Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Neurotrophin signaling is a central mechanism of salivary dysfunction after irradiation that disrupts myoepithelial differentiation

ABSTRACT: The mechanisms that prevent regeneration of irradiated (IR) salivary glands remain elusive. Bulk RNAseq of IR versus non-IR human salivary glands showed that neurotrophin signaling is highly disrupted post-radiation. Moreover, neurotrophin receptors (NTRs) are significantly upregulated in myoepithelial cells (MECs) post-IR, and scRNAseq revealed that MECs are a main source of neurotrophin ligands. Using two ex vivo models, we show that nerve growth factor (NGF) is essential for MEC differentiation during development, whereas upregulation of NTRs in adult MECs is associated with differentiation defects. The latter morphological abnormalities were confirmed in MECs of human IR glands. As MECs are required for proper acinar cell contraction and secretion, we propose that MEC-specific upregulation of NTRs post-IR disrupts MEC differentiation and potentially hinders the ability of the gland to regenerate.

ORGANISM(S): Homo sapiens

PROVIDER: GSE206878 | GEO | 2023/03/23

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Lacrimal gland myoepithelial cells are altered in a mouse model of dry eye disease

Project description:The purpose of this study was to determine the pathogenic changes that occur in myoepithelial cells (MECs) from lacrimal glands of a mouse model of Sjogren’s syndrome. MECs were cultured from lacrimal glands of C57BL/6J (wild type, WT), and thrombospondin 1 knockout null (TSP1 -/- ) mice. We used microarray to analyzed the differential expression of genes in cultured MECs of TSP1-/- and wild type (WT) mice.

2020-06-25 | GSE150771 | GEO

miR-22 and miR-205 drive tumor aggressiveness of mucoepidermoid carcinomas of salivary glands [miRNA]

Project description:We used miRNA expression arrays and integrated analysis to study mucoepidermoid carcinomas (MEC) to identify potential drivers involved with its pathogenesis. Normal salivary glands were used as controls.

2022-03-03 | GSE169692 | GEO

miR-22 and miR-205 drive tumor aggressiveness of mucoepidermoid carcinomas of salivary glands [mRNA]

Project description:We used mRNA expression arrays and integrated analysis to study mucoepidermoid carcinomas (MEC) to identify potential drivers involved with its pathogenesis. Normal salivary glands were used as controls.

2022-03-03 | GSE169753 | GEO

Long-term functional regeneration of radiation-damaged salivary glands through delivery of a neurogenic hydrogel

Project description:To investigate the timing of endogenous regenerative events in response to a single 10 Gy dose of IR, we sequeced the transcriptomes of glands from adult (6-7 wks)mice and 7- and 14-days post-IR. We then compared to the radiated glands to Non-IR (no radiation) controls, and performed differential expression analysis.

2022-12-28 | GSE209931 | GEO

scRNAseq of healthy and irradiated mouse parotid glands highlights crosstalk between immune and secretory cells during chronic injury

Project description:Translational frameworks to understand the chronic loss of salivary dysfunction that follows after clinical irradiation, and the development of regenerative therapies remain an unmet need. Advances in single cell (sc)RNAseq has made it possible to identify previously uncharacterized cell types within tissues and to uncover gene regulatory networks that mediate cell-cell communication and drive specific cell states. scRNAseq studies have been performed for virtually all major tissues including salivary glands; however, there are currently no scRNAseq studies on chronically irradiated salivary glands. Here, we present scRNAseq from control and irradiated parotid glands from mouse collected 10 months post-irradiation. We identify a previously uncharacterized population of epithelial cells in the gland defined by expression of Etv1, which could be a possible salivary precursor. Furthermore, our data suggests that CD8+ T-cells and secretory cells are the most transcriptionally affected during chronic injury with radiation, suggesting active immune involvement during chronic irradiation injury. Notably, scRNAseq of in vivo models of chronic IR injury has only been performed in liver, lung, and skin, and data is only publicly available for lung and skin. Thus, our study will also be an essential resource to better understand cell-specific responses to chronic irradiation in general.

