Understanding what role, if any, the N-ras gene plays in this metaplasia may lead to a better understanding of proliferative disorders such as proliferative vitreoretinopathy.
The presence of IL-1 beta, IL-6 and TNF alpha mRNA-positive cells within retinal membranes provides further evidence of a pathogenic role of these cytokines in proliferative vitreoretinopathy.
The presence of mRNA coding for the cytokines interleukin 1 beta (IL-1 beta), interleukin 6 (IL-6) and tumour necrosis factor alpha (TNF alpha) was investigated in 19 epiretinal membranes obtained from eyes undergoing vitrectomy for the treatment of retinal detachment complicated by proliferative vitreoretinopathy.
The presence of IL-1 beta, IL-6 and TNF alpha mRNA-positive cells within retinal membranes provides further evidence of a pathogenic role of these cytokines in proliferative vitreoretinopathy.
Interleukin-6 and genes that were related to melanogenesis were expressed in the proliferative membranes and may play an important role in the generation of proliferative vitreoretinopathy.
Local production of bFGF in epiretinal membranes was confirmed by nonisotopic in situ hybridisation for bFGF mRNA in some (4/7) examined PDR membranes and some (3/4) examined PVR membranes.
We examined 20 epiretinal membranes from patients with proliferative diabetic retinopathy (PDR) (n = 12) and proliferative vitreoretinopathy (PVR) (n = 8) for the presence of bFGF peptide, fibroblast growth factor receptor-1 (FGFR-1) and bFGF messenger ribonucleic acid (mRNA).
Confirmation of induced expression of MAP1B mRNA was obtained by PCR with specific primers and by immunocytochemical analysis in cultured RPE cells and in surgically removed epiretinal membranes from patients with proliferative vitreoretinopathy.
Gene expression for melanogenesis was determined by reverse transcriptase-polymerase chain reaction of tyrosinase and tyrosinase-related protein-1 genes in normal and cultured retinal pigment epithelial cells and in proliferative membranes in patients with proliferative vitreoretinopathy.
Gene expression for melanogenesis was determined by reverse transcriptase-polymerase chain reaction of tyrosinase and tyrosinase-related protein-1 genes in normal and cultured retinal pigment epithelial cells and in proliferative membranes in patients with proliferative vitreoretinopathy.
The presence of mRNA coding for HPRT, IL-6, IL-1beta, IL-8, and TNFalpha was investigated in 20 vitreous and subretinal fluid (SRF) samples from patients with PVR by reverse transcriptase polymerase chain reaction (RT-PCR).
Adrenomedullin mRNA levels in the tissues obtained from patients with intraocular or orbital tumors were significantly higher than those of patients with proliferative vitreoretinopathy (P <.05), proliferative diabetic retinopathy (P <.05), preretinal macular fibrosis (P <.005), and acute retinal necrosis (P <.01).
To detect the expression of mRNA of protooncogenes ets-1, c-jun, c-fos, and platelet-derived growth factor (PDGF) in proliferative membranes of patients with proliferative diabetic retinopathy (PDR) and proliferative vitreoretinopathy (PVR).
These results suggest that IL-8 may be involved in retinal inflammatory responses to injury and that DEX and/or CSA treatment may help control the inflammatory components of retinal diseases such as proliferative vitreoretinopathy.
To establish new strategies for the treatment of proliferative vitreoretinopathy (PVR), we investigated new members of a recently discovered apoptosis-inducing receptor-ligand system in human retinal pigment epithelial (RPE) cells.
The amount and activity of this enzyme appears to be related to the differentiation state of the RPE cells and their stimulation by TGF-beta2, a growth factor known to be increased in the vitreous of PVR.
Semiquantitative analysis in in situ hybridization and immunohistochemistry results demonstrated no notable differences in uPA, tPA or PAI-1 expression between PDR and PVR membranes.
Twenty PVR, PDR or pucker membranes were examined to identify the cells with cell specific markers and to detect the expression of urokinase (uPA), tissue-type plasminogen activator (tPA) or plasminogen activator inhibitor-1 (PAI-1) by in situ hybridization and by immunohistochemistry.