title: Enhanced protein expressions of sortilin and p75NTR in retina of rat following elevated intraocular pressure-induced retinal ischemia.
abstract: Elevated introcular pressure (IOP)-induced retinal neuron ischemic death includes an early phase of necrosis and prolonged phase of apoptosis. We used this ischemic model to observe the changes of sortilin and p75(NTR) protein expressions in rat retina. The results of Western blot analysis showed the expression of p75(NTR) at the band of 75 (mature form), 60 (non-glycosylated pieces) and 50 kDa (ectodomain shedding pieces), and the expression of sortilin at the 95 and 90 kDa (the mature form). The protein expressions of p75(NTR) (60 and 50 kDa pieces) and sortilin (90 kDa) increased significantly (p < 0.05) at days 3, 5 and 7 after retinal ischemia. This effect was also confirmed by immunofluorescence staining. Sortilin was primarily present in cell membrane of the ganglion cells layer (GCL) and large ganglion cell bodies by immunofluorescence labeling. There was little expression of p75(NTR) in the normal retina, while expression increased extensively in GCL, inner plexiform layer (IPL) and inner nuclear layer (INL) after retinal ischemia. p75(NTR) was shown to co-localize with neurofilament in the axons of neuronal cells by double-labeling. These results suggested that the protein expressions of 60 and 50 kDa forms of p75(NTR), and the 90 kDa mature form of sortilin increased in ischemia-induced retinal neuron of rats.
authors.affiliation: Beijing TongRen Eye Center, Beijing Tongren Hospital; Vision Science Laboratory, School of Ophthalmology, Capital Medical University, Beijing 100730, China.
authors.forename: Yong
authors.initials: Y
authors.lastname: Wei
authors.forename: Ningli
authors.initials: N
authors.lastname: Wang
authors.forename: Qingjun
authors.initials: Q
authors.lastname: Lu
authors.forename: Nan
authors.initials: N
authors.lastname: Zhang
authors.forename: Deyu
authors.initials: D
authors.lastname: Zheng
authors.forename: Junfa
authors.initials: J
authors.lastname: Li
mesh_terms: D008841:Actin Cytoskeleton / Q000378:metabolism / Q000473:pathology; D033942:Adaptor Proteins, Vesicular Transport; D000818:Animals; D001369:Axons / Q000378:metabolism / Q000473:pathology; D004195:Disease Models, Animal; D018450:Disease Progression; D005455:Fluorescent Antibody Technique; D007429:Intraocular Pressure; D007511:Ischemia / Q000209:etiology / Q000503:physiopathology*; D008297:Male; D008562:Membrane Glycoproteins / Q000737:chemistry / Q000378:metabolism*; D008970:Molecular Weight; D009410:Nerve Degeneration / Q000209:etiology / Q000378:metabolism / Q000473:pathology; D009419:Nerve Tissue Proteins / Q000737:chemistry / Q000378:metabolism*; D009798:Ocular Hypertension / Q000150:complications / Q000473:pathology / Q000503:physiopathology*; D020033:Protein Isoforms / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D020800:Receptor, Nerve Growth Factor / Q000737:chemistry / Q000378:metabolism*; D012160:Retina / Q000378:metabolism* / Q000473:pathology; D012162:Retinal Degeneration / Q000209:etiology / Q000378:metabolism* / Q000473:pathology; D012165:Retinal Ganglion Cells / Q000378:metabolism / Q000473:pathology; D015854:Up-Regulation; D000099183:Sortilin
chemical_list: D033942:Adaptor Proteins, Vesicular Transport; D008562:Membrane Glycoproteins; D009419:Nerve Tissue Proteins; D020033:Protein Isoforms; D020800:Receptor, Nerve Growth Factor; D000099183:Sortilin