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Aberrantly expressed lncRNAs and mRNAs after botulinum toxin type A inhibiting salivary secretion
Author(s) -
Mao QianYing,
Xie Shang,
Wu LiLing,
Xiang RuoLan,
Cai ZhiGang
Publication year - 2021
Publication title -
oral diseases
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.953
H-Index - 87
eISSN - 1601-0825
pISSN - 1354-523X
DOI - 10.1111/odi.13633
Subject(s) - competing endogenous rna , microarray analysis techniques , biology , microrna , messenger rna , microarray , long non coding rna , gene , secretion , rna , gene expression , computational biology , microbiology and biotechnology , genetics , endocrinology
Objective In this study, we sought to determine the expression profiles of long non‐coding RNAs (lncRNAs) and messenger RNAs (mRNAs) and construct functional networks to analyze their potential roles following botulinum toxin type A (BTXA)‐mediated inhibition of salivary secretion. Methods The submandibular gland of rats in the BTXA and control groups was injected with BTXA and saline, respectively. Microarray analysis was used to identify the differentially expressed lncRNAs and mRNAs. Gene ontology and pathway analysis were performed to examine the biological functions. Functional networks, including lncRNA‐mRNA co‐expression and competing endogenous RNA (ceRNA) networks, were constructed to reveal the interaction between the coding and non‐coding genes. Results Microarray analysis revealed that 254 lncRNAs and 631 mRNAs were differentially expressed between the BTXA and control groups. Bioinformatic analysis revealed that most of the mRNAs were closely related to transmembrane transporter activity. lncRNA‐mRNA co‐expression and ceRNA networks were constructed, and several critical mRNA‐lncRNA axes and key microRNAs related to salivary secretion were identified. Conclusions Our study identified differentially expressed lncRNAs and mRNAs through microarray analysis and explored the interactions between the coding and non‐coding genes through bioinformatic analysis. These findings provide new insights into the mechanism of BTXA‐mediated inhibition of salivary secretion.