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Related Concept Videos

Renewal of Intestinal Stem Cells01:23

Renewal of Intestinal Stem Cells

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The intestinal epithelial lining rapidly renews every 4 to 5 days. The renewal is facilitated by intestinal stem cells (ISCs) located at the base of the crypt– a gland located at the bottom of each villus. ISCs divide asymmetrically to form new stem cells and progenitor daughter cells. The daughter cells are called transit-amplifying (TA) cells which move upwards along the crypt and either differentiate into absorptive cells– the enterocytes or secretory cells– including the...
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MicroRNA (miRNA) are short, regulatory RNA transcribed from introns (non-coding regions of a gene) or intergenic regions (stretches of DNA present between genes). Several processing steps are required to form biologically active, mature miRNA. The initial transcript, called primary miRNA (pri-mRNA), base-pairs with itself, forming a stem-loop structure. Within the nucleus, an endonuclease enzyme, called Drosha, shortens the stem-loop structure into hairpin-shaped pre-miRNA. After the pre-miRNA...
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MicroRNA (miRNA) are short, regulatory RNA transcribed from introns—non-coding regions of a gene—or intergenic regions—stretches of DNA present between genes. Several processing steps are required to form biologically active, mature miRNA. The initial transcript, called primary miRNA (pri-mRNA), base-pairs with itself forming a stem-loop structure. Within the nucleus, an endonuclease enzyme, called Drosha, shortens the stem-loop structure into hairpin-shaped pre-miRNA. After...
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Role Of Notch Signalling In Intestinal Stem Cell Renewal01:12

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Notch signaling was first discovered in Drosophila melanogaster, where it is involved in cell lineage differentiation. Notch signaling regulates the maintenance and differentiation of intestinal stem cells or ISCs by controlling the expression of atonal homolog 1 or Atoh1. Atoh1 directs cells to differentiate into secretory cells.
Direct cell-to-cell contact is needed for the activation of Notch signaling. The signal is initiated when a notch ligand binds to a receptor on an adjacent cell, also...
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Adult Stem Cells01:33

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Stem cells are undifferentiated cells that divide and produce more stem cells or progenitor cells that differentiate into mature, specialized cell types. All the cells in the body are generated from stem cells in the early embryo, but small populations of stem cells are also present in many adult tissues including the bone marrow, brain, skin, and gut. These adult stem cells typically produce the various cell types found in that tissue—to replace cells that are damaged or to continuously...
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Induced Differentiation of M Cell-like Cells in Human Stem Cell-derived Ileal Enteroid Monolayers
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Functional Transcriptomics in Diverse Intestinal Epithelial Cell Types Reveals Robust MicroRNA Sensitivity in

Bailey C E Peck1,2, Amanda T Mah3, Wendy A Pitman2

  • 1From the Curriculum in Genetics and Molecular Biology, bpeck@email.unc.edu.

The Journal of Biological Chemistry
|January 6, 2017
PubMed
Summary
This summary is machine-generated.

Gut microbes influence intestinal epithelial stem cell (IESC) proliferation via microRNAs (miRNAs). Suppressing miR-375 in IESCs boosts their proliferation, revealing a key mechanism for gut homeostasis.

Keywords:
genomicsintestinal epitheliummicroRNA (miRNA)microbiomestem cells

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Area of Science:

  • Microbiology
  • Molecular Biology
  • Gastroenterology

Background:

  • Gut microbiota are crucial for host health, influencing immunity and metabolism.
  • Mechanisms linking microbiota and intestinal epithelial cells are not fully understood.
  • MicroRNAs (miRNAs) are key regulators of gene expression.

Purpose of the Study:

  • To investigate the role of miRNAs in mediating microbiota-host interactions in intestinal epithelial stem cells (IESCs).
  • To identify specific miRNAs regulated by microbiota in IESCs and their impact on proliferation.

Main Methods:

  • Analysis of miRNA expression profiles in distinct mouse jejunal epithelial cell types.
  • Cell type-specific assessment of miRNA responses to microbiota.
  • Ex vivo enteroid model for gene and miRNA knockdown in Lgr5+ IESCs.
  • Quantification of IESC proliferation following miR-375 knockdown.

Main Results:

  • Distinct miRNA profiles exist across intestinal epithelial cell types, with cell type-specific responses to microbiota.
  • IESCs show prominent microbiota-dependent miRNA regulation compared to other subtypes.
  • miR-375 is significantly suppressed by microbiota in IESCs.
  • Knockdown of miR-375 in IESCs leads to significantly increased proliferative capacity.

Conclusions:

  • Microbiota regulate IESC proliferation, in part, through cell type-specific modulation of miRNAs like miR-375.
  • This highlights a critical molecular network controlling intestinal homeostasis.
  • Findings suggest potential miRNA-based therapeutic strategies for gastrointestinal diseases linked to IESC dysfunction.