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Role Of Notch Signalling In Intestinal Stem Cell Renewal01:12

Role Of Notch Signalling In Intestinal Stem Cell Renewal

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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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Inflammatory Bowel Disease I: Ulcerative Colitis01:27

Inflammatory Bowel Disease I: Ulcerative Colitis

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Introduction
Inflammatory bowel disease, or IBD, encompasses a group of disorders characterized by chronic inflammation or ulceration of the gastrointestinal tract.
Risk Factors
The exact cause of IBD remains unclear, although it is believed to be due to a mix of genetic, environmental, microbial, and immune factors. Genetic factors are significant in determining susceptibility to IBD, with family history being a critical risk factor. Individuals with a first-degree relative who has IBD are at...
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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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Drugs for Treatment of Ulcerative Colitis in IBD01:29

Drugs for Treatment of Ulcerative Colitis in IBD

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Ulcerative colitis is a chronic inflammatory condition primarily affecting the colon and rectum. The primary drugs used in the treatment of ulcerative colitis are aminosalicylates. They exhibit anti-inflammatory and immunosuppressive properties. They modulate inflammatory mediators and inhibit the activity of nuclear factor κB (NF-κB). Aminosalicylates also reduce inflammation by inhibiting prostaglandin and leukotriene production and decreasing neutrophil chemotaxis and superoxide...
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Mucosal Barrier of the Stomach01:25

Mucosal Barrier of the Stomach

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The gastric glands contain parietal cells that secrete hydrochloric acid (HCl) for digestion. The cells secrete HCl because it is highly corrosive and essential for breaking down food. To achieve this, they secrete hydrogen and chloride ions into the lumen of the gastric glands, which combine to form HCl.
Within parietal cells, carbonic acid is first formed through the reaction of water and carbon dioxide. The dissociation of carbonic acid releases bicarbonate and hydrogen ions. The bicarbonate...
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Updated: Jan 7, 2026

An Intravital Microscopy-Based Approach to Assess Intestinal Permeability and Epithelial Cell Shedding Performance
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ST3Gal1は腸管バリア機能の調節に関与し、ヒト潰瘍性大腸炎に影響を与える

Yin Tian1, Yun Liu2, Yangyang Shang2

  • 1Department of Gastroenterology, The People's Hospital of Yubei District of Chongqing City, Chongqing 401120, P.R. China.

Molecular medicine reports
|December 19, 2025
PubMed
まとめ

ST3Gal1タンパク質は腸管バリア機能を調節する。ST3Gal1の発現抑制はバリア機能を強化し、過剰発現はそれを悪化させ、炎症性腸疾患の病原性に影響を与える。

キーワード:
ST3Gal1バリア炎症シアリル化トリプルカルチャーモデル

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Analyzing Beneficial Effects of Nutritional Supplements on Intestinal Epithelial Barrier Functions During Experimental Colitis
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科学分野:

  • 消化器病学
  • 細胞生物学
  • 生化学

背景:

  • 炎症性腸疾患（IBD）の病原性には、腸粘膜バリア機能不全が関与している。
  • タンパク質のシアリル化は、腸管バリア機能の維持に不可欠である。
  • IBDにおけるST3Gal1媒介α2,3-シアリル化の役割は、まだ十分に解明されていない。

研究 の 目的:

  • ST3Gal1触媒α2,3-シアリル化が腸管バリア機能に与える影響を調査すること。
  • 潰瘍性大腸炎（UC）の病原性におけるST3Gal1の役割を探求すること。

主な方法:

  • 健康および炎症性ヒト腸の状態をシミュレートしたinvitroトリプルカルチャーモデルを確立した。
  • 腸管上皮細胞（IEC）におけるST3Gal1のノックダウンおよび過剰発現のために、アデノウイルスおよびレンチウイルスベクターを利用した。
  • 経上皮電気抵抗およびFITCデキストラン透過性アッセイを用いて腸管バリア機能を評価した。

主要な成果:

  • UC患者および大腸炎マウスモデルにおいて、ST3Gal1の発現は大腸の炎症と相関していた。
  • ST3Gal1の発現抑制により腸管バリア機能は強化されたが、過剰発現はそれを悪化させた。
  • ST3Gal1はMUC2、TFF3、CDX2、p-STAT3、IL-1β、IL-6、IL-8の発現を調節し、バリア機能の完全性と炎症に影響を与えた。

結論:

  • ST3Gal1は腸管バリア機能の調節において重要な役割を果たしている。
  • ST3Gal1触媒α2,3-シアリル化は、バリア関連タンパク質および炎症性メディエーターに影響を与えることにより、UCの病原性に影響を与える。
  • ST3Gal1を標的とすることは、炎症性腸疾患の治療の可能性を提供するかもしれない。