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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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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.
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Erythropoietin-producing hepatocellular carcinoma receptor (Eph) and its ligand, Eph receptor-interacting protein (Ephrin) were first discovered in the human carcinoma cell line, hence the name. Ephrin-Eph interaction guides cells to reach their appropriate location in adult tissues. They also play an essential role in the immune system by helping in immune cell migration, adhesion, and activation. Based on their structure and function, Eph is divided into two classes — EphA and EphB.
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All blood and immune cells are produced from the multipotent hematopoietic stem cells (HSCs) by the process of hematopoiesis. However, they all have a limited life span. In addition, many are depleted in immune surveillance or combatting an injury or infection. This makes blood one of the most regenerative tissues. Hematopoiesis helps replenish these blood and immune cells, restoring the body's normal functioning. However, overproduction of blood and immune cells can make them cancerous or...
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Peptic ulcer disease, commonly called PUD, represents a multifaceted condition characterized by disruptions in the lining of the gastrointestinal (GI)  tract. Central to the protection of the gastrointestinal lining is the mucosal-bicarbonate barrier. This physiological defense mechanism is a formidable shield against the corrosive effects of gastric acid and pepsin secretion in the stomach. Its role is pivotal in maintaining the structural integrity of the stomach's inner lining.
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Epidermal stem cells (EpiSCs) are mainly located at the basal layer of the epidermis. These cells repair minor injuries of the skin and replace dead skin cells. However, EpiSCs’ cannot heal severe wounds such as major burns or those from diabetes or hereditary disorders. In such cases, culturing the epidermal stem cells from the patient is possible and has yielded successful treatment options, such as laboratory-grown skin grafts. These grafts are synthesized using a patient’s own...
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Related Experiment Video

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Inhibition of Soluble Stem Cell Factor Promotes Intestinal Mucosal Repair.

Vicky Garcia-Hernandez1, Arturo Raya-Sandino1, Veronica Azcutia1

  • 1Department of Pathology, University of Michigan Medical School, Ann Arbor, MI, USA.

Inflammatory Bowel Diseases
|January 23, 2023
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Summary

Stem cell factor (SCF) drives inflammatory bowel disease (IBD) and hinders gut healing. Neutralizing SCF, particularly the SCF248 isoform, reduces inflammation and promotes mucosal repair, offering a potential new therapy for IBD patients.

Keywords:
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Area of Science:

  • Gastroenterology
  • Immunology
  • Cell Biology

Background:

  • Inflammatory bowel disease (IBD) is a growing global health concern.
  • Current IBD treatments primarily manage symptoms, highlighting the need for therapies that also promote mucosal healing.
  • Increased stem cell factor (SCF) expression in inflamed IBD tissues suggests a potential role in disease pathogenesis.

Purpose of the Study:

  • To investigate the role of stem cell factor (SCF) in mediating intestinal inflammation and mucosal repair in inflammatory bowel disease (IBD).
  • To evaluate SCF expression patterns in the colon during homeostasis and dextran sodium sulfate (DSS)-induced colitis.
  • To assess the therapeutic potential of SCF neutralization in preclinical models of IBD.

Main Methods:

  • Compared SCF expression in colonic tissues of healthy mice versus those with DSS-induced colitis.
  • Utilized genetic deletion of SCF in intestinal epithelial cells and anti-SCF antibody administration in mouse models.
  • Assessed mucosal wound healing after biopsy and colitis severity after DSS treatment.

Main Results:

  • SCF is robustly expressed by intestinal epithelial cells during homeostasis, shifting to immune cell production during colitis.
  • Immune cell-derived SCF significantly contributes to colitis pathogenesis.
  • Neutralizing SCF, especially the SCF248 isoform, reduced immune cell infiltration and improved mucosal repair in both biopsy and DSS-induced colitis models.

Conclusions:

  • Stem cell factor (SCF) acts as a pro-inflammatory mediator in the gut mucosa.
  • Targeting SCF, specifically the SCF248 isoform, presents a promising therapeutic strategy for reducing inflammation and enhancing mucosal repair in IBD.