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Background: Pilocarpine is commonly used after angle surgery for glaucoma despite a host of side effects and risks. We hypothesized that a pharmacological miosis during the first two months does not improve short- and long-term results of trabectome-mediated ab interno trabeculectomy. Methods: In this retrospective comparative 1-year case series, we compared 187 trabectome surgery eyes with (P+) or without (P-) 1% pilocarpine for two months. Primary outcome measures were the surgical success defined as intraocular pressure (IOP) ≤ 21 mmHg and decreased ≥ 20%, and no secondary glaucoma surgery. Secondary outcome measures were the number of glaucoma medications, complications, and IOP. Results: We categorized 86 (46%) eyes as P- and 101 (54%) eyes as P+. The mean age was 69.8±10.1 in P- and 70.5±9.4 in P+ (P=0.617) with equal gender distribution (P=0.38). The cumulative probability of qualified success at 12 months was 78.1% in the P- and 81% in the P+ (P=0.35). The IOP was decreased significantly from 20.2±6.8 mmHg at baseline to 15.0±4.8 mmHg at 12 months follow-up in P- (P=0.001) and 18.8±5.3 and 14.7±4.0, respectively (P=0.001). The medications decreased significantly from 1.4±1.2 in P- and 1.4±1.2 in P+ at baseline to 1.0±1.2 and 0.7±1.0, respectively (P=0.183). P- and P+ did not differ in IOP or medications (all P>0.05). In Multivariate Cox Regression models, the baseline IOP and central corneal thickness were associated with failure. Conclusions: Use of postoperative pilocarpine does not improve the efficacy of trabectome surgery.
We aimed to assess whether the transcription factor PAX6 affects transcription of FMNL2. PAX6 is a transcription factor with significant roles in development of the eye and eye-related functions. FMNL2 encodes a member of the formin family of proteins and has roles in polymerization of actin and features of the cytoskeleton. The state of the cytoskeleton affects the flow of aqueous humor, disruption of which is a cornerstone of glaucoma pathology.
Sturge-Weber syndrome (SWS) or encephalotrigeminal angiomatosis is a non-inherited congenital disorder characterized by neurologic, skin, and ocular abnormalities. A somatic activating mutation (R183Q) in the GNAQ gene during early embryogenesis has been recently recognized as the etiology of vascular abnormalities in SWS. Approximately, half of the patients with SWS manifest ocular involvement including glaucoma as the most common ocular abnormality followed by choroidal hemangioma (CH). The underlying pathophysiology of glaucoma in SWS has not been completely understood yet. Early onset glaucoma comprising 60% of SWS glaucoma have lower success rates after medical and surgical treatments compared with primary congenital glaucoma. Primary angle surgery is associated with modest success in the early onset SWS glaucoma while the success rate significantly decreases in late onset glaucoma. Filtration surgery is associated with a higher risk of intraoperative and postoperative choroidal effusion and suprachoroidal hemorrhage. CH is reported in 40-50% of SWS patients. The goal of treatment in patients with CH is to induce involution of the hemangioma, with reduction of subretinal and intraretinal fluid and minimal damage to the neurosensory retina. The decision for treating diffuse CHs highly depends on the patient's visual acuity, the need for glaucoma surgery, the presence of subretinal fluid (SRF), its chronicity, and the potential for visual recovery.
Brain-derived neurotrophic factor (BDNF) is a well-known neuroprotectant and a potent therapeutic candidate for neurodegenerative diseases. However, there are several clinical concerns about its therapeutic applications. In the current study, we designed and developed BDNF-mimicking small peptides as an alternative to circumvent these problems. A phage-displayed peptide library was screened using BDNF receptor (neurotrophic tyrosine kinase receptor type2 [NTRK2]) and evaluated by ELISA. The peptide sequences showed similarity to loop2 of BDNF, they were recognized as discontinuous epitopes though. Interestingly, in silico molecular docking showed strong interactions between the peptide three-dimensional models and the surface residues of the NTRK2 protein at the IgC2 domain. A consensus peptide sequence was then synthesized to generate a mimetic construct (named as RNYK). The affinity binding and function of this construct was confirmed by testing against the native structure of NTRK2 in SH-SY5Y cells in vitro using flow-cytometry and MTT assays, respectively. RNYK at 5 ng/mL prevented neuronal degeneration of all- trans-retinoic acid-treated SH-SY5Y with equal efficacy to or even better than BDNF at 50 ng/mL.
