Search

Your search keyword '"Rolandsson Enes, Sara"' showing total 44 results
Start Over Author "Rolandsson Enes, Sara"
44 results on '"Rolandsson Enes, Sara"'

5. List of contributors

Author

Almendros, Isaac, primary, Althuwaybi, Abdullah Jaber A, additional, Blokland, Kaj E.C., additional, Burgess, Janette K., additional, Chen, Y-W., additional, Colt, Henri G., additional, de Hilster, Roderick H.J., additional, Elowsson, Linda, additional, Farré, Ramon, additional, Geiser, Thomas, additional, Gosens, Reinoud, additional, Guenat, Olivier T., additional, Hackett, Tillie-Louise, additional, Heijink, Irene H., additional, Hiemstra, Pieter S., additional, Ibáñez-Fonseca, Arturo, additional, Joglekar, Mugdha M., additional, John, T., additional, Khemasuwan, Danai, additional, Kistemaker, Loes EM, additional, Malakpour-Permlid, Atena, additional, Malmström, Anders, additional, Migulina, Nataliya, additional, Nawijn, Martijn C., additional, Ngassie, Maunick Lefin Koloko, additional, Nizamoglu, Mehmet, additional, Oredsson, Stina, additional, Otero, Jorge, additional, Rae, Brady, additional, Rea, M.G., additional, Rehnberg, Emil, additional, Rolandsson Enes, Sara, additional, Ryan, A.L., additional, Stegmayr, John, additional, Tas, Sinem, additional, Teitsma, Greta J., additional, van der Does, Anne M., additional, Vasse, Gwenda F., additional, Wagner, Darcy E., additional, Ward, Christopher, additional, Wasserstrom, Sebastian, additional, and Westergren-Thorsson, Gunilla, additional

Published
2022
Full Text
View/download PDF

13. Three dimensional lung models - Three dimensional extracellular matrix models

Author

Nizamoglu, Mehmet, Joglekar, Mugdha M., de Hilster, Roderick H.J., Ngassie, Maunick Lefin Koloko, Teitsma, Greta J., Migulina, Nataliya, Blokland, Kaj E.C., Burgess, Janette K., Westergren-Thorsson, Gunilla, Rolandsson Enes, Sara, Restoring Organ Function by Means of Regenerative Medicine (REGENERATE), and Groningen Research Institute for Asthma and COPD (GRIAC)

Subjects
collagen, gelatin, Extracellular matrix, hydrogel, decellularized matrices, in vitro models, lung
Abstract

In vitro models for investigating mechanisms underlying repair and regeneration in lung disease have advanced greatly in the last decades. Of these models, three-dimensional (3D) models are particularly interesting, owing to their enhanced resemblance of the physiological conditions in vivo. Three-dimensional in vitro models can be created using natural or synthetic biomaterials; where utilizing the extracellular matrix (ECM) from the lung itself or ECM-derived biomaterials have improved our understanding of lung disease and repair mechanisms. Homeostasis of lung ECM is critically important for the function of the lungs for gas exchange, and disruption of the ECM occurs in most chronic lung diseases. Reflecting the complexity of the architecture of lung tissue, several different types of in vitro models based on ECM have been developed. Materials derived from collagen, gelatin, hyaluronic acid, and their derivatives are among the most used single ECM protein-based models. Although these models lack the 3D architecture and organization of the native ECM, they facilitate the collection of extensive information via mimicking the lung microenvironment in health and disease. Decellularized lung matrices have been used as scaffolds for in vitro models, enabling the preservation of native architecture and composition within the ECM. However, reintroducing and imaging to localize cells pose some novel challenges in working within these 3D models. Hydrogels that are prepared using these decellularized lung matrices are emerging as a new opportunity, bringing the native lung ECM composition and the ability to control the model shape together. In this chapter we discuss the ECM-based 3D in vitro models for lung disease, repair, and regeneration. First, we briefly outline the lung ECM and the changes associated with chronic lung diseases. Then we summarize the progress and state-of-the-art research performed using these models, discussing the advantages and challenges related to these models and summarizing the properties of an ideal 3D model.

