An association between polymorphism of the heme oxygenase-1 and -2 genes and age-related macular degeneration

Iron may be implicated in the generation of oxidative stress by the catalyzing the Haber–Weiss or Fenton reaction. On the other hand, oxidative stress has been implicated in the pathogenesis of age-related macular degeneration (AMD) and heme oxygenase-1 (HO-1), encoded by the HMOX1 gene and heme oxygenase-2 (HO-2), encoded by the HMOX2 gene are important markers of iron-related oxidative stress and its consequences. Therefore, variability of the HMOX1 and HMOX2 genes might be implicated in the pathogenesis of AMD through the modulation of the cellular reaction to oxidative stress. In the present work, we investigated the association between AMD and a G → C transversion at the 19 position in the HMOX1 gene (the 19G>C-HMOX1 polymorphism, rs2071747) and a A → G transition at the −42 + 1444 position in the HMOX2 gene (the −42 + 1444A>G-HMOX2 polymorphism, rs2270363) and its modulation by some environmental factors. 279 patients with AMD and 105 controls were recruited in this study and the polymorphisms were typed by restriction fragment length polymorphism and allele-specific polymerase chain reaction (PCR). We observed an association between the occurrence of dry AMD and the G/A genotype of the −42 + 1444A>G-HMOX2 polymorphism (odds ratio (OR) 2.72), whereas the G/G genotype reduced the risk of dry AMD (OR 0.41). The G/C genotype and the C allele of the 19 G>C-HMOX1 polymorphism and the G/G genotype and the G allele of the −42 + 1444A>G-HMOX2 polymorphism were associated with progression of AMD from dry to wet form (OR 4.83, 5.20, 2.55, 1.69, respectively). On the other hand, the G/G genotype and the G allele of the 19 G>C-HMOX1 polymorphism and the A/G genotype and the A allele of the −42 + 1444A>G-HMOX2 polymorphism protected against AMD progression (OR 0.19, 0.19, 0.34, 0.59, respectively). Therefore, the 19G>C-HMOX1 and the −42 + 1444A>G-HMOX2 polymorphisms may be associated with the occurrence and progression of AMD

670-nm light treatment reduces complement propagation following retinal degeneration

AIM: Complement activation is associated with the pathogenesis of age-related macular degeneration (AMD). We aimed to investigate whether 670-nm light treatment reduces the propagation of complement in a light-induced model of atrophic AMD. METHODS: Sprague–Dawley (SD) rats were pretreated with 9 J/cm(2) 670-nm light for 3 minutes daily over 5 days; other animals were sham treated. Animals were exposed to white light (1,000 lux) for 24 h, after which animals were kept in dim light (5 lux) for 7 days. Expression of complement genes was assessed by quantitative polymerase chain reaction (qPCR), and immunohistochemistry. Counts were made of C3-expressing monocytes/microglia using in situ hybridization. Photoreceptor death was also assessed using outer nuclear layer (ONL) thickness measurements, and oxidative stress using immunohistochemistry for 4-hydroxynonenal (4-HNE). RESULTS: Following light damage, retinas pretreated with 670-nm light had reduced immunoreactivity for the oxidative damage maker 4-HNE in the ONL and outer segments, compared to controls. In conjunction, there was significant reduction in retinal expression of complement genes C1s, C2, C3, C4b, C3aR1, and C5r1 following 670 nm treatment. In situ hybridization, coupled with immunoreactivity for the marker ionized calcium binding adaptor molecule 1 (IBA1), revealed that C3 is expressed by infiltrating microglia/monocytes in subretinal space following light damage, which were significantly reduced in number after 670 nm treatment. Additionally, immunohistochemistry for C3 revealed a decrease in C3 deposition in the ONL following 670 nm treatment. CONCLUSIONS: Our data indicate that 670-nm light pretreatment reduces lipid peroxidation and complement propagation in the degenerating retina. These findings have relevance to the cellular events of complement activation underling the pathogenesis of AMD, and highlight the potential of 670-nm light as a non-invasive anti-inflammatory therapy

