerular endothelial cells were treated with podocyte-conditioned medium (PCM), and then podocytes were incubated with endothelial cell–conditioned medium (ECM). The levels of vascular endothelial growth factor-A (VEGF-A) in PCM and endothelin-1 in ECM were analyzed, and the injury of podocyte and glomerular endothelial cells were further evaluated. The pathological score of glomerular endothelial cell injury was correlated with FPW in LN complicated with thrombotic microangiopathy. In vitro study showed the following: 1. Stimulation of podocytes by IgG from LN led to decline in the expression of nephrin with cytoskeleton rearrangement, and reduction of VEGF-A levels. 2. Exposure of glomerular endothelial cells to PCM incubated with LN-derived IgG (PCM-LN) induced more endothelin-1 secretion and disruption of intercellular tight junction. 3. Exposure of podocytes to ECM stimulated with PCM-LN could induce cytoskeleton redistribution with decrease of nephrin. In conclusion, the pathological glomerular endothelial cell lesions were associated with FPW and the VEGF-endothelin-1 system might play a critical role in the endothelial cell-podocyte crosstalk in LN.

scholarly journals The Role of MicroRNA-155 in Glomerular Endothelial Cell Injury of Diabetic Nephropathy

2021 ◽  
Author(s):  
Kaiying He ◽  
Zhan Chen ◽  
Jing Zhao ◽  
Yang He ◽  
Rongrong Deng ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
High Glucose ◽  
Cell Injury ◽  
Inflammatory Factors ◽  
Glucose Stimulation ◽  
Endothelial Cell Injury ◽  
Glomerular Endothelial Cells ◽  
Human Glomerular Endothelial Cells

Abstract Objective: To investigate the role of microRNA-155-5p (miR-155-5p) on apoptosis and inflammatory response in human glomerular endothelial cells (HRGEC) cultured with high glucose.Methods: The primary human glomerular endothelial cells (HRGEC) were studied, QPCR, WB , IF were used to detect cell morphology, target gene ETS-1 (ETS-1), downstream factors VCAM-1 and MCP-1, and apoptosis of cells in each group after high glucose stimulation and transfection with miR-155 overexpression or inhibitor.Results:1.The expression of inflammatory factors and apoptosis of HRGEC cells increased under high glucose stimulation.2.The overexpression of miR-155 in HRGEC cells under high glucose stimulation decreased the expression of ETS-1, while the expression of ETS-1 increased when miR-155 was inhibited. These results suggest that miR-155 may be involved in endothelial cell injury by negatively regulating the expression of ETS-1.3.HRGEC cells were transfected with miR-155 mimic and ETS-1 siRNA with high glucose stimulation. The expression of ETS-1 was positively correlated with the expression of downstream factors VCAM-1 and MCP-1. These results suggest that ETS-1 can mediate endothelial cell inflammation by regulating VCAM-1 and MCP-1.

Human serum catalase decreases endothelial cell injury from hydrogen peroxide

1991 ◽  
Vol 71 (5) ◽  
pp. 1903-1906 ◽  
Author(s):  
J. A. Leff ◽  
M. A. Oppegard ◽  
L. S. Terada ◽  
E. C. McCarty ◽  
J. E. Repine
Keyword(s):  
Hydrogen Peroxide ◽  
Endothelial Cells ◽  
Endothelial Cell ◽  
Catalase Activity ◽  
Trichloroacetic Acid ◽  
Cell Injury ◽  
Human Subjects ◽  
Endothelial Cell Injury ◽  
Normal Human

Serum from normal human subjects contained variable amounts of catalase activity, which was inhibitable by heat, azide, trichloroacetic acid (TCA), or aminotriazole treatment. Serum also decreased hydrogen peroxide (H2O2) concentrations in vitro and H2O2-mediated injury to cultured endothelial cells. By comparison, heat-, azide-, TCA-, or aminotriazole-treated serum neither decreased H2O2 concentrations in vitro nor reduced H2O2-mediated damage to endothelial cells. We conclude that serum catalase activity can alter H2O2-dependent reactions. We speculate that variations in serum catalase activity may alter individual susceptibility to oxidant-mediated vascular disease or be a factor when added to test systems in vitro.