Published
2022

15. Mesenchymal stromal cells-derived extracellular vesicles reprogramme macrophages in ARDS models through the miR-181a-5p-PTEN-pSTAT5-SOCS1 axis

Author

Su, Yue, primary, Silva, Johnatas Dutra, additional, Doherty, Declan, additional, Simpson, David A, additional, Weiss, Daniel J, additional, Rolandsson-Enes, Sara, additional, McAuley, Daniel F, additional, O'Kane, Cecilia M, additional, Brazil, Derek P, additional, and Krasnodembskaya, Anna D, additional

Published
2022
Full Text
View/download PDF

16. Mesenchymal stromal cells-derived extracellular vesicles reprogramme macrophages in ARDS models through the miR-181a-5p-PTEN-pSTAT5-SOCS1 axis.

Author

Yue Su, Silva, Johnatas Dutra, Doherty, Declan, Simpson, David A., Weiss, Daniel J., Rolandsson-Enes, Sara, McAuley, Daniel F., O'Kane, Cecilia M., Brazil, Derek P., and Krasnodembskaya, Anna D.

Subjects
EXTRACELLULAR vesicles, MACROPHAGES, ADULT respiratory distress syndrome, MEDICAL sciences, GENE expression, MACROPHAGE inflammatory proteins
Published
2023
Full Text
View/download PDF

22. Mesenchymal stromal cells-derived extracellular vesicles reprogramme macrophages in ARDS models through the miR-181a-5p-PTEN-pSTAT5-SOCS1 axis

Author

Su, Yue, Silva, Johnatas Dutra, Doherty, Declan, Simpson, David A, Weiss, Daniel J, Rolandsson-Enes, Sara, McAuley, Daniel F, O'Kane, Cecilia M, Brazil, Derek P, and Krasnodembskaya, Anna D

Abstract

RationaleA better understanding of the mechanism of action of mesenchymal stromal cells (MSCs) and their extracellular vesicles (EVs) is needed to support their use as novel therapies for acute respiratory distress syndrome (ARDS). Macrophages are important mediators of ARDS inflammatory response. Suppressor of cytokine signalling (SOCS) proteins are key regulators of the macrophage phenotype switch. We therefore investigated whether SOCS proteins are involved in mediation of the MSC effect on human macrophage reprogramming.MethodsHuman monocyte-derived macrophages (MDMs) were stimulated with lipopolysaccharide (LPS) or plasma samples from patients with ARDS (these samples were previously classified into hypo-inflammatory and hyper-inflammatory phenotype) and treated with MSC conditioned medium (CM) or EVs. Protein expression was measured by Western blot. EV micro RNA (miRNA) content was determined by miRNA sequencing. In vivo: LPS-injured C57BL/6 mice were given EVs isolated from MSCs in which miR-181a had been silenced by miRNA inhibitor or overexpressed using miRNA mimic.ResultsEVs were the key component of MSC CM responsible for anti-inflammatory modulation of human macrophages. EVs significantly reduced secretion of tumour necrosis factor-α and interleukin-8 by LPS-stimulated or ARDS plasma-stimulated MDMs and this was dependent on SOCS1. Transfer of miR-181a in EVs downregulated phosphatase and tensin homolog (PTEN) and subsequently activated phosphorylated signal transducer and activator of transcription 5 (pSTAT5) leading to upregulation of SOCS1 in macrophages. In vivo, EVs alleviated lung injury and upregulated pSTAT5 and SOCS1 expression in alveolar macrophages in a miR181-dependent manner. Overexpression of miR-181a in MSCs significantly enhanced therapeutic efficacy of EVs in this model.ConclusionmiR-181a-PTEN-pSTAT5-SOCS1 axis is a novel pathway responsible for immunomodulatory effect of MSC EVs in ARDS.

