SHED‐exos promote saliva secretion by suppressing p‐ERK1/2‐mediated apoptosis in glandular cells

Author:

Chu Wei‐Xia12,Ding Chong2ORCID,Du Zhi‐Hao3,Wei Pan4,Wang Yi‐Xiang2,Ge Xue‐Jun1,Yu Guang‐Yan3

Affiliation:

1. Department of Periodontics Shanxi Medical University School and Hospital of Stomatology Taiyuan Shanxi P.R. China

2. Center Laboratory Peking University School and Hospital of Stomatology Beijing P.R. China

3. Department of Oral and Maxillofacial Surgery Peking University School and Hospital of Stomatology Beijing P.R. China

4. Department of Oral Medicine Peking University School and Hospital of Stomatology & National Center of Stomatology & National Clinical Research Center for Oral Diseases & National Engineering Research Center of Oral Biomaterials and Digital Medical Devices Beijing P.R. China

Abstract

AbstractObjectivesConfirm that stem cells from human exfoliated deciduous teeth‐derived exosomes (SHED‐exos) can limit inflammation‐triggered epithelial cell apoptosis and explore the molecular mechanism.MethodsSHED‐exos were injected into the submandibular glands (SMGs) of non‐obese diabetic (NOD) mice, an animal model of Sjögren's syndrome (SS). Cell death was evaluated by western blotting and terminal deoxynucleotidyl transferase‐mediated dUTP nick‐end labelling staining.ResultsSHED‐exos treatment promoted the saliva flow rates of NOD mice, accompanied by decreased cleaved caspase‐3 levels and apoptotic cell numbers in SMGs. SHED‐exos inhibited autophagy, pyroptosis, NETosis, ferroptosis, necroptosis and oxeiptosis marker expression in SS‐damaged glands. Mechanistically, Kyoto Encyclopedia of Genes and Genomes analysis of exosomal miRNAs suggested that the rat sarcoma virus (RAS)/mitogen‐activated protein kinase kinase (MEK)/extracellular signal‐regulated kinase (ERK) pathway might play an important role. In vivo, the expression of Kirsten RAS, Harvey RAS, MEK1/2 and p‐ERK1/2 was upregulated in SMGs, and this change was blocked by SHED‐exos treatment. In vitro, SHED‐exos suppressed p‐ERK1/2 activation and increased cleaved caspase‐3 and apoptotic cell numbers, which were induced by IFN‐γ.ConclusionSHED‐exos suppress epithelial cell death, which is responsible for promoting salivary secretion. SHED‐exos inhibited inflammation‐triggered epithelial cell apoptosis by suppressing p‐ERK1/2 activation, which is involved in these effects.

Publisher

Wiley

Subject

General Dentistry,Otorhinolaryngology

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