scholarly journals Polymer Optical Waveguide Grating-Based Biosensor to Detect Effective Drug Concentrations of Ginkgolide A for Inhibition of PMVEC Apoptosis

Biosensors ◽  
2021 ◽  
Vol 11 (8) ◽  
pp. 264
Author(s):  
Chunxue Wang ◽  
Pengfei Yi ◽  
Jiang Li ◽  
Haibing Dong ◽  
Changming Chen ◽  
...  
Keyword(s):  
Core Layer ◽  
Optical Biosensor ◽  
Effective Drug ◽  
Microvascular Endothelial Cell ◽  
Waveguide Grating ◽  
Drug Concentrations ◽  
Photosensitive Polymer ◽  
Ginkgolide A ◽  
Pulmonary Microvascular Endothelial Cell ◽  
Writing Technology

In this work, we successfully developed a fluorinated cross-linked polymer Bragg waveguide grating-based optical biosensor to detect effective drug concentrations of ginkgolide A for the inhibition of pulmonary microvascular endothelial cell (PMVEC) apoptosis. Fluorinated photosensitive polymer SU-8 (FSU-8) as the sensing core layer and polymethyl methacrylate (PMMA) as the sensing window cladding were synthesized. The effective drug concentration range (5–10 µg/mL) of ginkgolide A for inhibition of PMVEC apoptosis was analyzed and obtained by pharmacological studies. The structure of the device was optimized to be designed and fabricated by direct UV writing technology. The properties of the biosensor were simulated with various refractive indices of different drug concentrations. The actual sensitivity of the biosensor was measured as 1606.2 nm/RIU. The resolution and detection limit were characterized as 0.05 nm and 3 × 10−5 RIU, respectively. The technique is suitable for safe and accurate detection of effective organic drug dosages of Chinese herbal ingredients.

scholarly journals Pseudomonas aeruginosa exoenzymes U and Y induce a transmissible endothelial proteinopathy

2016 ◽  
Vol 310 (4) ◽  
pp. L337-L353 ◽  
Author(s):  
K. Adam Morrow ◽  
Cristhiaan D. Ochoa ◽  
Ron Balczon ◽  
Chun Zhou ◽  
Laura Cauthen ◽  
...  
Keyword(s):  
Molecular Weight ◽  
Pseudomonas Aeruginosa ◽  
High Molecular Weight ◽  
Cell Injury ◽  
Microvascular Endothelial Cell ◽  
Gap Formation ◽  
Conditional Expression ◽  
Pulmonary Microvascular Endothelial Cell ◽  
Injury Characteristic ◽  
Type 3

We tested the hypothesis that Pseudomonas aeruginosa type 3 secretion system effectors exoenzymes Y and U (ExoY and ExoU) induce release of a high-molecular-weight endothelial tau, causing transmissible cell injury characteristic of an infectious proteinopathy. Both the bacterial delivery of ExoY and ExoU and the conditional expression of an activity-attenuated ExoU induced time-dependent pulmonary microvascular endothelial cell gap formation that was paralleled by the loss of intracellular tau and the concomitant appearance of high-molecular-weight extracellular tau. Transfer of the high-molecular-weight tau in filtered supernatant to naïve endothelial cells resulted in intracellular accumulation of tau clusters, which was accompanied by cell injury, interendothelial gap formation, decreased endothelial network stability in Matrigel, and increased lung permeability. Tau oligomer monoclonal antibodies captured monomeric tau from filtered supernatant but did not retrieve higher-molecular-weight endothelial tau and did not rescue the injurious effects of tau. Enrichment and transfer of high-molecular-weight tau to naïve cells was sufficient to cause injury. Thus we provide the first evidence for a pathophysiological stimulus that induces release and transmissibility of high-molecular-weight endothelial tau characteristic of an endothelial proteinopathy.

