UVB-Induced Murine Bone Marrow Derived Macrophages and Apoptosis

Abstract

A major part of the mutagenic and carcinogenic properties of sunlight has been attributed to UV rays. UV radiation in the middle-wavelength range between 290 and 320 nm (UVB) represents one of the most relevant environmental dangers because of its hazardous effects. Like other adverse agents (alkylating chemicals, oxidants), UVB induces apoptosis in mammalian cells. Elucidation of the underlying molecular mechanisms is of primary importance for the understanding of how UVB can damage cells. To exert its biological effects, UVB must be first absorbed by a cellular chromophore, which transfers the energy into a biochemical signal. DNA damage is regarded as an important reservoir for transferring the biochemical signals of UVB. We have examined the signal mechanism of UVB induced apoptosis in bone marrow derived macrophages. Macrophages exposed to 50 mJ/cm² doses and above of UVB irradiation showed the morphological characteristics of apoptotic cells, and electrophoresis of DNA isolated from these cells showed characteristic fragmentation. The DNA fragmentation induced in macrophages with 50 mJ/cm² UVB exposure appeared to be sufficient for activating p53, Bax, Caspase-3 and PARP cleavage. This study provides evidence that UVB can cause the apoptosis in bone marrow derived macrophages induced by DNA damage providing an useful experimental model for research and investigational purposes.

Keywords:

• UVB
• Bone marrow derived macrophages
• Apoptosis
• Bax
• Caspase-3

Notes

Kerr, J. F. R., Harmon, B. V. (1991). Definition and incidence of apoptosis: an historical perspective. In: Tomei, L. D., Cope, F. O., eds. Curr. Commun. Cell Mol. Biology Apoptosis: The molecular basis of cell death. Cold Spring Harbor Laboratory Press, Cold Spring Harbor, New York, 3:5–29.