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        <identifier>oai:figshare.com:article/33946489</identifier>
        <datestamp>2026-09-30T10:03:30Z</datestamp>
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        <oai_dc:dc xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance"  xmlns:oai_dc="http://www.openarchives.org/OAI/2.0/oai_dc/" xmlns:dc="http://purl.org/dc/elements/1.1/" xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/oai_dc/ http://www.openarchives.org/OAI/2.0/oai_dc.xsd">
          <dc:title>Dataset for &lt;b&gt;miR-433-3p protects against cadmium-induced intestinal injury via targeting &lt;/b&gt;&lt;b&gt;&lt;i&gt;MAPK8&lt;/i&gt;&lt;/b&gt;&lt;b&gt; to repress the JNK-JUN signaling pathway&lt;/b&gt;</dc:title>
          <dc:creator>yuanwei wan (25075915)</dc:creator>
          <dc:creator>Zhimin Wu (25079120)</dc:creator>
          <dc:creator>Bingchen Wang (25079126)</dc:creator>
          <dc:creator>Huimin Zhang (18421069)</dc:creator>
          <dc:creator>Shuo Yan (18421060)</dc:creator>
          <dc:creator>Ting Wang (25079130)</dc:creator>
          <dc:creator>Xinyue Cheng (25079136)</dc:creator>
          <dc:creator>Zimeng Ma (25079138)</dc:creator>
          <dc:creator>Siqin Bao (18421094)</dc:creator>
          <dc:creator>Xihe Li (18421091)</dc:creator>
          <dc:creator>Jiuzhi Xu (25079143)</dc:creator>
          <dc:creator>Yongli Song (18421097)</dc:creator>
          <dc:subject>Animal growth and development</dc:subject>
          <dc:subject>Hu sheep; Cadmium; miR-433-3p; MAPK8; JNK-JUN signaling; Intestinal inflammation</dc:subject>
          <dc:description>&lt;p dir="ltr"&gt;Cadmium (Cd), a widespread environmental pollutant with potent bioaccumulation and persistent toxicity to animals, primarily targets the gastrointestinal tract. Although Cd induces intestinal inflammation, the molecular mechanisms governing this pathological process, particularly post-transcriptional regulatory events, remain largely unclear. Here we constructed a Cd-exposed Hu sheep model and found that Cd accumulation caused significant intestinal inflammatory injury, elevated pro-inflammatory cytokine levels and disrupted intestinal homeostasis. Integrated transcriptomics identified miR-433-3p as a candidate regulatory miRNA markedly downregulated upon Cd treatment. Functional assays demonstrated that miR-433-3p overexpression substantially alleviated Cd-induced inflammatory responses, whereas miR-433-3p inhibition aggravated inflammation. Pathway enrichment identified MAPK signaling as the key downstream cascade modulated by miR-433-3p. Mechanistically, Cd activated the JNK/MAPK8-JUN pathway, while miR-433-3p restoration suppressed this cascade. Bioinformatics prediction combined with dual-luciferase reporter assays verified &lt;i&gt;MAPK8&lt;/i&gt; as a direct target of miR-433-3p. In Cd-challenged mice, &lt;i&gt;in vivo&lt;/i&gt; administration of miR-433-3p mimics significantly repressed JNK/MAPK8-JUN signaling activation, thereby ameliorating Cd-provoked intestinal damage and inflammatory responses. Collectively, our findings &lt;a href="" target="_blank"&gt;reveal a previously unrecognized post-transcriptional regulatory mechanism&lt;/a&gt;: Cd-driven miR-433-3p reduction de-represses MAPK8 to hyperactivate the JNK-JUN inflammatory cascade, where miR‑433‑3p serves as a critical negative regulator (molecular brake) of this inflammatory axis. Our study provides new insights into Cd-induced intestinal injury and suggests miR-433-3p as a potential therapeutic target against heavy-metal-associated intestinal toxicity.&lt;/p&gt;&lt;p&gt;&lt;br&gt;&lt;/p&gt;</dc:description>
          <dc:date>2026-09-29T00:00:00Z</dc:date>
          <dc:type>Dataset</dc:type>
          <dc:type>Dataset</dc:type>
          <dc:identifier>10.6084/m9.figshare.33946489.v1</dc:identifier>
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          <dc:rights>CC BY 4.0</dc:rights>
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