Evaluating the transcriptional landscape and cell-cell communication networks in chronically irradiated parotid glands.
| Autor: | Rheinheimer BA; Nutritional Sciences Department, University of Arizona, Tucson, AZ 85721, USA., Pasquale MC; Matrix and Morphogenesis Section, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, MD 20892, USA., Limesand KH; Nutritional Sciences Department, University of Arizona, Tucson, AZ 85721, USA., Hoffman MP; Matrix and Morphogenesis Section, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, MD 20892, USA., Chibly AM; Matrix and Morphogenesis Section, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, MD 20892, USA. |
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| Jazyk: | angličtina |
| Zdroj: | IScience [iScience] 2023 Apr 11; Vol. 26 (5), pp. 106660. Date of Electronic Publication: 2023 Apr 11 (Print Publication: 2023). |
| DOI: | 10.1016/j.isci.2023.106660 |
| Abstrakt: | 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. Competing Interests: The authors declare no competing interests. |
| Databáze: | MEDLINE |
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