Published
2023
Full Text
View/download PDF

23. Healthy versus inflamed lung environments differentially affect mesenchymal stromal cells.

Author

Rolandsson Enes, Sara and Rolandsson Enes, Sara

Abstract

BackgroundDespite increased interest in mesenchymal stromal cell (MSC)-based cell therapies for acute respiratory distress syndrome (ARDS), clinical investigations have not yet been successful and our understanding of the potential in vivo mechanisms of MSC actions in ARDS remains limited. ARDS is driven by an acute severe innate immune dysregulation, often characterised by inflammation, coagulation and cell injury. How this inflammatory microenvironment influences MSC functions remains to be determined.AimThe aim of this study was to comparatively assess how the inflammatory environment present in ARDS lungs versus the lung environment present in healthy volunteers alters MSC behaviour.MethodsClinical-grade human bone marrow-derived MSCs (hMSCs) were exposed to bronchoalveolar lavage fluid (BALF) samples obtained from ARDS patients or from healthy volunteers. Following exposure, hMSCs and their conditioned media were evaluated for a broad panel of relevant properties, including viability, levels of expression of inflammatory cytokines, gene expression, cell surface human leukocyte antigen expression, and activation of coagulation and complement pathways.ResultsPro-inflammatory, pro-coagulant and major histocompatibility complex (self-recognition) related gene expression was markedly upregulated in hMSCs exposed ex vivo to BALF obtained from healthy volunteers. These changes were less apparent and often opposite in hMSCs exposed to ARDS BALF samples.ConclusionThese data provide new insights into how hMSCs behave in healthy versus inflamed lung environments, and strongly suggest that the inflamed environment in ARDS induces hMSC responses that are potentially beneficial for cell survival and actions. This further highlights the need to understand how different disease environments affect hMSC functions.

Published
2021

26. Healthy versus inflamed lung environments differentially affect mesenchymal stromal cells

Author

Rolandsson Enes, Sara, primary, Hampton, Thomas H., additional, Barua, Jayita, additional, McKenna, David H., additional, dos Santos, Claudia C., additional, Amiel, Eyal, additional, Ashare, Alix, additional, Liu, Kathleen D., additional, Krasnodembskaya, Anna D., additional, English, Karen, additional, Stanton, Bruce A., additional, Rocco, Patricia R.M., additional, Matthay, Michael A., additional, and Weiss, Daniel J., additional

Published
2021
Full Text
View/download PDF

27. Differential effects of the cystic fibrosis lung inflammatory environment on mesenchymal stromal cells

Author

Abreu, Soraia C., primary, Hampton, Thomas H., additional, Hoffman, Evan, additional, Dearborn, Jacob, additional, Ashare, Alix, additional, Singh Sidhu, Karatatiwant, additional, Matthews, Dwight E., additional, McKenna, David H., additional, Amiel, Eyal, additional, Barua, Jayita, additional, Krasnodembskaya, Anna, additional, English, Karen, additional, Mahon, Bernard, additional, Dos Santos, Claudia, additional, Cruz, Fernanda F., additional, Chambers, Daniel C., additional, Liu, Kathleen D., additional, Matthay, Michael A., additional, Cramer, Robert A., additional, Stanton, Bruce A., additional, Rocco, Patricia R. M., additional, Wargo, Matthew J., additional, Weiss, Daniel J., additional, and Rolandsson Enes, Sara, additional

Published
2020
Full Text
View/download PDF

29. Stem Cells, Cell Therapies, and Bioengineering in Lung Biology and Disease 2019

Author

Wagner, Darcy E., primary, Ikonomou, Laertis, additional, Gilpin, Sarah E., additional, Magin, Chelsea M., additional, Cruz, Fernanda, additional, Greaney, Allison, additional, Magnusson, Mattias, additional, Chen, Ya-Wen, additional, Davis, Brian, additional, Vanuytsel, Kim, additional, Rolandsson Enes, Sara, additional, Krasnodembskaya, Anna, additional, Lehmann, Mareike, additional, Westergren-Thorsson, Gunilla, additional, Stegmayr, John, additional, Alsafadi, Hani N., additional, Hoffman, Evan T., additional, Weiss, Daniel J., additional, and Ryan, Amy L., additional

