scholarly journals Urinary Trypsin Inhibitor Protects Tight Junctions of Septic Pulmonary Capillary Endothelial Cells by Regulating the Functions of Macrophages

2021 ◽  
Vol Volume 14 ◽  
pp. 1973-1989
Author(s):  
Ruijie Wang ◽  
Wenliang Song ◽  
Chengyuan Xie ◽  
Wenhong Zhong ◽  
Hui Xu ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Tight Junctions ◽  
Trypsin Inhibitor ◽  
Urinary Trypsin Inhibitor ◽  
Pulmonary Capillary ◽  
Capillary Endothelial Cells

scholarly journals miR-181c-5p mediates apoptosis of vascular endothelial cells induced by hyperoxemia via ceRNA crosstalk

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Jizhi Wu ◽  
Guangqi Zhang ◽  
Hui Xiong ◽  
Yuguang Zhang ◽  
Gang Ding ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Oxygen Therapy ◽  
Vascular Endothelial Cells ◽  
Inhibitory Effect ◽  
Vascular Endothelial ◽  
Pulmonary Capillaries ◽  
Pulmonary Capillary ◽  
Capillary Endothelial Cells ◽  
Nasal Inhalation ◽  
Induced Apoptosis

AbstractOxygen therapy has been widely used in clinical practice, especially in anesthesia and emergency medicine. However, the risks of hyperoxemia caused by excessive O2 supply have not been sufficiently appreciated. Because nasal inhalation is mostly used for oxygen therapy, the pulmonary capillaries are often the first to be damaged by hyperoxia, causing many serious consequences. Nevertheless, the molecular mechanism by which hyperoxia injures pulmonary capillary endothelial cells (LMECs) has not been fully elucidated. Therefore, we systematically investigated these issues using next-generation sequencing and functional research techniques by focusing on non-coding RNAs. Our results showed that hyperoxia significantly induced apoptosis and profoundly affected the transcriptome profiles of LMECs. Hyperoxia significantly up-regulated miR-181c-5p expression, while down-regulated the expressions of NCAPG and lncRNA-DLEU2 in LMECs. Moreover, LncRNA-DLEU2 could bind complementarily to miR-181c-5p and acted as a miRNA sponge to block the inhibitory effect of miR-181c-5p on its target gene NCAPG. The down-regulation of lncRNA-DLEU2 induced by hyperoxia abrogated its inhibition of miR-181c-5p function, which together with the hyperoxia-induced upregulation of miR-181c-5p, all these significantly decreased the expression of NCAPG, resulting in apoptosis of LMECs. Our results demonstrated a ceRNA network consisting of lncRNA-DLEU2, miR-181c-5p and NCAPG, which played an important role in hyperoxia-induced apoptosis of vascular endothelial injury. Our findings will contribute to the full understanding of the harmful effects of hyperoxia and to find ways for effectively mitigating its deleterious effects.

Endothelial Metabolism in Pulmonary Vascular Homeostasis and Acute Respiratory Distress Syndrome

2021 ◽  
Author(s):  
Reece P Stevens ◽  
Sunita S. Paudel ◽  
Santina C Johnson ◽  
Troy Stevens ◽  
Ji Young Lee
Keyword(s):  
Endothelial Cells ◽  
Acute Respiratory Distress Syndrome ◽  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Distress Syndrome ◽  
Epigenetic Landscape ◽  
Pulmonary Capillary ◽  
Capillary Endothelial Cells ◽  
Insight Into ◽  
Alveolar Capillary

Capillary endothelial cells possess a specialized metabolism necessary to adapt to the unique alveolar-capillary environment. Here, we highlight how endothelial metabolism preserves the integrity of the pulmonary circulation by controlling vascular permeability, defending against oxidative stress, facilitating rapid migration and angiogenesis in response to injury, and regulating the epigenetic landscape of endothelial cells. Recent reports on single cell RNA sequencing reveal subpopulations of pulmonary capillary endothelial cells with distinctive reparative capacities which potentially offers new insight into their metabolic signature. Lastly, we discuss broad implications of pulmonary vascular metabolism on acute respiratory distress syndrome, touching on emerging findings of endotheliitis in Coronavirus Disease 2019 (COVID-19) lungs.

Urinary trypsin inhibitor may have a protective effect on endothelial cells in preeclampsia

1994 ◽  
Vol 73 (10) ◽  
pp. 755-757 ◽  
Author(s):  
Emad El Maradny ◽  
Naohiro Kanayama ◽  
Abdul Halim ◽  
Kayoko Maehara ◽  
Toshihiko Terao
Keyword(s):  
Endothelial Cells ◽  
Protective Effect ◽  
Trypsin Inhibitor ◽  
Urinary Trypsin Inhibitor

scholarly journals The upregulation of miR-204-3p in LPS-induced acute lung injury aggravated pulmonary endothelial cells apoptosis via targeting sulfatase 2

2021 ◽  
Author(s):  
Liya Zhang ◽  
Zhengyu Zhu ◽  
Qian Zhang ◽  
Zhengdao Mao
Keyword(s):  
Endothelial Cells ◽  
Acute Lung Injury ◽  
Lung Injury ◽  
Cell Structure ◽  
Alveolar Epithelial Cells ◽  
Alveolar Epithelial ◽  
Pulmonary Endothelial Cells ◽  
Pulmonary Capillary ◽  
Capillary Endothelial Cells ◽  
Lps Treatment

