14 May 2009

Level of cellular stress determines longevity of retinal cells


Studies by scientists at Rockefeller University revealed how the process of cell apoptosis in fruit fly retinal cell could be halted with the use of gene knockout technique. Cell apoptosis is a programmed cell death which can occur in response to a stress as a way of removing the damaged cell. It was shown that knocking out a gene called NinaA in retinal neurons switched off the intracellular apoptotic signals which induce the cell suicide and consequently stopped their descent toward death.

NinaA encodes for a protein which makes up rhodopsin, photosensitive pigment in rod cells, responsible for the vision in low light intensity. With the absence of NinaA in the cells, rhodopsin cannot be formed properly and accumulation of the protein in the endoplasmic reticulum called ER stress occurs. As a result repair pathway is activated and thus halting the cell’s self-destruction. It is also thought that cellular exposure to mild ER stress may cause upregulation of antioxidant genes which result in the protection of the cells from exogenous stress especially UV radiations from the sun.   

As it is now unveiled that
the absence of NinaA and non-lethal level of ER stress determines the cellular decision of its termination and its longevity in retinal neurons, the further study in this field could bring a cure for diseases like Alzheimer’s, diabetes and cancer.

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