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ORIGINAL RESEARCH article

Front. Mar. Sci.
Sec. Marine Pollution
Volume 12 - 2025 | doi: 10.3389/fmars.2025.1528020

Increased miRNA-375 causes oxidative damage but promotes apoptosis resistance and cell migration in the clam Ruditapes philippinarum

Provisionally accepted
Ming Cong Ming Cong *Wenwen Tian Wenwen Tian Zhaoshun Li Zhaoshun Li Yixian Yu Yixian Yu Yu Che Yu Che Jiasen Lv Jiasen Lv
  • Yantai University, Yantai, China

The final, formatted version of the article will be published soon.

    Abstract:MicroRNA is an important regulatory factor at the post-transcriptional level. Previous miRNAomics analysis found miRNA-375 steadily up-expressed in the clam Ruditapes philippinarum upon ammonia nitrogen exposure. However, we have no idea about its regulatory mechanism, yet. In this study, the clams were challenged by injection of miRNA-375 mimics/inhibitor in vivo. Then, combined approaches of qRT-PCR, enzyme assay and ultra-structure observation were applied to investigate its regulatory effects on the related genes, cellular parameters and histological structures, respectively. Results showed that increased expression of miRNA-375 interfered the expression levels of both its target genes and ammonia toxicity-related genes which would probably lead to oxidative stress, migration of damaged cells, apoptosis resistance, and increased possibility of tumor formation. Also, miRNA-375 increased MDA content but decreased glutamate content, and caused serious structure-damage to the clam gills. Thus, increased miRNA-375 probably brings a disastrous fate to the clams R. philippinarum by inducing oxidative damage but promoting apoptosis resistance and cell migration. Overall, this study revealed for the first time about the regulatory effects of miRNA-375 in the clams and gave valuable clues to understand the toxicological mechanisms of ammonia nitrogen on the marine bivalve.

    Keywords: Ruditapes philippinarum, miRNA-375, NH3-N exposure, Oxidative damage, Apoptosis Resistance

    Received: 14 Nov 2024; Accepted: 15 Jan 2025.

    Copyright: © 2025 Cong, Tian, Li, Yu, Che and Lv. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

    * Correspondence: Ming Cong, Yantai University, Yantai, China

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