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Injured hepatocyte-released microvesicles induce bone marrow-derived mononuclear cells differentiation
Laura Simon1, Mónica López1, Carolina Uribe-Cruz2
1Gene Therapy Center, Hospital de Clínicas de Porto Alegre, Porto Alegre, Brazil; Post-Graduation Program on Genetics and Molecular Biology, Universidade Federal do Rio Grande do Sul, Porto Alegre, Brazil.
Differentiation; Research in Biological Diversity
|September 29, 2015
Summary
Injured hepatocytes promote bone marrow-derived mononuclear cell (BMMC) differentiation into hepatocyte-like cells. Microvesicles from injured hepatocytes carry specific mRNAs and are absorbed by BMMCs, suggesting a role in cell plasticity.
Area of Science:
- Cell Biology
- Hepatology
- Stem Cell Research
Background:
- Bone marrow-derived mononuclear cells (BMMCs) can differentiate into hepatocyte-like cells.
- The specific conditions and mechanisms driving this differentiation require further investigation.
Purpose of the Study:
- To investigate the effect of carbon tetrachloride (CCl4)-injured hepatocytes on the differentiation of the non-adherent (NAD) fraction of BMMCs.
- To analyze the role of microvesicles (MVs) in this differentiation process.
Main Methods:
- Co-culture of NAD cells with CCl4-injured or healthy hepatocytes.
- Analysis of cell differentiation via gene/protein expression and urea production at 2, 6, and 24 hours.
- Characterization of microvesicles in cell supernatants and their uptake by NAD cells.
Main Results:
- NAD cells exhibited hepatocyte-like characteristics after 24h co-culture with injured hepatocytes, but not with healthy hepatocytes.
- Microvesicles containing hepatocyte-specific mRNAs (Albumin, Coagulation factor V, Alpha-fetoprotein, Cytokeratin 18) were found in the supernatant of differentiated cells.
- NAD cells incorporated MVs derived from injured hepatocytes, indicating a potential role in inducing cell plasticity.
Conclusions:
- CCl4-injured hepatocytes induce differentiation of BMMC-derived NAD cells into hepatocyte-like cells.
- Microvesicles released by injured hepatocytes play a significant role in mediating this cell plasticity and differentiation.
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