Research Highlights | Published:

Cell biology

p53 triggers cell death in stroke

Nature volume 486, pages 442443 (28 June 2012) | Download Citation


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.

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