Related Experiment Videos
Ultrastructural study of liver sinusoids of mice during invasion by leukemic myelocytes
Abstract:
Results of an ultrastructural study of liver of RF mice during invasion by leukemic myelocytes were reported. In early stages of infiltration, leukemia cells adhered to the endothelial cells of the sinusoidal wall; gaps 1-4 mu in diameter then developed in the endothelium, and leukemia cells passed through the gaps to enter the extravascular space. Other sinusoids became occluded by leukemic myelocytes, the endotheilium disintegrated, and the occluding cells thus became extravascular. In late stages of infiltration, when leukemia cells migrated back into the sinusoids, the endothelium was continuous and leukemia cells passed through temporary pores located within endothelial cells.
Insights
Leukemic myelocytes invade the liver by adhering to and passing through the sinusoidal endothelium. In later stages, cells re-enter circulation via temporary pores within intact endothelial cells.
Area of Science:
- Hepatology
- Hematology
- Cell Biology
Background:
- Leukemic myelocytes can infiltrate various organs, including the liver.
- Understanding the mechanism of leukemic cell invasion is crucial for disease progression studies.
Purpose of the Study:
- To investigate the ultrastructural changes in the liver during leukemic myelocyte invasion.
- To elucidate the pathways of leukemic cell transmigration across the liver sinusoidal endothelium.
Main Methods:
- Ultrastructural analysis of liver tissue from RF mice with experimentally induced leukemia.
- High-resolution microscopy to observe cellular interactions and structural modifications.
Main Results:
- Early invasion: Leukemic myelocytes adhere to sinusoidal endothelial cells, forming gaps for extravasation.
- Occlusion: Disintegration of endothelium allows leukemic cells to become extravascular.
- Late stage: Leukemic cells re-enter sinusoids through transient pores in continuous endothelium.
Conclusions:
- Leukemic myelocyte liver invasion involves distinct ultrastructural mechanisms for extravasation and re-entry.
- Endothelial cell integrity and transient pore formation are key in late-stage leukemic cell migration.