Reduced neuropathy target esterase in pre‐eclampsia suppresses tube formation of HUVECs via dysregulation of phospholipid metabolism

2020 ◽  
Author(s):  
Mo Li ◽  
Xin Shen ◽  
Hui Liu ◽  
Bei Yang ◽  
Siying Lu ◽  
...  
Keyword(s):  
Phospholipid Metabolism ◽  
Tube Formation ◽  
Neuropathy Target Esterase

Ultrastructural characteristics of sporidia of Ustilago

1989 ◽  
Vol 47 ◽  
pp. 786-787
Author(s):  
Patricia N. Hackney
Keyword(s):  
Electron Microscope ◽  
Type System ◽  
Tube Formation ◽  
High Voltage Electron Microscopy ◽  
Voltage Electron ◽  
University Of Wisconsin ◽  
Transmission Electron ◽  
Ustilago Hordei ◽  
Silene Alba ◽  
The University

Ustilago hordei and Ustilago violacea are yeast-like basidiomycete pathogens ofHordeum vulgare and Silene alba respectively. The mating type system in both species of Ustilago is bipolar, with alleles, A,a, (U.hordei) and a1, a2 (U.violacea) at a single locus. Haploid sporidia maintain the asexual phase by budding, while the sexual phase is initiated by conjugation tube formation between the mating types during budding and conjugation.For observation of budding, sporidia were prepared by culturing the four types on YEG (yeast extract glucose) broth for 24 hours. After centrifugation at 5000g cells were either left unmated or mated in a1/a2,A/a combinations. The sporidia were then mixed 1:1 with 4% agar and the resulting 1mm cubes fixed in 8% gluteraldehyde and post fixed in osmium tetroxide. After dehydration and embedding cubes were thin sectioned with a LKB ultratome and photographed in a Zeiss 9s transmission electron microscope or in an AE1 electron microscope of MK11 1MEV at the High Voltage Electron Microscopy Center of the University of Wisconsin-Madison.

Non-genomic effects of thyroid hormones on endothelial cell tube formation

2016 ◽  
Author(s):  
Kathrin A Schmohl ◽  
Maike Dohmann ◽  
Alexandra Wechselberger ◽  
Peter J Nelson ◽  
Christine Spitzweg
Keyword(s):  
Endothelial Cell ◽  
Thyroid Hormones ◽  
Tube Formation ◽  
Genomic Effects

Phospholipid metabolism in patients with type I and 2 diabetes mellitus

2020 ◽  
Author(s):  
Gulnora Artykbaeva ◽  
Talat Saatov
Keyword(s):  
Diabetes Mellitus ◽  
Phospholipid Metabolism ◽  
Type I

scholarly journals PTPRD-inactivation-induced CXCL8 promotes angiogenesis and metastasis in gastric cancer and is inhibited by metformin

2019 ◽  
Vol 38 (1) ◽  
Author(s):  
Won Jung Bae ◽  
Ji Mi Ahn ◽  
Hye Eun Byeon ◽  
Seokwhi Kim ◽  
Dakeun Lee
Keyword(s):  
Microarray Analysis ◽  
Protein Tyrosine Phosphatase ◽  
Cancer Metastasis ◽  
Tyrosine Phosphatase ◽  
Underlying Mechanism ◽  
Tube Formation ◽  
Potential Therapeutic Target ◽  
Efficient Treatment ◽  
Stat3 Signaling

Abstract Background Protein tyrosine phosphatase receptor delta (PTPRD) is frequently inactivated in various types of cancers. Here, we explored the underlying mechanism of PTPRD-loss-induced cancer metastasis and investigated an efficient treatment option for PTPRD-inactivated gastric cancers (GCs). Methods PTPRD expression was evaluated by immunohistochemistry. Microarray analysis was used to identify differentially expressed genes in PTPRD-inactivated cancer cells. Quantitative reverse transcription (qRT-PCR), western blotting, and/or enzyme-linked immunosorbent assays were used to investigate the PTPRD-CXCL8 axis and the expression of other related genes. An in vitro tube formation assay was performed using HUVECs. The efficacy of metformin was assessed by MTS assay. Results PTPRD was frequently downregulated in GCs and the loss of PTPRD expression was associated with advanced stage, worse overall survival, and a higher risk of distant metastasis. Microarray analysis revealed a significant increase in CXCL8 expression upon loss of PTPRD. This was validated in various GC cell lines using transient and stable PTPRD knockdown. PTPRD-loss-induced angiogenesis was mediated by CXCL8, and the increase in CXCL8 expression was mediated by both ERK and STAT3 signaling. Thus, specific inhibitors targeting ERK or STAT3 abrogated the corresponding signaling nodes and inhibited PTPRD-loss-induced angiogenesis. Additionally, metformin was found to efficiently inhibit PTPRD-loss-induced angiogenesis, decrease cell viability in PTPRD-inactivated cancers, and reverse the decrease in PTPRD expression. Conclusions Thus, the PTPRD-CXCL8 axis may serve as a potential therapeutic target, particularly for the suppression of metastasis in PTPRD-inactivated GCs. Hence, we propose that the therapeutic efficacy of metformin in PTPRD-inactivated cancers should be further investigated.

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