CD8+iTregs attenuate glomerular endothelial cell injury in lupus-prone mice through blocking the activation of p38 MAPK and NF-κB

2018 ◽  
Vol 103 ◽  
pp. 133-143 ◽  
Author(s):  
Ya Liu ◽  
Weijuan Deng ◽  
Qiaoyun Meng ◽  
Xiaonan Qiu ◽  
Dong Sun ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
P38 Mapk ◽  
Cell Injury ◽  
Glomerular Endothelial Cell ◽  
Endothelial Cell Injury

Peptide5 attenuates rtPA related brain microvascular endothelial cells reperfusion injury via the Wnt/β-catenin signalling pathway

2021 ◽  
Vol 18 ◽  
Author(s):  
Weimin Ren ◽  
Chuyi Huang ◽  
Heling Chu ◽  
Yuping Tang ◽  
Xiaobo Yang
Keyword(s):  
Endothelial Cells ◽  
Ischemic Stroke ◽  
Endothelial Cell ◽  
Cell Injury ◽  
Time Window ◽  
Microvascular Endothelial Cells ◽  
Brain Microvascular Endothelial Cells ◽  
Endothelial Cell Injury ◽  
Endothelial Cell Death ◽  
Therapeutic Time Window

Aims: Brain vascular endothelial cell dysfunction after rtPA treatment is a significant factor associated with poor prognosis, suggesting that alleviation of rtPA-related endothelial cell injury may represent a potential beneficial strategy along with rtPA thrombolysis. Background: Thrombolysis with recombinant tissue plasminogen activator (rtPA) is beneficial for acute ischemic stroke but may increase the risk of hemorrhagic transformation (HT), which is considered ischemia-reperfusion injury. The underlying reason may contribute to brain endothelial injury and dysfunction related to rtPA against ischemic stroke. As previous studies have demonstrated that transiently blocked Cx43 using peptide5 (Cx43 mimetic peptide) during retinal ischemia reduced vascular leakage, it is necessary to know whether this might help decrease side effect of rtPA within the therapeutic time window. Objective: This study aims to investigate the effects of peptide5 on rtPA-related cell injury during hypoxia/reoxygenation (H/R) within the therapeutic time window. Methods: In this study, we established a cell hypoxia/reoxygenation H/R model in cultured primary rat brain microvascular endothelial cells (RBMECs) and evaluated endothelial cell death and permeability after rtPA treatment with or without transient peptide5. In addition, we also investigated the potential signaling pathway to explore the underlying mechanisms preliminarily. Results: The results showed that peptide5 inhibited rtPA-related endothelial cell death and permeability. It also slightly increased tight junction (ZO-1, occluding, claudin-5) and β-catenin mRNA expression, demonstrating that peptide5 might attenuate endothelial cell injury by regulating the Wnt/β-catenin pathway. The following bioinformatic exploration from the GEO dataset GSE37239 was also consistent with our findings. Conclusion: This study showed that the application of peptide5 maintained cell viability and permeability associated with rtPA treatment, revealing a possible pathway that could be exploited to limit rtPA-related endothelial cell injury during ischemic stroke. Furthermore, the altered Wnt/β-catenin signaling pathway demonstrated that signaling pathways associated with Cx43 might have potential applications in the future. This study may provide a new way to attenuate HT and assist the application of rtPA in ischemic stroke.

scholarly journals Omentin-1 Ameliorated Free Fatty Acid-Induced Impairment in Proliferation, Migration, and Inflammatory States of HUVECs

2020 ◽  
Vol 2020 ◽  
pp. 1-9
Author(s):  
Yubin Chen ◽  
Fen Liu ◽  
Fei Han ◽  
Lizhi Lv ◽  
Can-e Tang ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Fatty Acid ◽  
Endothelial Cell ◽  
Free Fatty Acid ◽  
Cell Injury ◽  
Umbilical Vein ◽  
Quantitative Polymerase Chain Reaction ◽  
Cell Counting ◽  
Endothelial Cell Injury ◽  
Umbilical Vein Endothelial Cells

