ScRNAseq of healthy and irradiated mouse parotid glands highlights crosstalk between immune and secretory cells during chronic injury
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ABSTRACT:
PROVIDER: PRJNA926633 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR23193990.fastq.gz | Fastqsanger.gz | |||
| SRR23193991.fastq.gz | Fastqsanger.gz | |||
| SRR23193992.fastq.gz | Fastqsanger.gz | |||
| SRR23193993.fastq.gz | Fastqsanger.gz | |||
| SRR23193994.fastq.gz | Fastqsanger.gz |
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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.
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Project description:Gene expression of 4 human parotid gland samples were comapred with 4 mouse parotid gland samples. Human and mouse parotid gland gene expression was screened using custom-designed targeted cDNA containing probes for 198 genes which encode for ion/water transporter (75 genes) and receptor/regulatory (101 genes) proteins potentially involved in the fluid secretion mechanism, as well as 11 secretory protein genes and 11 control genes
2007-08-13 | E-GEOD-6017 | biostudies-arrayexpress
Project description:As the largest salivary gland in oral cavity, the parotid gland plays an important role in initial digesting and lubricating food. The abnormal secretory function of parotid gland can lead to dental caries and oral mucosal inflammation. In recent years, single-cell RNA sequencing (scRNA-seq) has been used to explore the heterogeneity and diversity of cells in various organs and tissues. However, the transcription profile of human parotid gland at single-cell resolution has not been reported yet. In this study, we constructed the cell atlas of human parotid gland using 10x Genomics platform. Characteristic gene analysis identified the biological functions of serous acinar cell populations in secreting digestive enzymes and antibacterial proteins. We revealed the specificity and similarity of parotid gland comparing to other digestive glands through comparative analyses of other published scRNA-seq datasets. We also identified the cell-specific expression of hub genes for Sjogren’s syndrome in human parotid gland by integrating the results of GWAS and bulk RNA-seq, which highlighted the importance of immune cell dysfunction in parotid Sjogren’s syndrome pathogenesis.
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Project description:We applied both single cell and bulk RNA-sequencing to characterize and identify uniqueness in gene expression of the mouse Parotid gland compared to other tissues including the submandibular gland
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Project description:Adult parotid gland RNA-seq libraries and embryonic submandibular gland RNA-seq libraries were created to examine the mRNA species present in these secretory glands, as part of a project to understand acinar glands in general.
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Project description:Worldwide, 500,000 cases of head and neck cancer (HNC) are reported each year and the primary treatment for HNC is radiotherapy. Although the goal of radiotherapy is to target the tumor, secondary exposure occurs in surrounding normal tissues, such as the salivary glands. As a result, despite successful treatment of the cancer, patients are left with long-term side effects due to direct damage to the salivary glands. The effect is chronic and currently there is no treatment. Stem cells are an attractive therapeutic option for treatment of radiation-induced glandular dysfunction because of the potential to regenerate damaged cell populations and restore salivary gland function. However, limited knowledge about the endogenous stem cell population post irradiation hinders the development for stem cell-based therapies. In this study, an ex vivo sphere formation cell culture system was utilized to assess the self-renewal capacity of cells derived from parotid salivary glands at a chronic time point following radiation. Salivary glands from irradiated mice generate significantly fewer salispheres, but can be stimulated with fetal bovine serum (FBS) to generate an equivalent number of salispheres as unirradiated salivary glands. Interestingly, the number and size of salispheres formed is dependent on the concentration of FBS supplemented into the media. Salispheres derived from irradiated glands and cultured in FBS media were found to contain cells that proliferate and express progenitor and acinar cell markers such as Keratin 5, Keratin 14, Aquaporin 5, and NKCC1. Utilization of insulin-like growth factor (IGF1) injections following radiation treatment restores salivary gland function and improves salisphere generation. These findings indicate that stimulation of these cellular populations may provide a promising avenue for the development of cell-based therapies for radiation-induced salivary gland damage.
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Project description:Radiotherapy plays a major role in the curative treatment of head and neck cancer, either as a single modality therapy, or in combination with surgery or chemotherapy, or both. Despite advances to limit radiation-induced side-effects, the major salivary glands are often affected. This frequently leads to hyposalivation which causes an increased risk for xerostomia, dental caries, mucositis, and malnutrition culminating in a significant impact on patients' quality of life. Previous research demonstrated that loss of salivary function is associated with a decrease in polarity regulators and an increase in nuclear Yap localization in a putative stem and progenitor cell (SPC) population. Yap activation has been shown to be essential for regeneration in intestinal injury models; however, the highest levels of nuclear Yap are observed in irradiated salivary SPCs that do not regenerate the gland. Thus, elucidating the inputs that regulate nuclear Yap localization and determining the role that Yap plays within the entire tissue following radiation damage and during regeneration is critical. In this study, we demonstrate that radiation treatment increases nuclear Yap localization in acinar cells and Yap-regulated genes in parotid salivary tissues. Conversely, administration of insulin-like growth factor 1 (IGF1), known to restore salivary function in mouse models, reduces nuclear Yap localization and Yap transcriptional targets to levels similar to untreated tissues. Activation of Rho-associated protein kinase (ROCK) using calpeptin results in increased Yap-regulated genes in primary acinar cells while inhibition of ROCK activity (Y-27632) leads to decreased Yap transcriptional targets. These results suggest that Yap activity is dependent on ROCK activity and provides new mechanistic insights into the regulation of radiation-induced hyposalivation.
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Project description:Understanding the transcriptional landscape that results in chronic salivary hypofunction after irradiation will help identify injury mechanisms and develop regenerative therapies. We present scRNA-seq analysis from control and irradiated murine parotid glands collected 10 months after irradiation. We identify a population of secretory cells defined by specific expression of Etv1, which may be an acinar cell precursor. Acinar and Etv1+ secretory express Ntrk2 and Erbb3, respectively while the ligands for these receptors are expressed in myoepithelial and stromal cells. Furthermore, our data suggests that secretory cells and CD4+CD8+T-cells are the most transcriptionally affected during chronic injury with radiation, suggesting active immune involvement. Lastly, evaluation of cell-cell communication networks predicts that neurotrophin, neuregulin, ECM, and immune signaling are dysregulated after irradiation, and thus may play a role in the lack of repair. This resource will be helpful to understand cell-specific pathways that may be targeted to repair chronic damage in irradiated glands.
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Project description:Gene expression of 4 human parotid gland samples were comapred with 4 mouse parotid gland samples. Keywords: Comparative Gene Expression
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