Pseudoexfoliation Syndrome

Purpose: The purpose of the present study was to evaluate the aqueous humor endocan and endostatin levels in patients with pseudoexfoliation (PEX) syndrome and to compare the results with healthy individuals. Materials and Methods: Twenty nine cataract patients with PEX syndrome (PEX group) and 32 cataract patients without PEX syndrome (control group) were enrolled in the study. Endocan and endostatin were measured in the aqueous humor of the PEX and control groups by enzyme-linked immunosorbent assay. Results: There was no difference between the PEX and control groups in terms of age (P=0.721) and sex (P=0.902). The aqueous levels of endocan in patients with PEX (26.39 +/- 5.80 pg/mL) was significantly higher than in the control group (11.42 +/- 2.44 pg/mL) (P=0.039). The aqueous levels of endostatin was 12.00 +/- 1.35 ng/mL in the PEX group and 14.22 +/- 3.31 ng/mL in the control group, however, the difference was not statistically significant (P=0.41). Conclusions: The findings of the present study could suggest that the increased levels of aqueous endocan may be related to pathogenesis of PEX. However, levels of aqueous endostatin did not show any significant difference in PEX.C1 [Yagci, Ramazan] Pamukkale Univ, Sch Med, Dept Ophthalmol, Denizli, Turkey.[Dervisogullari, Serdar] Baskent Univ, Adana Dr Turgut Noyan Clin & Res Ctr, Ankara, Turkey.[Guler, Emre] Ercis State Hosp, Eye Clin, Van, Turkey.[Totan, Yueksel] Turgut Ozal Univ, Dept Ophthalmol, Sch Med, Ankara, Turkey.[Hepsen, Ibrahim F.] Gazi Univ, Sch Med, Dept Ophthalmol, Ankara, Turkey

Evaluation of Aqueous Endocan and Endostatin Levels in Patients With Pseudoexfoliation Syndrome.

PURPOSE: The purpose of the present study was to evaluate the aqueous humor endocan and endostatin levels in patients with pseudoexfoliation (PEX) syndrome and to compare the results with healthy individuals. MATERIALS AND METHODS: Twenty nine cataract patients with PEX syndrome (PEX group) and 32 cataract patients without PEX syndrome (control group) were enrolled in the study. Endocan and endostatin were measured in the aqueous humor of the PEX and control groups by enzyme-linked immunosorbent assay. RESULTS: There was no difference between the PEX and control groups in terms of age (P=0.721) and sex (P=0.902). The aqueous levels of endocan in patients with PEX (26.39±5.80 pg/mL) was significantly higher than in the control group (11.42±2.44 pg/mL) (P=0.039). The aqueous levels of endostatin was 12.00±1.35 ng/mL in the PEX group and 14.22±3.31 ng/mL in the control group, however, the difference was not statistically significant (P=0.41). CONCLUSIONS: The findings of the present study could suggest that the increased levels of aqueous endocan may be related to pathogenesis of PEX. However, levels of aqueous endostatin did not show any significant difference in PEX

McCune-Albright syndrome progressing with severe fibrous dysplasia

WOS: 000071544100017PubMed ID: 9558573We present the case of an 11-year-old girl with McCune-Albright syndrome associated with severe fibrous dysplasia. In addition to bone lesions, she has apparent manifestations of precocious puberty. In examination, a mass at the mentum spreading to mandibular corpus bilaterally was seen. This mass has affected the mandibular teeth. It was nearly 20 x 20 x 15 cm in size and had local necrotic regions on it. The lower lip was expanded too much by the mass. Another mass filled the left maxillary sinus, expanding the left zygomatic region outwardly and closing the left nasal fossa completely. A rectangular skull shape was related to the involvement of cranial bones. After stainless steel, custom-made mandibular prosthesis was prepared, the patient underwent surgery. A partial mandibulectomy was performed, and resulting mandibular bone defect was reconstructed by steel prosthesis. Craniofacial involvement occurs in 100% of disseminated cases. In the dental literature, mandibular involvement was found in 20% of cases. However, in studied literature, we did not find a dramatic mandibular lesion as severe as that presented here