Published
2020
Full Text
View/download PDF

32. ERS International Congress, Madrid, 2019: highlights from the Basic and Translational Science Assembly

Author

Ubags, Niki D., primary, Baker, Jonathan, additional, Boots, Agnes, additional, Costa, Rita, additional, El-Merhie, Natalia, additional, Fabre, Aurélie, additional, Faiz, Alen, additional, Heijink, Irene H., additional, Hiemstra, Pieter S., additional, Lehmann, Mareike, additional, Meiners, Silke, additional, Rolandsson Enes, Sara, additional, and Bartel, Sabine, additional

Published
2020
Full Text
View/download PDF

33. Functional role of glycosaminoglycans in decellularized lung extracellular matrix

Author

Uhl, Franziska E., primary, Zhang, Fuming, additional, Pouliot, Robert A., additional, Uriarte, Juan J., additional, Rolandsson Enes, Sara, additional, Han, Xiaorui, additional, Ouyang, Yilan, additional, Xia, Ke, additional, Westergren-Thorsson, Gunilla, additional, Malmström, Anders, additional, Hallgren, Oskar, additional, Linhardt, Robert J., additional, and Weiss, Daniel J., additional

Published
2020
Full Text
View/download PDF

35. Lung inflammatory environments differentially alter mesenchymal stromal cell behavior

Author

Abreu, Soraia C., primary, Rolandsson Enes, Sara, additional, Dearborn, Jacob, additional, Goodwin, Meagan, additional, Coffey, Amy, additional, Borg, Zachary D., additional, dos Santos, Claúdia C., additional, Wargo, Matthew J., additional, Cruz, Fernanda F., additional, Loi, Roberto, additional, DeSarno, Michael, additional, Ashikaga, Takamuru, additional, Antunes, Mariana A., additional, Rocco, Patricia R. M., additional, Liu, Kathleen D., additional, Lee, Jae-Woo, additional, Matthay, Michael A., additional, McKenna, David H., additional, and Weiss, Daniel J., additional

Published
2019
Full Text
View/download PDF

36. CD105+CD90+CD13+ identifies a clonogenic subset of adventitial lung fibroblasts.

Author

Kadefors, Måns, Rolandsson Enes, Sara, Åhrman, Emma, Michaliková, Barbora, Löfdahl, Anna, Dellgren, Göran, Scheding, Stefan, and Westergren-Thorsson, Gunilla

Subjects
*TISSUE remodeling, *LUNG diseases, *TRANSCRIPTOMES, *REGENERATION (Biology)
Abstract

Mesenchymal cells are important components of specified niches in the lung, and can mediate a wide range of processes including tissue regeneration and repair. Dysregulation of these processes can lead to improper remodeling of tissue as observed in several lung diseases. The mesenchymal cells responsible remain poorly described, partially due to the heterogenic nature of the mesenchymal compartment and the absence of appropriate markers. Here, we describe that CD105+CD90+ mesenchymal cells can be divided into two populations based on their expression of CD13/aminopeptidase N (CD105+CD90+CD13− and CD105+CD90+CD13+). By prospective isolation using FACS, we show that both these populations give rise to clonogenic fibroblast-like cells, but with an increased clonogenic and proliferative capacity of CD105+CD90+CD13+ cells. Transcriptomic and spatial analysis pinpoints an adventitial fibroblast subset as the origin of CD105+CD90+CD13+ clonogenic mesenchymal cells in human lung. [ABSTRACT FROM AUTHOR]

Published
2021
Full Text
View/download PDF

43. Differential effects of the cystic fibrosis lung inflammatory environment on mesenchymal stromal cells.

Author

Abreu SC, Hampton TH, Hoffman E, Dearborn J, Ashare A, Singh Sidhu K, Matthews DE, McKenna DH, Amiel E, Barua J, Krasnodembskaya A, English K, Mahon B, Dos Santos C, Cruz FF, Chambers DC, Liu KD, Matthay MA, Cramer RA, Stanton BA, Rocco PRM, Wargo MJ, Weiss DJ, and Rolandsson Enes S

