The protein p53 is known to suppress tumour growth, which it does in part by initiating apoptosis, or programmed cell death. However, p53 also triggers another form of cell death — necrosis — that occurs in conditions such as stroke.
Ute Moll at Stony Brook University in New York and her team studied the effects of adding purified p53 to mitochondria — the cell's power-generating organelles — isolated from mouse cells. The authors found that p53 causes certain pores in the mitochondrial membrane to open up by interacting with a protein, cyclophilin D, that regulates the pore. Treating cells with an oxidizing chemical kicks off this process, which ultimately leads to necrosis.
The researchers detected the two-protein complex in injured brain tissue from mice in which a cerebral artery had been temporarily blocked as a model of stroke. Preventing complex formation protected against stroke-induced injury.