Thus, in contrast to CNTF upregulation, FGF2 appears to be regulated as a response to injury type of tissue reaction in the TGR rat. The Muiller cell and astrocyte, which interconnect vessels and neurons through their end-foot processes, participate in neuroprotection and neuronal repair after injury. Thus, increased GFAP expression as early as after 1 month suggests that glial activation occurs in response to neuronal degeneration in TGR rats. However, upregulation of GFAP is unspecific, as it occurs in various retinal injury models such as axotomy, retinal ischemia, retinal detachment and diabetic retinopathy. In contrast to the diabetic model, glial activation in the TGR model was not sufficient to induce VEGF, while bFGF upregulation is possibly the result of glial activation. Mutations in cilia genes or defective cilia genes are associated with renal abnormalities, retinal degeneration, liver and respiratory diseases in patients. In a previous study using the TGR rat, defective polycystin-2 gene was found in the region of connection cilia of outer and inner segments of rod and cone photoreceptors. However, electron microscopy studies did not reveal any morphological cilia defects except photoreceptor degeneration in the TGR. The Cardamonin precise function of polycystin-2 in the retinal cilia remains unclear. Changes of polycystin-2 gene expression in the retinal cilia may lead to defective transport of functional proteins through this apparatus, although no change in the morphology of cilia in the TGR retina has been detected so far. The link between the genetic defect of polycystin-2 and the apoptosis of photoreceptors requires Aceglutamide further investigations. Since the genetic makeup of the TGR rat has no human correlate, the model must not be considered as an animal model reflecting a specific human disease. In summary, this study provides insight into the relationship between neurodegeneration, glial activation and vessel regression. Further evaluation of the molecular mechanisms involved in vasoregression in the TGR rat and comparative studies with models of vasoregression of diabetic origin supposedly yield novel targets for intervention of retinal vasoregression.