Serum deprivation induced apoptosis in macrophage is mediated by autocrine secretion of type I IFNs.
Apoptosis can be triggered by different forms of cellular stress. We here show that serum deprivation induces the expression and secretion of type I interferons and results in apoptosis in RAW 264.7 cell in a caspase dependent manner. Administration of either IFN-alpha or IFN-beta antibody partially inhibits apoptosis while the two antibodies used together totally prevents RAW264.7 cell from apoptosis. GM-CSF, but not M-CSF and IL-3, protects serum deprivation induced apoptosis. Inhibition of JAKs also prevents macrophages from apoptosis. Activation of MAPKs is not required for serum deprivation induced apoptosis. Our results are the first to demonstrate that serum deprivation-induced apoptosis acts through autocrine secretion of type I interferons.
National Key Laboratory of Protein Engineering and Plant Genetic Engineering, College of Life Science, Peking University, Beijing, 100871, China.
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J
Wei
Z
Z
Sun
Q
Q
Chen
J
J
Gu
D000818:Animals; D017209:Apoptosis; D019898:Autocrine Communication; D020169:Caspases / Q000378:metabolism; D002460:Cell Line; D016895:Culture Media, Serum-Free; D007370:Interferon Type I / Q000037:antagonists & inhibitors / Q000378:metabolism*; D008264:Macrophages / Q000166:cytology / Q000201:enzymology / Q000276:immunology*; D051379:Mice; D011505:Protein-Tyrosine Kinases / Q000037:antagonists & inhibitors
D016895:Culture Media, Serum-Free; D007370:Interferon Type I; D011505:Protein-Tyrosine Kinases; D020169:Caspases