intestinal epithelial cell migration

Definition

Target type: biologicalprocess

The orderly movement of an intestinal epithelial cell from one site to another, often during the development of a multicellular organism. [GOC:dph]

Intestinal epithelial cell migration is a complex and highly regulated process essential for maintaining the integrity of the intestinal lining. It plays a crucial role in wound healing, tissue repair, and normal epithelial turnover. Here's a detailed breakdown of the process:

1. **Initiation:** Migration is triggered by various stimuli, including:
* **Growth factors:** Epidermal growth factor (EGF), transforming growth factor-α (TGF-α), hepatocyte growth factor (HGF), and fibroblast growth factor (FGF) stimulate cell proliferation and migration.
* **Cytokines:** Interleukin-1 (IL-1), IL-6, and tumor necrosis factor-α (TNF-α) can trigger migration in response to injury or inflammation.
* **Extracellular matrix (ECM) components:** Integrins, cell surface receptors, bind to ECM proteins like fibronectin and laminin, initiating intracellular signaling cascades that regulate migration.

2. **Cell Polarization:** The migrating cell undergoes a dramatic change in its morphology, becoming polarized with distinct front and rear regions:
* **Leading edge:** The front of the cell extends protrusions called lamellipodia and filopodia. Lamellipodia are sheet-like extensions rich in actin filaments, providing the driving force for movement. Filopodia are thin, finger-like projections that explore the environment and sense chemoattractant signals.
* **Trailing edge:** The rear of the cell forms a stable structure called the uropod, anchoring the cell and facilitating detachment from the substrate.

3. **Motility:** The cell moves forward by a coordinated process of:
* **Protrusion:** Actin polymerization at the leading edge drives lamellipodia extension, pushing the cell membrane forward.
* **Adhesion:** Integrins at the leading edge bind to ECM proteins, forming temporary attachments that anchor the cell.
* **Contraction:** Myosin motor proteins interact with actin filaments, generating contractile forces that pull the cell body forward.
* **Detachment:** At the trailing edge, integrin-ECM interactions are broken, allowing the cell to detach and move forward.

4. **Regulation:** Intestinal epithelial cell migration is tightly controlled by intracellular signaling pathways:
* **Rho GTPases:** These small GTP-binding proteins play crucial roles in regulating actin polymerization, cell adhesion, and migration direction.
* **PI3K/Akt pathway:** This pathway promotes cell survival, proliferation, and migration by activating downstream targets.
* **MAPK signaling:** Mitogen-activated protein kinases (MAPKs) are involved in regulating cell proliferation, differentiation, and migration.
* **Calcium signaling:** Calcium ions act as second messengers, modulating cytoskeletal dynamics and cell motility.

5. **Consequences of Impaired Migration:** Defects in intestinal epithelial cell migration can lead to:
* **Delayed wound healing:** Impaired migration slows down the repair of intestinal lesions, increasing the risk of infections and complications.
* **Inflammatory bowel disease:** Dysregulated migration contributes to chronic inflammation and tissue damage in diseases like Crohn's disease and ulcerative colitis.
* **Cancer metastasis:** Cancer cells exploit migration pathways to spread to distant sites, leading to secondary tumors.

6. **Future Directions:** Further research is ongoing to understand the intricate molecular mechanisms underlying intestinal epithelial cell migration. This knowledge could lead to novel therapeutic strategies for treating intestinal diseases and preventing cancer metastasis.'
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Compounds (24)