FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2562104493> ?p ?o ?g. }

• W2562104493 abstract "Background: In colon cancer, the majority of metastatic cells end up in the liver. In order to elucidate metastasis migration, a possible road of investigation may lie in exosomes, a biological nanoparticle. Usually, exosomes range from 80-150 nm and medicate cell-to-cell communication. Additionally, exosomes house up to hundred proteins, oligonucleotides, lipids, and receptors that may contribute to affecting the inflammatory response in cancer cell lines. The aim of the study is to show preferential uptake of Caco2BBE exosomes by HepG2 cells under an inflammatory stimulus. Whereas Caco2BBE cells prohibits HepG2 exosomes uptake under an inflammatory stimulus. Methods: Exosomes was isolated by differential centrifugation from Caco2BBE, HepG2, and Raw 264.7 cell culture media stimulated with and without 10 ug/mL of LPS. Once collected, exosomes were characterized for size and charge by dynamic light scatter (DLS), atomic force microscopy (AFM), and transmission electron microcopy (TEM). Additional characterization of exosomes included toxicity as well as fluorescent microscopy to explore the specificity of Coumarin-6 labelled exosomes (C-6 Exo). Finally, the biological effects of exosomes on inflammatory markers in vitro were examined by Western blot and RT-qPCR. Results: The different measurements of exosomes size indicates an average diameter of 70-100 nm. Additionally, the exosomes extracted from each cells were not toxic to any cells. Interestingly, the uptake of C-6 Exo showed a striking find that Caco2BBE cells uptake HepG2 extracted exosomes under normal conditions. Whereas LPS stimulation of Caco2BBE cells prohibits the uptake of HepG2 exosomes. Then conversely, HepG2 cells were taking up Caco2BBE extracted exosomes when stimulated with LPS. These findings correlate with Western blot and RT-qPCR data that shows up-regulation of IL-6, TNFα, and MMP9 by Caco2BBE exosomes on HepG2 cells. Again, the LPS stimulation on HepG2 cells treated with Caco2BBE exosomes causes decrease of IL-6, TNFα, MMP9, and NF-κB. Conclusions: The characterization of these exosomes showed about 100 nm non-toxic particles that effect IL-6, TNF-α, MMP9, and NFκB on HepG2 cells treated with Caco2BBE exosomes. These effects on inflammatory markers mediate the uptake of these exosomes and especially with an inflammatory stimulation such as LPS, which can either prohibit or promote this process. Together, our data could lead to understanding the role of exosomes on the translocation of metastatic cells to the liver and could open a new therapeutics option. Citation Format: Jenniffer L. Stetler, Brandon SB Canup, Russell P. Puckett, XiangXiao Meng, Ma Qiang, Hamed Laroui. In vitro cellular inflammation caused by Caco2BBE and HepG2 cells secreted exosomes. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 3177. doi:10.1158/1538-7445.AM2015-3177" @default.
• W2562104493 created "2017-01-06" @default.
• W2562104493 creator A5045846019 @default.
• W2562104493 creator A5047010785 @default.
• W2562104493 creator A5052402540 @default.
• W2562104493 creator A5053912244 @default.
• W2562104493 creator A5077689249 @default.
• W2562104493 creator A5084535940 @default.
• W2562104493 date "2015-08-01" @default.
• W2562104493 modified "2023-09-26" @default.
• W2562104493 title "Abstract 3177:In vitrocellular inflammation caused by Caco2BBE and HepG2 cells secreted exosomes" @default.
• W2562104493 doi "https://doi.org/10.1158/1538-7445.am2015-3177" @default.
• W2562104493 hasPublicationYear "2015" @default.
• W2562104493 type Work @default.
• W2562104493 sameAs 2562104493 @default.
• W2562104493 citedByCount "0" @default.
• W2562104493 crossrefType "proceedings-article" @default.
• W2562104493 hasAuthorship W2562104493A5045846019 @default.
• W2562104493 hasAuthorship W2562104493A5047010785 @default.