Objectives. Endothelial cell injury is a critical pathological change during the development of atherosclerosis. Here, we explored the effect of omentin-1 on free fatty acid- (FFA-) induced endothelial cell injury. Methods. An FFA-induced endothelial cell injury model was established to investigate the role of omentin-1 in this process. Cell proliferation was analyzed with the Cell Counting Kit assay and flow cytometry. Scratch and transwell assays were used to evaluate cell migration. Factors secreted by endothelial cells after injury were detected by western blotting, reverse-transcription quantitative polymerase chain reaction, and cellular fluorescence assay. Results. Omentin-1 rescued the FFA-induced impaired proliferation and migration capabilities of human umbilical vein endothelial cells (HUVECs). It decreased the number of THP-1 cells attached to HUVECs in response to injury and inhibited the FFA-induced proinflammatory state of HUVECs. Conclusion. Omentin-1 could partly ameliorate FFA-induced endothelial cell injury.

scholarly journals Reduced Krüppel-Like Factor 2 Aggravates Glomerular Endothelial Cell Injury and Kidney Disease in Mice with Unilateral Nephrectomy

2016 ◽  
Vol 186 (8) ◽  
pp. 2021-2031 ◽  
Author(s):  
Fang Zhong ◽  
Sandeep K. Mallipattu ◽  
Chelsea Estrada ◽  
Madhav Menon ◽  
Fadi Salem ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Kidney Disease ◽  
Cell Injury ◽  
Unilateral Nephrectomy ◽  
Glomerular Endothelial Cell ◽  
Endothelial Cell Injury

scholarly journals Human Endothelial Cell Injury Mechanisms in Vitro

1977 ◽  
Author(s):  
R.T. Wall ◽  
L.A. Harker ◽  
G. Striker ◽  
L. Quadracci
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Dose Response ◽  
Cell Injury ◽  
Cultured Cells ◽  
Test Material ◽  
51Cr Release ◽  
Injury Mechanisms ◽  
Cell Antibody

Since endothelial cell desquamation constitutes the initial event leading to acute and chronic vascular diseases, we have developed an in vitro system for studying injury mechanisms using cultured cells. The system involves the incubation of test material with confluent, 51Cr-labeled, cultured human umbilical vein endothelial cells in 100% pooled human serum; injury was measured as% endothelial cell 51Cr release (ECR) into the supernatant media. Baseline spontaneous ECR was 6.0% ± 1.5 while specific rabbit antihuman endothelial cell antibody (1:64 dilution) in the presence of fresh complement released 90% ± 3 of the total releasable 51Cr activity. Consistent with in vivo predictions, homocysteine in concentrations of 0.5-40 mM iduced dose response ECR up to 20%. Neither methionine nor homocystine increased ECR over controls. Also as expected from experimental work endotoxin (S. enteritidis) caused dose response ECR, i.e., 24% ± 2 at 10 ug/ml. Control studies with cultured human smooth muscle cells (SMC) demonstrated no ECR with homocysteine but significant release occurred with endotoxin.Specific complement dependent cytotoxic anti-endothelial cell antibody was demonstrated in the secum of two thrombotic thrombocytopenic purpura (TTP) patients at a 1:1 dilution, inducing ECR of 23.1% ± 1.4 and 21.0% ± 0.25. The antibody was also demonstrated by immunoflourescent techniques and was absorbed from the serum using human endothelial cells. One disease-free, six month survivor showed no cytotoxic activity. Serum from a patient with adult hemolytic-uremic syndrome demonstrated antibody dependent cell mediated cytotoxicity with release of 22% ± 1.1 when normal non-immune lymphocytes were added to heat inactivated seriun. Control studies with SMC showed no ECR with TTP sera. We conclude that assays of endothelial cell 51Cr release are stable, reproducible and useful in the characterization of injury mechanisms.

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