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Pradimicin, a mannose-binding antibiotic, induced carbohydrate-mediated apoptosis in U937 cells
1Toyama Prefectural University, Biotechnology Research Center, Japan. oki@pu-toyama.ac.jp
Abstract:
Pradimicin (PRM), a mannose-binding antifungal antibiotic, recognizes a D-mannoside in the presence of calcium. We demonstrated that BMY-28864, a semi-synthetic analog of PRM, induced apoptosis in U937 cells which had been incubated with 1-deoxymannojirimycin (DMJ). Characteristic morphological changes such as formation of apoptotic bodies and DNA fragmentation were observed in apoptotic cells.
Insights
The antifungal pradimicin analog BMY-28864 triggers apoptosis in U937 cells. This cell death, induced by 1-deoxymannojirimycin, involves DNA fragmentation and apoptotic bodies.
Area of Science:
- Pharmacology
- Cell Biology
- Mycology
Background:
- Pradimicin (PRM) is a mannose-binding antifungal antibiotic.
- PRM requires calcium to recognize D-mannoside structures.
Purpose of the Study:
- To investigate the effect of BMY-28864, a semi-synthetic PRM analog, on U937 cells.
- To determine if BMY-28864 induces apoptosis in U937 cells, particularly after incubation with 1-deoxymannojirimycin (DMJ).
Main Methods:
- U937 cells were incubated with 1-deoxymannojirimycin (DMJ).
- BMY-28864 was administered to DMJ-treated U937 cells.
- Apoptosis was assessed by observing morphological changes and DNA fragmentation.
Main Results:
- BMY-28864 induced apoptosis in U937 cells pre-incubated with DMJ.
- Key apoptotic features, including the formation of apoptotic bodies, were observed.
- DNA fragmentation was a characteristic finding in the apoptotic cells.
Conclusions:
- BMY-28864, a pradimicin analog, effectively induces apoptosis in U937 cells.
- The induction of apoptosis is potentiated by prior incubation with 1-deoxymannojirimycin.
- Morphological and molecular evidence confirms apoptosis, highlighting BMY-28864's potential cytotoxic effects.