Blocking PTEN may reactivate the PI3K/Akt pathway and attenuate photoreceptor apoptosis by suppressing the mitochondrial pathway. Phosphatase and tensin homology deleted on chromosome 10 ( PTEN) participates in the apoptosis of photoreceptors after RD. In addition, bpV treatment increased the levels of p-BAD and Bcl-2, and decreased the expression levels of cytosolic Cyt c and cleaved caspase-3 after RD. Compared to vehicle-treated RD groups, levels of p-Akt and p-PDK1 were significantly upregulated in bpV-treated RD groups. Subretinal injection of bpV(pic) effectively reduced the apoptosis of photoreceptors and preserved the retinal thickness of the ONL after RD. The expression of PTEN gradually increased after RD, peaking at 3 days and then decreasing to normal by 7 days after RD. The thickness of the outer nuclear layer (ONL) also was recorded. Apoptosis of photoreceptors was detected using the TUNEL assay. We measured phosphatidylinositol 3,4,5-triphosphate (PIP3) by ELISA. Levels of phosph-phosphoinositide–dependent kinase 1 (p-PDK1), phospho–Bcl-2 death promotor (p-BAD), cytosolic cytochrome c (Cyt c), and cleaved Caspase-3 were detected by Western blotting. We documented the expression and distribution of phospho-Akt (p-Akt) and B-cell lymphoma 2 (Bcl-2) in the retina by Western blot analysis and immunofluorescence. Some of the rats were given subretinal injections of bisperoxovanadium compound (bpV) after RD. This study evaluated the role of PTEN in photoreceptor cell apoptosis caused by retinal detachment (RD).Ī rat model of RD was established, and PTEN expression changes were detected at different time points by Western blotting and immunofluorescence. Phosphatase and tensin homology deleted on chromosome 10 ( PTEN) is crucial in neuronal apoptosis.
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