Background: To determine the predictive value of postoperative bleb morphological features and intraocular pressure (IOP) on the success rate of trabeculectomy. Methods: In this prospective interventional case series, we analyzed for one year 80 consecutive primary open angle glaucoma patients who underwent mitomycin-augmented trabeculectomy. Bleb morphology was scored using the Indiana bleb appearance grading scale (IBAGS). Success was defined as IOP ≤15 mmHg at 12 months. We applied a multivariable regression analysis and determined the area under the receiver operating characteristic curve (AUC). Results: The mean age of participants was 62±12.3 years in the success and 63.2±16.3 years in the failure group (P= 0.430) with equal gender distribution (P=0.911). IOPs on day 1, 7 and 30 were similar in both (P= 0.193, 0.639, and 0.238, respectively.) The AUC of IOP at day 1, day 7 and 30 for predicting a successful outcome was 0.355, 0.452, and 0.80, respectively. The AUC for bleb morphology parameters of bleb height, extension, and vascularization, on day 14 were 0.368, 0.408, and 0.549, respectively. Values for day 30 were 0.428, 0.563, and 0.654. IOP change from day 1 to day 30 was a good predictor of failure (AUC=0.838, 95% CI: 0.704 to 0.971) with a change of more than 3 mmHg predicting failure with a sensitivity of 82.5% (95% CI: 68 to 91%) and a specificity of 87.5% (95% CI: 53 to 98%). Conclusions: IOP on day 30 had a fair to good accuracy while bleb features failed to predict success except bleb vascularity that had a poor to fair accuracy. An IOP increase more than 3 mmHg during the first 30 days was a good predictor of failure.
To assess for the first time the possible contribution of latent transforming growth factor (TGF)-beta binding protein 2 (LTBP2), an extracellular matrix (ECM) protein that associates with fibrillin-1-containing microfibrils, to the etiology of primary open angle glaucoma (POAG) and pseudoexfoliation (PEX) syndrome. Mutations in LTBP2 have previously been shown to be the cause of primary congenital glaucoma (PCG) and other disorders that often manifest as secondary glaucoma.
This review article aimed to evaluate ocular biometric changes after trabeculectomy. The PubMed database was searched using the keywords "axial length" (AL), "anterior chamber depth" (ACD), "corneal astigmatism," "corneal topography" and "trabeculectomy." The extracted studies were categorized based on the evaluated parameters and the biometry method (contact and non-contact). Comparable studies with respect to their sample size were combined for statistical analysis. Twenty-five studies including 690 individuals which met the inclusion criteria were selected. After trabeculectomy, a significant and persistent AL reduction, with a range of 0.1-0.19 and 0.1-0.9 mm measured with contact and non-contact methods, respectively, was observed. With respect to topographic changes, 0.38-1.4 diopters (D) with-the-rule (WTR) astigmatism was induced postoperatively. All studies revealed ACD reduction immediately after surgery, which gradually deepened and approximated its preoperative levels on day 14. ACD reduction was not significant after that period in the majority of cases. In conclusion, changes in ACD is of small amount and of short period, thus it can be ignored; however, reported changes in AL and keratometry are of sufficient magnitude and can affect the refractive prediction of combined cataract surgery and trabeculectomy.
To identify genes whose expressions in primary human trabecular meshwork (TM) cell cultures are affected by the transcription factor pituitary homeobox 2 (PITX2) and to identify genes that may have roles in glaucoma. Known glaucoma causing genes account for disease in a small fraction of patients, and we aimed at identification of other genes that may have subtle and accumulative effects not easily identifiable by a genetic approach.