Subjects
Bronchoalveolar Lavage Fluid microbiology, Cystic Fibrosis metabolism, Humans, Lung metabolism, Lung microbiology, Anti-Inflammatory Agents therapeutic use, Cystic Fibrosis therapy, Mesenchymal Stem Cell Transplantation methods, Mesenchymal Stem Cells cytology
Abstract

Growing evidence demonstrates that human mesenchymal stromal cells (MSCs) modify their in vivo anti-inflammatory actions depending on the specific inflammatory environment encountered. Understanding this better is crucial to refine MSC-based cell therapies for lung and other diseases. Using acute exacerbations of cystic fibrosis (CF) lung disease as a model, the effects of ex vivo MSC exposure to clinical bronchoalveolar lavage fluid (BALF) samples, as a surrogate for the in vivo clinical lung environment, on MSC viability, gene expression, secreted cytokines, and mitochondrial function were compared with effects of BALF collected from healthy volunteers. CF BALF samples that cultured positive for Aspergillus sp. (Asp) induced rapid MSC death, usually within several hours of exposure. Further analyses suggested the fungal toxin gliotoxin as a potential mediator contributing to CF BALF-induced MSC death. RNA sequencing analyses of MSCs exposed to either Asp+ or Asp- CF BALF samples identified a number of differentially expressed transcripts, including those involved in interferon signaling, antimicrobial gene expression, and cell death. Toxicity did not correlate with bacterial lung infections. These results suggest that the potential use of MSC-based cell therapies for CF or other lung diseases may not be warranted in the presence of Aspergillus .

Published
2020
Full Text
View/download PDF

44. Lung inflammatory environments differentially alter mesenchymal stromal cell behavior.

Author

Abreu SC, Rolandsson Enes S, Dearborn J, Goodwin M, Coffey A, Borg ZD, Dos Santos CC, Wargo MJ, Cruz FF, Loi R, DeSarno M, Ashikaga T, Antunes MA, Rocco PRM, Liu KD, Lee JW, Matthay MA, McKenna DH, and Weiss DJ

Subjects
Cystic Fibrosis immunology, Cystic Fibrosis pathology, Humans, Mesenchymal Stem Cell Transplantation, Mesenchymal Stem Cells drug effects, Mesenchymal Stem Cells metabolism, Pneumonia immunology, Pneumonia pathology, Respiratory Distress Syndrome immunology, Respiratory Distress Syndrome pathology, Anti-Inflammatory Agents pharmacology, Bronchoalveolar Lavage Fluid chemistry, Culture Media, Conditioned pharmacology, Cystic Fibrosis therapy, Mesenchymal Stem Cells cytology, Pneumonia therapy, Respiratory Distress Syndrome therapy
Abstract

Mesenchymal stromal (stem) cells (MSCs) are increasingly demonstrated to ameliorate experimentally induced lung injuries through disease-specific anti-inflammatory actions, thus suggesting that different in vivo inflammatory environments can influence MSC actions. To determine the effects of different representative inflammatory lung conditions, human bone marrow-derived MSCs (hMSCs) were exposed to in vitro culture conditions from bronchoalveolar lavage fluid (BALF) samples obtained from patients with either the acute respiratory distress syndrome (ARDS) or with other lung diseases including acute respiratory exacerbations of cystic fibrosis (CF) (non-ARDS). hMSCs were subsequently assessed for time- and BALF concentration-dependent effects on mRNA expression of selected pro- and anti-inflammatory mediators, and for overall patterns of gene and mRNA expression. Both common and disease-specific patterns were observed in gene expression of different hMSC mediators, notably interleukin (IL)-6. Conditioned media obtained from non-ARDS BALF-exposed hMSCs was more effective in promoting an anti-inflammatory phenotype in monocytes than was conditioned media from ARDS BALF-exposed hMSCs. Neutralizing IL-6 in the conditioned media promoted generation of anti-inflammatory monocyte phenotype. This proof of concept study suggest that different lung inflammatory environments potentially can alter hMSC behaviors. Further identification of these interactions and the driving mechanisms may influence clinical use of MSCs for treating lung diseases.

Published
2019
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results