{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Mizikova I"],"funding":["German Research Foundation","Frederick Banting and Charles Best Doctoral Scholarship","Finnish Foundation for Pediatric Research","Deutsche Forschungsgemeinschaft","Canadian Lung Association—Breathing","Molly Towel Perinatal Research Foundation Postdoctoral Fellowship","Finnish Sigrid Juselius Foundation","Canadian Institutes of Health Research","CIHR"],"pagination":["479-492"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9199848"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["40(5)"],"pubmed_abstract":["Late lung development is a period of alveolar and microvascular formation, which is pivotal in ensuring sufficient and effective gas exchange. Defects in late lung development manifest in premature infants as a chronic lung disease named bronchopulmonary dysplasia (BPD). Numerous studies demonstrated the therapeutic properties of exogenous bone marrow and umbilical cord-derived mesenchymal stromal cells (MSCs) in experimental BPD. However, very little is known regarding the regenerative capacity of resident lung MSCs (L-MSCs) during normal development and in BPD. In this study we aimed to characterize the L-MSC population in homeostasis and upon injury. We used single-cell RNA sequencing (scRNA-seq) to profile in situ Ly6a+ L-MSCs in the lungs of normal and O2-exposed neonatal mice (a well-established model to mimic BPD) at 3 developmental timepoints (postnatal days 3, 7, and 14). Hyperoxia exposure increased the number and altered the expression profile of L-MSCs, particularly by increasing the expression of multiple pro-inflammatory, pro-fibrotic, and anti-angiogenic genes. In order to identify potential changes induced in the L-MSCs transcriptome by storage and culture, we profiled 15 000 Ly6a+ L-MSCs after in vitro culture. We observed great differences in expression profiles of in situ and cultured L-MSCs, particularly those derived from healthy lungs. Additionally, we have identified the location of Ly6a+/Col14a1+ L-MSCs in the developing lung and propose Serpinf1 as a novel, culture-stable marker of L-MSCs. Finally, cell communication analysis suggests inflammatory signals from immune and endothelial cells as main drivers of hyperoxia-induced changes in L-MSCs transcriptome."],"journal":["Stem cells (Dayton, Ohio)"],"pubmed_title":["Single-Cell RNA Sequencing-Based Characterization of Resident Lung Mesenchymal Stromal Cells in Bronchopulmonary Dysplasia."],"pmcid":["PMC9199848"],"funding_grant_id":["#MI 2505_1-1"],"pubmed_authors":["Mizikova I","Bardin P","Vanderhyden BC","Zhong S","Hanninen SM","Vadivel A","Lesage F","Carpen O","Cyr-Depauw C","Cook DP","Hurskainen M","Thebaud B"],"additional_accession":[]},"is_claimable":false,"name":"Single-Cell RNA Sequencing-Based Characterization of Resident Lung Mesenchymal Stromal Cells in Bronchopulmonary Dysplasia.","description":"Late lung development is a period of alveolar and microvascular formation, which is pivotal in ensuring sufficient and effective gas exchange. Defects in late lung development manifest in premature infants as a chronic lung disease named bronchopulmonary dysplasia (BPD). Numerous studies demonstrated the therapeutic properties of exogenous bone marrow and umbilical cord-derived mesenchymal stromal cells (MSCs) in experimental BPD. However, very little is known regarding the regenerative capacity of resident lung MSCs (L-MSCs) during normal development and in BPD. In this study we aimed to characterize the L-MSC population in homeostasis and upon injury. We used single-cell RNA sequencing (scRNA-seq) to profile in situ Ly6a+ L-MSCs in the lungs of normal and O2-exposed neonatal mice (a well-established model to mimic BPD) at 3 developmental timepoints (postnatal days 3, 7, and 14). Hyperoxia exposure increased the number and altered the expression profile of L-MSCs, particularly by increasing the expression of multiple pro-inflammatory, pro-fibrotic, and anti-angiogenic genes. In order to identify potential changes induced in the L-MSCs transcriptome by storage and culture, we profiled 15 000 Ly6a+ L-MSCs after in vitro culture. We observed great differences in expression profiles of in situ and cultured L-MSCs, particularly those derived from healthy lungs. Additionally, we have identified the location of Ly6a+/Col14a1+ L-MSCs in the developing lung and propose Serpinf1 as a novel, culture-stable marker of L-MSCs. Finally, cell communication analysis suggests inflammatory signals from immune and endothelial cells as main drivers of hyperoxia-induced changes in L-MSCs transcriptome.","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 May","modification":"2025-04-22T11:56:26.043Z","creation":"2025-04-06T00:10:00.628Z"},"accession":"S-EPMC9199848","cross_references":{"pubmed":["35445270"],"doi":["10.1093/stmcls/sxab023"]}}