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10.1172/jci.insight.140750 http://scihub22266oqcxt.onion/10.1172/jci.insight.140750 33830084!8119180!33830084     free     free     free Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       JCI+Insight 2021 ; 6 (7): ä Nephropedia Template TP {{tp|p=33830084|t=2021. A mechanism for matrikine regulation in acute inflammatory lung injury |pdf=|usr=}}{{33830084}} gab.com Text A mechanism for matrikine regulation in acute inflammatory lung injury JO: JCI Insight http://www.kidney.de/pget.php?&tw=1&pmid=33830084 #FOAvip Proline-glycine-proline (PGP) and its acetylated form (Ac-PGP) are neutrophil chemoattractants generated by collagen degradation, and they have been shown to play a role in chronic inflammatory disease. However, the mechanism for matrikine regulation in acute inflammation has not been well established. Here, we show that these peptides are actively transported from the lung by the oligopeptide transporter, PEPT2. Following intratracheal instillation of Ac-PGP in a mouse model, there was a rapid decline in concentration of the labeled peptide in the bronchoalveolar lavage (BAL) over time and redistribution to extrapulmonary sites. In vitro knockdown of the PEPT2 transporter in airway epithelia or use of a competitive inhibitor of PEPT2, cefadroxil, significantly reduced uptake of Ac-PGP. Animals that received intratracheal Ac-PGP plus cefadroxil had higher levels of Ac-PGP in BAL and lung tissue. Utilizing an acute LPS-induced lung injury model, we demonstrate that PEPT2 blockade enhanced pulmonary Ac-PGP levels and lung inflammation. We further validated this effect using clinical samples from patients with acute lung injury in coculture with airway epithelia. This is the first study to our knowledge to determine the in vitro and in vivo significance of active matrikine transport as a mechanism of modulating acute inflammation and to demonstrate that it may serve as a potential therapeutic target. Twit Text FOAVip A mechanism for matrikine regulation in acute inflammatory lung injury ????JCI Insight http://www.kidney.de/pget.php?&tw=1&pmid=33830084 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=33830084 #FOAvip English Wikipedia <ref>{{Cite pmid|33830084}}</ref> A mechanism for matrikine regulation in acute inflammatory lung injury #MMPMID33830084 Robison SW; Li J; Viera L; Blackburn JP; Patel RP; Blalock JE; Gaggar A; Xu X JCI Insight 2021[Apr]; 6 (7): ä PMID33830084show ga Proline-glycine-proline (PGP) and its acetylated form (Ac-PGP) are neutrophil chemoattractants generated by collagen degradation, and they have been shown to play a role in chronic inflammatory disease. However, the mechanism for matrikine regulation in acute inflammation has not been well established. Here, we show that these peptides are actively transported from the lung by the oligopeptide transporter, PEPT2. Following intratracheal instillation of Ac-PGP in a mouse model, there was a rapid decline in concentration of the labeled peptide in the bronchoalveolar lavage (BAL) over time and redistribution to extrapulmonary sites. In vitro knockdown of the PEPT2 transporter in airway epithelia or use of a competitive inhibitor of PEPT2, cefadroxil, significantly reduced uptake of Ac-PGP. Animals that received intratracheal Ac-PGP plus cefadroxil had higher levels of Ac-PGP in BAL and lung tissue. Utilizing an acute LPS-induced lung injury model, we demonstrate that PEPT2 blockade enhanced pulmonary Ac-PGP levels and lung inflammation. We further validated this effect using clinical samples from patients with acute lung injury in coculture with airway epithelia. This is the first study to our knowledge to determine the in vitro and in vivo significance of active matrikine transport as a mechanism of modulating acute inflammation and to demonstrate that it may serve as a potential therapeutic target. |*COVID-19/immunology/metabolism[MESH] |*Oligopeptides/immunology/pharmacology[MESH] |*Symporters/antagonists & inhibitors/metabolism[MESH] |Acute Lung Injury/*immunology[MESH] |Animals[MESH] |Anti-Bacterial Agents/pharmacology[MESH] |Biological Transport, Active/immunology[MESH] |Cefadroxil/*pharmacology[MESH] |Cells, Cultured[MESH] |Chemotactic Factors/immunology/pharmacology[MESH] |Chemotaxis, Leukocyte/immunology[MESH] |Disease Models, Animal[MESH] |Extracellular Matrix[MESH] |Extracellular Matrix Proteins/metabolism[MESH] |Humans[MESH] |Inflammation/*metabolism[MESH] |Mice[MESH]A mechanism for matrikine regulation in acute inflammatory lung injury(epmc).pdf DeepDyve Pubget Overpricing