Albumin and Ricinus communis agglutinin decrease endothelial permeability via interactions with matrix

1993 ◽  
Vol 265 (2) ◽  
pp. C439-C446 ◽  
Author(s):  
R. Qiao ◽  
A. Siflinger-Birnboim ◽  
H. Lum ◽  
C. Tiruppathi ◽  
A. B. Malik
Keyword(s):  
Endothelial Cell ◽  
Ricinus Communis ◽  
Endothelial Permeability ◽  
Microvascular Endothelial Cell ◽  
Unit Surface Area ◽  
Ulex Europaeus ◽  
Liquid Flux ◽  
Ricinus Communis Agglutinin ◽  
Pulmonary Microvascular Endothelial Cell ◽  
Relationship Of

We studied the effects of albumin and the lectin Ricinus communis agglutinin (RCA) on hydraulic conductivity (Lp) of bovine pulmonary microvascular endothelial cell monolayers (BPMVEC) because of the evidence that albumin and RCA can interfere with transendothelial albumin permeability (Siflinger-Birnboim, A., J. Schnitzer, H. Lum, F. Blumenstock, C. Shen, P. Del Vecchio, and A. Malik. J. Cell. Physiol. 149: 575-584, 1991). BPMVEC were seeded on microporous polycarbonate filters, and the liquid flux was measured by collecting effluent into a tubing of known inner diameter at transendothelial hydrostatic pressures (P) ranging from 5 to 20 cmH2O. Lp was calculated as the slope of the relationship of liquid flux per unit surface area (Jv) vs. P. Addition of RCA (50 micrograms/ml) or albumin (5 mg/ml) to the endothelial cell medium containing albumin-free Hanks' balanced saline solution (HBSS) decreased total Lp (expressed x 10(-6) cm.s-1 x cmH2O-1) from 17.2 +/- 3.6 during HBSS to 4.7 +/- 0.9 during albumin and 5.7 +/- 1.6 during RCA (P < 0.01 for both). The RCA effect, but not that of albumin, was prevented by the addition of D-galactose (0.1 M) (the cognate hapten monosaccharide of RCA). We determined the contribution of the extracellular matrix (ECM) in decreasing the Lp by obtaining ECM after treatment of the monolayers with 0.025 M NH4OH to detach endothelial cells from the ECM. Basal ECM Lp (expressed x 10(-6) cm.s-1 x cmH2O-1) was 57.0 +/- 15.3, and it decreased to 19.7 +/- 4.3 and 17.5 +/- 2.9 during RCA and albumin, respectively (P < 0.01 for both). In contrast, RCA and albumin did not alter the filter Lp values. Another lectin, Ulex europaeus agglutinin, and the protein immunoglobulin G had no effect on Lp values.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals MiR-375-3p regulates rat pulmonary microvascular endothelial cell activity by targeting Notch1 during hypoxia

2020 ◽  
Vol 48 (7) ◽  
pp. 030006052092685
Author(s):  
Yuan An ◽  
Ziquan Liu ◽  
Hui Ding ◽  
Qi Lv ◽  
Haojun Fan ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Cell Activity ◽  
Tube Formation ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Microvascular Endothelial Cell ◽  
Adaptation To Hypoxia ◽  
Pulmonary Microvascular Endothelial Cell ◽  
Reporter Assays ◽  
Microvascular Endothelial

Objective Pulmonary microvascular endothelial cells (PMECs) exhibit specific responses in adaptation to hypoxia. However, the mechanisms regulating PMEC activities during hypoxia remain unclear. This study investigated the potential involvement of a microRNA, miR-375-3p, in the regulation of PMEC activities. Methods Primary PMECs were isolated from rats. The expression levels of miR-375-3p and Notch1 in the PMECs were detected by quantitative PCR and western blotting. Luciferase reporter assays were performed to explore the transcriptional regulation of Notch1 by miR-375-3p. The proliferation and chemotaxis of the PMECs were measured with the Cell Counting Kit-8 and Transwell invasion assays, respectively. Additionally, the capacity of hypoxia-treated PMECs for angiogenesis and inflammatory response was determined with tube formation assays and ELISA, respectively. Results The expression of miR-375-3p and Notch1 in the PMECs was significantly down-regulated and up-regulated during hypoxia, respectively. The results demonstrated that miR-375-3p directly targets Notch1 in PMECs, thereby suppressing the transcriptional expression of Notch1. It was further revealed that miR-375-3p regulates the proliferation, chemotaxis, angiogenesis, and inflammatory response of PMECs. Conclusions Our findings revealed the important role of miR-375-3p in the regulation of PMEC function and suggest the potential involvement of miR-375-3p in the development of lung diseases.

