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Full-Text Articles in Medicine and Health Sciences
Microrna Cargo Of Extracellular Vesicles From Alcohol-Exposed Monocytes Signals Naive Monocytes To Differentiate Into M2 Macrophages, Banishree Saha, Fatemeh Momen-Heravi, Karen Kodys, Gyongyi Szabo
Microrna Cargo Of Extracellular Vesicles From Alcohol-Exposed Monocytes Signals Naive Monocytes To Differentiate Into M2 Macrophages, Banishree Saha, Fatemeh Momen-Heravi, Karen Kodys, Gyongyi Szabo
Gyongyi Szabo
Membrane-coated extracellular vesicles (EVs) released by cells can serve as vehicles for delivery of biological materials and signals. Recently, we demonstrated that alcohol-treated hepatocytes cross-talk with immune cells via exosomes containing microRNA (miRNAs). Here, we hypothesized that alcohol-exposed monocytes can communicate with naive monocytes via EVs. We observed increased numbers of EVs, mostly exosomes, secreted by primary human monocytes and THP-1 monocytic cells in the presence of alcohol in a concentration- and time-dependent manner. EVs derived from alcohol-treated monocytes stimulated naive monocytes to polarize into M2 macrophages as indicated by increased surface expression of CD68 (macrophage marker), M2 markers (CD206 …
Structural Basis For Mutation-Induced Destabilization Of Profilin 1 In Als, Sivakumar Boopathy, Tania Silvas, Maeve Tischbein, Silvia Jansen, Shivender Shandilya, Jill Zitzewitz, John Landers, Bruce Goode, Celia Schiffer, Daryl Bosco
Structural Basis For Mutation-Induced Destabilization Of Profilin 1 In Als, Sivakumar Boopathy, Tania Silvas, Maeve Tischbein, Silvia Jansen, Shivender Shandilya, Jill Zitzewitz, John Landers, Bruce Goode, Celia Schiffer, Daryl Bosco
Celia A. Schiffer
Mutations in profilin 1 (PFN1) are associated with amyotrophic lateral sclerosis (ALS); however, the pathological mechanism of PFN1 in this fatal disease is unknown. We demonstrate that ALS-linked mutations severely destabilize the native conformation of PFN1 in vitro and cause accelerated turnover of the PFN1 protein in cells. This mutation-induced destabilization can account for the high propensity of ALS-linked variants to aggregate and also provides rationale for their reported loss-of-function phenotypes in cell-based assays. The source of this destabilization is illuminated by the X-ray crystal structures of several PFN1 proteins, revealing an expanded cavity near the protein core of the …
Erythrocyte Aggregation And Neutrophil Function In An Aging Population, Rhys Christy, Oguz Baskurt, Gregory Gass, A. Gray, Sonya Marshall-Gradisnik
Erythrocyte Aggregation And Neutrophil Function In An Aging Population, Rhys Christy, Oguz Baskurt, Gregory Gass, A. Gray, Sonya Marshall-Gradisnik
A. Bon Gray
There are limited investigations which have examined the relationship between neutrophil activation and erythrocyte aggregation in older persons. The purpose of the present study was to investigate the relationship between neutrophil activation and erythrocyte aggregation (EA) in an aging population. Twenty-eight male and female subjects were allocated into one of four groups with 7 participants in each group (group 1, 20–29 years; group 2, 30–39 years; group 3, 40–49 years; group 4, 50–59 years). EA was determined using the Myrenne aggregometer. Neutrophil function (respiratory burst and phagocytic activity) was assessed using flow cytometry. EA was found to increase with age. …
Erythrocyte Aggregation And Neutrophil Function In An Aging Population, Rhys Christy, Oguz Baskurt, Gregory Gass, A. Gray, Sonya Marshall-Gradisnik
Erythrocyte Aggregation And Neutrophil Function In An Aging Population, Rhys Christy, Oguz Baskurt, Gregory Gass, A. Gray, Sonya Marshall-Gradisnik
Sonya Marshall-Gradisnik
There are limited investigations which have examined the relationship between neutrophil activation and erythrocyte aggregation in older persons. The purpose of the present study was to investigate the relationship between neutrophil activation and erythrocyte aggregation (EA) in an aging population. Twenty-eight male and female subjects were allocated into one of four groups with 7 participants in each group (group 1, 20–29 years; group 2, 30–39 years; group 3, 40–49 years; group 4, 50–59 years). EA was determined using the Myrenne aggregometer. Neutrophil function (respiratory burst and phagocytic activity) was assessed using flow cytometry. EA was found to increase with age. …