Forkhead box C1 (FOXC1) is a transcription factor that affects eye development. FOXC1 is implicated in the etiology of glaucoma because mutations in the gene are among the causes of Axenfeld-Rieger syndrome which is often accompanied by glaucoma. Glaucoma is the second leading cause of blindness. It is a complex disorder whose genetic basis in most patients remains unknown. Microarrays expression analysis was performed to identify genes in human trabecular meshwork (TM) primary cultures that are affected by FOXC1 and genes that may have roles in glaucoma. This represents the first genome wide analysis of FOXC1 target genes in any tissue. FOXC1 knock down by siRNAs affected the expression of 849 genes. Results on selected genes were confirmed by real time PCR, immunoblotting, and dual luciferase reporter assays. Observation of MEIS2 as a FOXC1 target and consideration of FOXC1 as a potential target of miR-204 prompted testing the effect of this micro RNA on expression of FOXC1 and several genes identified by array analysis as FOXC1 target genes. It was observed that miR-204 caused decreased expression of FOXC1 and the FOXC1 target genes CLOCK, PLEKHG5, ITGβ1, and MEIS2 in the TM cultures. Expression of CLOCK, PLEKHG5, ITGβ1 has not previously been reported to be affected by miR-204. The data suggest existence of a complex regulatory pathway in the TM part of which includes interactions between FOXC1, miR-204, MEIS2, and ITGβ1. All these molecules are known to have TM relevant functions, and the TM is strongly implicated in the etiology of glaucoma.
The transcription factor PITX2 is implicated in glaucoma pathology. In an earlier study we had used microarray analysis to identify genes in the trabecular meshwork (TM) that are affected by knock down of PITX2. Here, those studies were pursued to identify genes that are direct targets of PITX2 and that may be relevant to glaucoma. Initially, bioinformatics tools were used to select among the genes that had been affected by PITX2 knock down those that have PITX2 binding sites and that may be involved in glaucoma related functions. Subsequently, the effect of PITX2 was tested using the dual luciferase assay in four cell cultures including two primary TM cultures co-transfected with vectors containing promoter fragments of six candidate genes upstream of a luciferase gene and a vector that expressed PITX2. Finally, the effect of PITX2 on endogenous expression of two genes was assessed by over expression and knock down of PITX2 in TM cells. Thirty four genes were found to contain PITX2 binding sites in their putative promoter regions, and 16 were found to be associated with TM-specific and/or glaucoma associated functions. Results of dual luciferase assays confirmed that two of six genes tested were directly targeted by PITX2. The two genes were CXCL6 (chemokine (C-X-C motif) ligand 6) and BBS5 (Bardet-Biedl syndrome 5). Over expression and knock down of PITX2 showed that this transcription factor affects endogenous expression of these two genes in TM cells. CXCL6 encodes a pro-inflammatory cytokine, and many studies have suggested that cytokines and other immune system functions are involved in glaucoma pathogenesis. BBS5 is a member of the BBS family of genes that affect ciliary functions, and ciliary bodies in the anterior chamber of the eye produce the aqueous fluid that affects intraocular pressure. Immune related functions and intraocular pressure are both important components of glaucoma pathology. The role of PITX2 in glaucoma may be mediated partly by regulating the expression of CXCL6 and BBS5 and thus affecting immune functions and intraocular pressure.
An earlier meta-analysis on gene expression data derived from four microarray, two cDNA library, and one SAGE experiment had identified RGS5 as one of only ten non-housekeeping genes that were reported to be expressed in human trabecular meshwork (TM) cells by all studies. RGS5 encodes regulator of G-protein signaling-5. The TM tissue is the route of aqueous fluid outflow, and is relevant to the pathology of glaucoma. MicroRNAs constitute the most recently identified components of the cellular machinery for gene regulation in eukaryotic cells. Given our long standing interest in glaucoma, we aimed to identify miRNAs that may target RGS5.
To determine peripapillary retinal nerve fiber layer (RNFL) thickness values by three-dimensional optical coherence tomography (3D-OCT) in a normal Iranian population and to evaluate the concordance of these measurements with those obtained by the second generation of optical coherence tomography (OCT II).
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