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Long Noncoding RNA, MicroRNA, Zn Transporter Zip14 (Slc39a14) and Inflammation in Mice.

Felix R Jimenez-Rondan1, Courtney H Ruggiero1, Robert J Cousins1

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Summary

Deleting the zinc transporter Zip14 in intestinal cells alters specific long non-coding RNAs (lncRNAs) and microRNAs (miRNAs). This change involves inflammatory transcription factors binding to lncRNA promoters, impacting nutrient metabolism and zinc homeostasis.

Keywords:
epigeneticsintestineorganoidszinczinc transporter

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Area of Science:

  • Molecular Biology
  • Genetics
  • Physiology

Background:

  • Non-coding RNAs, including long non-coding RNAs (lncRNAs) and microRNAs (miRNAs), play crucial roles in animal physiology, notably in nutrient metabolism.
  • Cellular zinc homeostasis is tightly regulated by 23 transporter proteins, with Zip14 (Slc39a14) identified as a transporter responsive to proinflammatory stimuli.

Purpose of the Study:

  • To investigate the role of the zinc transporter Zip14 in the regulation of non-coding RNAs within the intestinal epithelium.
  • To elucidate the molecular mechanisms by which enterocyte-specific Zip14 deletion influences gene expression and inflammatory signaling pathways.

Main Methods:

  • Utilized enterocyte-specific Zip14 knockout mice.
  • Performed transcriptome profiling of the proximal small intestine using RNA-sequencing and quantitative polymerase chain reaction (qPCR) on whole intestine tissue, isolated intestinal epithelial cells (IECs), and intestinal organoids.
  • Conducted chromatin immunoprecipitation (ChIP) assays to assess transcription factor binding to specific gene promoters.

Main Results:

  • Enterocyte-specific deletion of Zip14 led to significant changes in the expression of several lncRNAs, including H19, U90926, Meg3, Bvht, Pvt1, and Neat1, and miR-7027, primarily within the intestine.
  • These changes were specific to the intestine, as similar alterations were not observed in skeletal muscle.
  • Chromatin immunoprecipitation assays revealed enhanced binding of proinflammatory transcription factors, signal transducer and activator of transcription 3 (STAT3) and nuclear factor kappa beta (NF-ĸβ), to the promoters of H19, Meg3, and U90926 following Zip14 deletion.

Conclusions:

  • Enterocyte-specific ablation of Zip14 restricts the observed changes in specific lncRNAs and miRNAs to the intestinal tissue.
  • The increased binding of NF-ĸβ and STAT3 to the promoters of H19, Meg3, and U90926 suggests a model where Zip14 deficiency leads to enhanced transcription factor occupancy.
  • This enhanced transcription factor binding provides a mechanism for the epigenetic regulation of specific lncRNA genes in response to Zip14 deletion, impacting intestinal physiology and potentially nutrient metabolism.