RNA-seq of murine lung mesenchymal stromal cells (LMSCs) during tumor progress
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE179315 | GEO | 2021/07/03
REPOSITORIES: GEO
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Project description:Purpose: The goals of this study are to explore the function of lung MSCs during tumor development Methods: mRNA profiles of lung MSCs (murine) were generated by deep sequencing.
2021-09-18 | GSE125591 | GEO
Project description:Stromal support is critical to the achievement of lung homeostasis and the maintenance of an effective epithelial barrier, and yet previous studies have found a positive association between the number of mesenchymal stromal cell populations (MSCs) isolated from the alveolar space and human diseases associated with epithelial dysfunctional. We hypothesised that alveolar MSCs (A-MSCs) represent a dysfunctional population which would be distinct from lung tissue MSCs (LT-MSCs) and which would not be recoverable from healthy humans. In this study, we comprehensively interrogated the phenotype and transcriptome of human A-MSCs and LT-MSCs. We found that MSCs were rarely recoverable from the alveolar space in healthy humans, but were readily isolated from lung transplant recipients, where they expressed a CD90Hi, CD73Hi, CD45Neg, CD105Lo immunophenotype and were bipotent, lacking adipogenic potential. In contrast, MSCs were readily recoverable from healthy lung tissue and were CD90Hi or Lo, CD73Hi, CD45Neg, CD105Int and had full tri-lineage potential. Transcriptome profiling of the two populations confirmed their status as MSCs and revealed a high degree of similarity between each other and the archetypal bone-marrow MSC. 105 genes were differentially expressed, with genes involved in fibroblast activation, extracellular matrix deposition and tissue remodelling being up-regulated in A-MSCs. Finally, we found the fibroblast markers collagen 1 and α-smooth muscle actin was increased in A-MSCs. Our data suggest that in healthy humans, lung MSCs reside within the tissue, but in disease can differentiate to acquire a profibrotic phenotype and so move out of their niche into the alveolar space. Total RNA obtained from in vitro expanded MSCs (p2-4)
2016-07-04 | E-GEOD-74284 | biostudies-arrayexpress
Project description:Stromal support is critical to the achievement of lung homeostasis and the maintenance of an effective epithelial barrier, and yet previous studies have found a positive association between the number of mesenchymal stromal cell populations (MSCs) isolated from the alveolar space and human diseases associated with epithelial dysfunctional. We hypothesised that alveolar MSCs (A-MSCs) represent a dysfunctional population which would be distinct from lung tissue MSCs (LT-MSCs) and which would not be recoverable from healthy humans. In this study, we comprehensively interrogated the phenotype and transcriptome of human A-MSCs and LT-MSCs. We found that MSCs were rarely recoverable from the alveolar space in healthy humans, but were readily isolated from lung transplant recipients, where they expressed a CD90Hi, CD73Hi, CD45Neg, CD105Lo immunophenotype and were bipotent, lacking adipogenic potential. In contrast, MSCs were readily recoverable from healthy lung tissue and were CD90Hi or Lo, CD73Hi, CD45Neg, CD105Int and had full tri-lineage potential. Transcriptome profiling of the two populations confirmed their status as MSCs and revealed a high degree of similarity between each other and the archetypal bone-marrow MSC. 105 genes were differentially expressed, with genes involved in fibroblast activation, extracellular matrix deposition and tissue remodelling being up-regulated in A-MSCs. Finally, we found the fibroblast markers collagen 1 and α-smooth muscle actin was increased in A-MSCs. Our data suggest that in healthy humans, lung MSCs reside within the tissue, but in disease can differentiate to acquire a profibrotic phenotype and so move out of their niche into the alveolar space.
2016-07-04 | GSE74284 | GEO
Project description:Expression profiling of lung derived mesenchymal stromal cells to lung fibrblasts and cord blood derived mesenchymal stromal cells We have previously isolated mesenchymal stromal cells (MSCs) from the tracheal aspirates of premature neonates with respiratory distress. While isolation of MSCs correlates with the development of bronchopulmonary dysplasia, the physiologic role of these cells remains unclear. To address this, we further characterized the cells, focusing on the issues of gene expression, origin and cytokine expression. Microarray comparison of early passage neonatal lung MSC gene expression to cord blood MSCs and human fetal and neonatal lung fibroblast lines demonstrated that the neonatal lung MSCs differentially expressed 971 gene probes compared to cord blood MSCs, including the transcription factors Tbx2, Tbx3, Wnt5a, FoxF1 and Gli2, each of which have been associated with lung development. Compared to lung fibroblasts, 710 gene probe transcripts were differentially expressed by the lung MSCs, including IL-6 and IL-8/CXCL8. Further, neonatal lung MSCs exhibited a pattern of Hox gene expression distinct from cord-blood MSCs but similar to human fetal lung fibroblasts, consistent with a lung origin. Together, these data suggest that MSCs isolated from neonatal tracheal aspirates originate in the lung and are distinct from lung fibroblasts.
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Project description:We report the correlation between lung-derived neonatal MSCs and 2 clinical variables among preterm newborns: corrected gestational age (CGA) at collection and the severity of bronchopulmonary dysplasia (BPD)
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Project 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 three 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 vitroculture. 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.
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Project description:RNA-seq of murine lung mesenchymal stromal cells (LMSCs) during tumor progress
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Project description:Mesenchymal stromal cells (MSCs) are multipotent cells that reside in various tissues, including bone marrow, adipose tissue or dental pulp. They can differentiate into different cell lineages, including osteoblasts, chondrocytes, and adipocytes. MSCs are recruited and stimulate the progression of renal cancer. However, the exact mechanisms that govern MSCs homing to renal tumors are largely unknown. Here, we found that renal cancer cells secrete piR_004153 encapsulated in exosomes that are taken-up by MSCs to induce transcriptional reprograming, and stimulate their migration towards renal cancer cells. To explore the impact of piRNA on MSCs, we transfected them with piR_004153 or non-targeting scrambled control oligonucleotide and analyzed their transcriptome using microarrays.
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Project description:Major depressive disorder (MDD) is one of the most common and disabling mental disorders, and current strategies remain inadequate. Although mesenchymal stromal cells (MSCs) have shown beneficial effects in experimental models of depression, underlying mechanisms remain elusive. Here, using murine depression models, we demonstrated that MSCs could alleviate depressive and anxiety-like behaviors not due to a reduction in proinflammatory cytokines, but rather activation of dorsal raphe nucleus (DRN) 5-hydroxytryptamine (5-HT) neurons. Mechanistically, peripheral delivery of MSCs activated pulmonary innervating vagal sensory neurons, which projected to the nucleus tractus solitarius, inducing the release of 5-HT in DRN. Furthermore, MSC-secreted brain-derived neurotrophic factor activated lung sensory neurons through tropomyosin receptor kinase B (TrkB), and inhalation of a TrkB agonist also achieved significant therapeutic effects in male mice. This study reveals a role of peripheral MSCs in regulating central nervous system function and demonstrates a potential "lung vagal-to-brain axis" strategy for MDD.
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