• W2562104493 hasAuthorship W2562104493A5052402540 @default.
• W2562104493 hasAuthorship W2562104493A5053912244 @default.
• W2562104493 hasAuthorship W2562104493A5077689249 @default.
• W2562104493 hasAuthorship W2562104493A5084535940 @default.
• W2562104493 hasConcept C104317684 @default.
• W2562104493 hasConcept C145059251 @default.
• W2562104493 hasConcept C1491633281 @default.
• W2562104493 hasConcept C153911025 @default.
• W2562104493 hasConcept C185592680 @default.
• W2562104493 hasConcept C202751555 @default.
• W2562104493 hasConcept C203014093 @default.
• W2562104493 hasConcept C20518536 @default.
• W2562104493 hasConcept C2776415932 @default.
• W2562104493 hasConcept C2776914184 @default.
• W2562104493 hasConcept C502942594 @default.
• W2562104493 hasConcept C54355233 @default.
• W2562104493 hasConcept C55493867 @default.
• W2562104493 hasConcept C81885089 @default.
• W2562104493 hasConcept C86803240 @default.
• W2562104493 hasConcept C95444343 @default.
• W2562104493 hasConceptScore W2562104493C104317684 @default.
• W2562104493 hasConceptScore W2562104493C145059251 @default.
• W2562104493 hasConceptScore W2562104493C1491633281 @default.
• W2562104493 hasConceptScore W2562104493C153911025 @default.
• W2562104493 hasConceptScore W2562104493C185592680 @default.
• W2562104493 hasConceptScore W2562104493C202751555 @default.
• W2562104493 hasConceptScore W2562104493C203014093 @default.
• W2562104493 hasConceptScore W2562104493C20518536 @default.
• W2562104493 hasConceptScore W2562104493C2776415932 @default.
• W2562104493 hasConceptScore W2562104493C2776914184 @default.
• W2562104493 hasConceptScore W2562104493C502942594 @default.
• W2562104493 hasConceptScore W2562104493C54355233 @default.
• W2562104493 hasConceptScore W2562104493C55493867 @default.
• W2562104493 hasConceptScore W2562104493C81885089 @default.
• W2562104493 hasConceptScore W2562104493C86803240 @default.
• W2562104493 hasConceptScore W2562104493C95444343 @default.
• W2562104493 hasLocation W25621044931 @default.
• W2562104493 hasOpenAccess W2562104493 @default.
• W2562104493 hasPrimaryLocation W25621044931 @default.
• W2562104493 hasRelatedWork W2348891403 @default.
• W2562104493 hasRelatedWork W2349601235 @default.
• W2562104493 hasRelatedWork W2349899029 @default.
• W2562104493 hasRelatedWork W2350329074 @default.
• W2562104493 hasRelatedWork W2353052064 @default.
• W2562104493 hasRelatedWork W2359200052 @default.
• W2562104493 hasRelatedWork W2359732052 @default.
• W2562104493 hasRelatedWork W2364229519 @default.
• W2562104493 hasRelatedWork W2369484357 @default.
• W2562104493 hasRelatedWork W2371679593 @default.
• W2562104493 hasRelatedWork W2382437268 @default.
• W2562104493 hasRelatedWork W2389980820 @default.
• W2562104493 hasRelatedWork W2409484787 @default.
• W2562104493 hasRelatedWork W2541410040 @default.
• W2562104493 hasRelatedWork W2752894229 @default.
• W2562104493 hasRelatedWork W3025333533 @default.
• W2562104493 hasRelatedWork W3028966471 @default.
• W2562104493 hasRelatedWork W3031105918 @default.
• W2562104493 hasRelatedWork W3032831540 @default.
• W2562104493 hasRelatedWork W3054859583 @default.
• W2562104493 isParatext "false" @default.
• W2562104493 isRetracted "false" @default.
• W2562104493 magId "2562104493" @default.
• W2562104493 workType "article" @default.