Arg-Gly-Asp peptide increases endothelial hydraulic conductivity: comparison with thrombin response

1995 ◽  
Vol 269 (1) ◽  
pp. C110-C117 ◽  
Author(s):  
R. L. Qiao ◽  
W. Yan ◽  
H. Lum ◽  
A. B. Malik
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Hydraulic Conductivity ◽  
Cell Monolayer ◽  
Endothelial Permeability ◽  
Microvascular Endothelial Cell ◽  
Ecm Proteins ◽  
Pulmonary Microvascular Endothelial Cell ◽  
Intercellular Gaps ◽  
Strength Of Adhesion

The contribution of integrin receptors to the regulation of endothelial permeability was studied using cultured bovine pulmonary microvascular endothelial cell (BPMVEC) monolayers by the measurement of hydraulic conductivity (Lp). Treatment of monolayers with a peptide containing the sequence Gly-Arg-Gly-Asp-Ser-Pro (GRGDSP) (0.85 mM) to compete for the RGD sequence of extracellular matrix (ECM) proteins increased endothelial Lp threefold, whereas the control peptide Gly-Arg-Gly-Glu-Ser-Pro had no effect on Lp. This action of GRGDSP on Lp was not significantly altered by dibutyryl adenosine 3',5'-cyclic monophosphate (DBcAMP; 0.5 mM). Endothelial Lp increased twofold when the monolayers were challenged with alpha-thrombin (5 x 10(-8) M for 10 min), and this response was completely reversed by DBcAMP. The strength of adhesion of endothelial cells was estimated by evaluating the ability of endothelial cells to remain attached to ECM after treating the monolayers with 0.05% trypsin plus 0.5 mM EDTA. Exposure of the monolayers to either GRGDSP or alpha-thrombin significantly reduced the strength of adhesion to the ECM. DBcAMP prevented the antiadhesive effect of alpha-thrombin but not that of GRGDSP. Treatment of the monolayers with either alpha-thrombin or GRGDSP caused formation of intercellular gaps, but only the thrombin-induced intercellular gaps were accompanied by reorganization of actin filaments. These results indicate that integrin binding to ECM proteins regulates an important determinant of endothelial permeability and that alpha-thrombin and GRGDSP increase endothelial cell monolayer permeability by different mechanisms.

Lung retinol storing cells synthesize and secrete retinoic acid, an inducer of alveolus formation

2004 ◽  
Vol 286 (2) ◽  
pp. L249-L256 ◽  
Author(s):  
Ghenima Dirami ◽  
Gloria DeCarlo Massaro ◽  
Linda Biadasz Clerch ◽  
Una S. Ryan ◽  
Peter R. Reczek ◽  
...  
Keyword(s):  
Retinoic Acid ◽  
Retinoic Acid Receptor ◽  
Retinol Binding Protein ◽  
Microvascular Endothelial Cell ◽  
Alveolar Wall ◽  
Retinoid Signaling ◽  
All Trans Retinoic Acid ◽  
Wall Cell ◽  
Pulmonary Microvascular Endothelial Cell ◽  
Storage Granules

Retinoids play a key role in the formation of pulmonary alveoli. Lipid interstitial cells (LICs) of the alveolar wall store retinol and are concentrated at sites of alveolus formation, suggesting they are an endogenous source of retinoids for alveolus formation. We show in cultured rat lung cells that LICs synthesize and secrete all- trans retinoic acid (ATRA); its secretion is halved by dexamethasone, an inhibitor of alveolus formation. In a second alveolar wall cell, the pulmonary microvascular endothelial cell (PMVC), ATRA increases expression of the mRNA of cellular retinol binding protein-I (CRBP-I), a protein involved in ATRA synthesis. Serum-free, exogenous ATRA-free medium conditioned by LICs rich in retinol storage granules caused a 10-fold greater increase of CRBP-I mRNA in PMVCs than media conditioned by LICs with few retinol storage granules. This action of medium conditioned by retinol storage granule-rich LICs is decreased by a retinoic acid receptor pan-antagonist and by a retinoid X receptor pan-antagonist, suggesting the responsible molecule(s) is a retinoid and that retinoid signaling occurs in a paracrine fashion.

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