2023-03-23 | GSE223516 | GEO

Neurotrophin NT3 promotes ovarian primordial to primary follicle transition

Project description:Neurotrophins are growth factors that are known to have a role in promoting cell survival and differentiation. The focus of the current study is to examine the role of neurotrophins in regulating ovarian primordial follicle development. Ovaries from 4-day old rats were placed into organ culture and cultured for 10 days in the absence or presence of neurotrophin-3 (NT3), brain-derived neurotrophic factor (BDNF), or nerve growth factor (NGF). Treatment of ovaries with NT3 resulted in a significant (P<0.01) increase in primordial follicle development (i.e. primordial to primary follicle transition). Treatment with BDNF at high doses of 100â250 ng/ml also significantly (P<0.01) increased primordial follicle development, but NGF had no effect. Immunohistochemical studies determined that NT3 was present in granulosa cells, interstitial tissue, and in the oocytes of primordial and primary follicles. The NT3 receptor NTRK3 was present in oocytes at all stages of development. Analysis of ovaries that contain predominantly primordial follicles demonstrated the transcripts for NT3, NTRK3, NGF, and the BDNF/neurotrophin-4 (NT4) receptor NTRK2 are expressed, while BDNF, NT4, and the NGF receptor NTRK1 are not detectable. Inhibition of the NTRK3 receptor with the tyrophostin AG 879 resulted in oocyte death and a significant (P<0.01) reduction in follicle pool size. Inhibition of the NTRK receptors with K252a slowed primordial to primary follicle transition. A microarray analysis demonstrated that a small number of genes were differentially expressed after NT3 treatment. Observations indicate that the neurotrophin NT3, acting through the NTRK3 receptor in oocytes, promotes the primordial to primary follicle transition. Reproduction (2009) 138, pp. 697-707 We used microarrays to determine genes expressed differentially between control and NT3 (neurotrophin-3) treated P4 ovary. RNA samples from 3 control groups are compared to 3 NT3 treated ovary groups.

2010-02-21 | E-GEOD-20358 | biostudies-arrayexpress

Expression data from sheroids cultured in medium that promotes myoepithelial or proacinar differentiation

Project description:We identifiied culture conditions that promoted the differentiation of the murine salivary gland epithelial cell line, mSG-PAC1 towards myoepithelial or proacinar cell fates, which were characterized by the expression of known cell type markers. Differentiation gene expression was analyzed and GSEA was performed comparing the resulting transcirptomes and published sc_RNA seq data for murine salivary gland myoepithleial and acinar cells

2022-03-02 | GSE197652 | GEO

The effects of Lef-1 overexpression on culture-expanded MECs

Project description:The mouse trachea is thought to contain two distinct stem cell compartments that contribute to airway repair—basal cells in the surface airway epithelium (SAE) and an unknown submucosal gland (SMG) cell type. Whether a lineage relationship exists between these two stem cell compartments remains unclear. Using lineage tracing of glandular myoepithelial cells (MECs), we demonstrate that MECs can give rise to seven cell types of the SAE and SMGs following severe airway injury. MECs progressively adopted a basal cell phenotype on the SAE and established lasting progenitors capable of further regeneration following reinjury. MECs activate Wnt-regulated transcription factors (Lef-1/TCF7) following injury and Lef-1 induction in cultured MECs promoted transition to a basal cell phenotype. Surprisingly, dose-dependent MEC conditional activation of Lef-1 in vivo promoted self-limited airway regeneration in the absence of injury. Thus, modulating the Lef-1 transcriptional program in MEC-derived progenitors may have regenerative medicine applications for lung diseases.

2018-04-30 | GSE111650 | GEO

Progesterone and estrogen receptors segregate into different cell subpopulations in the normal human breast

Project description:Gene expression profiles of normal human mammary epithelial cell subsets enriched for luminal or myoepithelial characteristics on the basis of EpCAM and CD49f expression. Transcription profiles were compared between luminal- and myoepithelial-enriched human MEC subsets following 3D culture from 4 individuals. Gene expression profiles of normal human mammary epithelial cell subsets enriched for mature, luminal progenitor or bipotent progenitor-enriched characteristics on the bais of CD49f, MUC1, CD10, CD133 and Thy1 expression Transcription profiles were compared between unsorted, mature, luminal progenitor-enriched and bipotent progenitor-enriched human MEC subsets following 3D culture from 2 individuals. Four replicates of luminal-enriched human MECs and 3 replicates of myoepithelial-enriched MECs Transcription profiles of two replicates of unsorted, mature, luminal progenitor-enriched and bipotent progenitor-enriched human MEC subsets were analysed following 3D culture

2012-08-17 | E-GEOD-31429 | biostudies-arrayexpress

The adipose microenvironment dysregulates the mammary myoepithelial cells and could participate to the progression of breast cancer

Project description:Overweight and obesity are now recognized as established risk factors for breast cancer in postmenopausal women. Reciprocal interactions have been described between adipose and cancer cells. Among the cell types present in the breast, myoepithelial cells (MECs) are considered "tumour suppressor" cells. During the transition from ductal carcinoma in situ to invasive cancer, disorganization or even the disappearance of MECs is observed. As the adipose microenvironment is now considered as a central actor in the progression of breast cancer, our objective was to evaluate if it could be involved in MEC functional modifications, leading to the transition of in situ to invasive carcinoma, particularly in obese patients. Through a co-culture model, we found that adipose cells could decrease the viability of the MECs. The adipose cells could also disrupt the expression of the genes involved in the maintenance of the extracellular matrix and to amplify the expression of leptin and inflammatory markers. The metabolite analyses revealed specific profiles that may be involved in the growth of neoplastic cells. All of these perturbations could thus be responsible for the loss of tumour suppressor status of MECs and promote the transition from in situ to invasive carcinoma.

2020-11-24 | MSV000086515 | MassIVE

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data