title: Up-regulation of integrin-linked kinase in the streptozotocin-induced diabetic rat retina.
abstract: OBJECTIVE
  This study investigated whether integrin-linked kinase (ILK) is involved in the pathogenesis of diabetic retinopathy, by analyzing the expression and activity of ILK in the retina from a streptozotocin (STZ)-induced rat model of diabetes.
  
  
  METHODS
  ILK expression in the retina from both control and STZ-induced diabetic rats was measured by reverse transcription polymerase chain reaction, immunohistochemistry and Western blot analysis. The expressions of Akt and FOXO1A, the downstream molecules of ILK, were also examined.
  
  
  RESULTS
  The present study showed that the STZ-induced diabetes was associated with the increase in the vascular permeability in the retina. This elevated vascular permeability increased with the progression of diabetic retinopathy. Meanwhile, the results also showed that the expression of ILK increased in protein and mRNA levels in the retina of STZ-induced diabetic rats. Immunohistochemistry showed that immunostaining of ILK was localized in the outer plexiform layer (OPL), the inner nuclear layer (INL), the inner plexiform layer (IPL), the ganglion cell layer (GCL) and the retinal microvasculature of rats. However, the expression of Akt was reduced in the retinas at 8 and 12 weeks and increased in the retinas at 4 weeks after induction of diabetes. Meanwhile, the expression of the FOXO1A protein increased in the retinas at 8 and 12 weeks and decreased in the retinas at 4 weeks after induction of diabetes. The FOXO1A immunostaining was also observed in the retinal microvasculature and in the OPL, INL, IPL and GCL of rat retinas.
  
  
  CONCLUSIONS
  These results indicate that diabetes affects the expression of ILK in the retina. ILK may be involved in the diabetes-induced damage and/or alterations of neural and microvascular structures.
authors.affiliation: Department of Ophthalmology, Xijing Hospital, The Fourth Military Medical University and Eye Institute of PLA, Xian 710032, People's Republic of China. liyjun@fmmu.edu.cn
authors.forename: Yang-Jun
authors.initials: YJ
authors.lastname: Li
authors.forename: Yan-Nian
authors.initials: YN
authors.lastname: Hui
authors.forename: Feng
authors.initials: F
authors.lastname: Yan
authors.forename: Zhao-Jiang
authors.initials: ZJ
authors.lastname: Du
mesh_terms: D000818:Animals; D015153:Blotting, Western; D002199:Capillary Permeability; D003921:Diabetes Mellitus, Experimental / Q000201:enzymology*; D003930:Diabetic Retinopathy / Q000201:enzymology*; D051858:Forkhead Transcription Factors; D007150:Immunohistochemistry; D008297:Male; D009419:Nerve Tissue Proteins; D017346:Protein Serine-Threonine Kinases / Q000235:genetics / Q000378:metabolism*; D051057:Proto-Oncogene Proteins c-akt; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D020133:Reverse Transcriptase Polymerase Chain Reaction; D015854:Up-Regulation / Q000502:physiology*; D000099200:Scaffold Protein ILK; D000071161:Forkhead Box Protein O1
chemical_list: D051858:Forkhead Transcription Factors; D009419:Nerve Tissue Proteins; D017346:Protein Serine-Threonine Kinases; D051057:Proto-Oncogene Proteins c-akt; D012333:RNA, Messenger; D000099200:Scaffold Protein ILK; C074639:Foxo1 protein, rat; D000071161:Forkhead Box Protein O1