Acute lung injury (ALI) results from the injury of alveolar epithelial cells and pulmonary capillary endothelial cells, with a high mortality rate ranging from 29% to 42%. Therefore, more efficient therapeutic strategies for ALI are necessary. Numerous studies revealed that miRNAs play a role in the regulation of ALI. Lipopolysaccharide (LPS) can induce an inflammatory response and has been widely applied in the establishment of the mouse ALI model. Here, we reported that miR-204-3p expression was upregulated by LPS treatment with increased cytokine secretion. LPS treatment promoted cell apoptosis, accompanied by abnormal cell structure and unobvious alveolar structure. These effects could be prevented by down-regulation of miR-204-3p, and promoted by miR-204-3p overexpression. Sulfatase 2 (SULF2) appeared to be the target of miR-204-3p predicted by TargetScan. Downregulation of miR-204-3p enhanced the protein level of SULF2, indicating that SULF2 was a target of miR-204-3p, which could negatively regulate the expression of SULF2. Thus, targeting miR-204-3p may be a potential therapeutic strategy for ALI.

scholarly journals Effects of gold and PCL- or PLLA-coated silica nanoparticles on brain endothelial cells and the blood–brain barrier

2019 ◽  
Vol 10 ◽  
pp. 941-954 ◽  
Author(s):  
Aniela Bittner ◽  
Angélique D Ducray ◽  
Hans Rudolf Widmer ◽  
Michael H Stoffel ◽  
Meike Mevissen
Keyword(s):  
Endothelial Cells ◽  
Silica Nanoparticles ◽  
Tight Junctions ◽  
Blood Brain Barrier ◽  
Medical Application ◽  
Brain Barrier ◽  
Brain Endothelial Cells ◽  
Blood Brain ◽  
Functional Aspects ◽  
Capillary Endothelial Cells

Nanomedicine is a constantly expanding field, facilitating and improving diagnosis and treatment of diseases. As nanomaterials are foreign objects, careful evaluation of their toxicological and functional aspects prior to medical application is imperative. In this study, we aimed to determine the effects of gold and polymer-coated silica nanoparticles used in laser tissue soldering on brain endothelial cells and the blood–brain barrier using rat brain capillary endothelial cells (rBCEC4). All types of nanoparticles were taken up time-dependently by the rBCEC4 cells, albeit to a different extent, causing a time- and concentration-dependent decrease in cell viability. Nanoparticle exposure did not change cell proliferation, differentiation, nor did it induce inflammation. rBCEC4 cells showed blood–brain barrier characteristics including tight junctions. None of the nanoparticles altered the expression of tight junctions or impaired the blood–brain barrier permeability. The findings suggest that effects of these nanoparticles on the metabolic state of cells have to be further characterized before use for medical purposes.

Low Molecular Weight Trypsin-Plasmin Inhibitors Isolated from Papain Treated Urinary Trypsin Inhibitor

1982 ◽  
Vol 47 (01) ◽  
pp. 014-018 ◽  
Author(s):  
H Sumi ◽  
N Toki ◽  
S Takasugi ◽  
S Maehara ◽  
M Maruyama ◽  
...  
Keyword(s):  
Trypsin Inhibitor ◽  
Gel Electrophoresis ◽  
Specific Activity ◽  
Polyacrylamide Gel Electrophoresis ◽  
Sodium Dodecyl ◽  
Gel Chromatography ◽  
Urinary Trypsin Inhibitor ◽  
Plasmin Activity ◽  
Molecular Weights ◽  
Plasmin Inhibitors

SummaryPapain treatment of human urinary trypsin inhibitor (UTI67; mol. wt. 43,000 by SDS-polyacrylamide gel electrophoresis, specific activity 1,897 U/mg protein) produced four new protease inhibitors, which were highly purified by gel chromatography on Sephadex G-100 and isoelectric focusing. The purified inhibitors (UTI26, UTI9-I, UTI9-II, and UTI9-III) were shown to be homogeneous by polyacrylamide disc gel electrophoresis, and had apparent molecular weights of 26,000, 9,000, 9,000, and 9,800, respectively, by sodium dodecyl sulfate gel electrophoresis. During enzymatic degradation of UTI67, the amino acid compositions changed to more basic, and the isoelectric point increased from pH 2.0 (UTI67) to pHs 4.4, 5.2, 6.6, and 8.3 (UTI26, UTI9-I, UTI9-II, and UTI9-III), respectively. Both the parent and degraded inhibitors had anti-plasmin activity as well as antitrypsin and anti-chymotrypsin activities. Much higher anti-plasmin/anti-trypsin and anti-plasmin/anti-chymotrypsin activities were observed in the degraded inhibitors than in the parent UTI67. They competitively inhibited human plasmin with Ki values of 1.13 X 10-7 - 2.12 X 10-6 M (H-D-Val-Leu-Lys-pNA substrate). The reactions were very fast and the active site of the inhibitors to plasmin was thought to be different from that to trypsin or chymotrypsin.

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