- Laser Capture Microdissection of Highly Pure Trabecular Meshwork from Mouse Eyes for Gene Expression Analysis. [Journal Article]
- JVJ Vis Exp 2018 Jun 03; (136)
- Laser capture microdissection (LCM) has allowed gene expression analysis of single cells and enriched cell populations in tissue sections. LCM is a great tool for the study of the molecular mechanism...
Laser capture microdissection (LCM) has allowed gene expression analysis of single cells and enriched cell populations in tissue sections. LCM is a great tool for the study of the molecular mechanisms underlying cell differentiation and the development and progression of various diseases, including glaucoma. Glaucoma, which comprises a family of progressive optic neuropathies, is the most common cause of irreversible blindness worldwide. Structural changes and damage within the trabecular meshwork (TM) can result in increased intraocular pressure (IOP), which is a major risk factor for developing glaucoma. However, the precise molecular mechanisms involved are still poorly understood. The ability to perform gene expression analysis will be crucial in obtaining further insights into the function of these cells and its role in the regulation of IOP and glaucoma development. To achieve this, a reproducible method for isolating highly enriched TM from frozen sections of mouse eyes and a method for downstream gene expression analysis, such as RT-qPCR and RNA-Seq is needed. The method described herein is developed to isolate highly pure TM from mouse eyes for downstream digital PCR and microarray analysis. In addition, this technique can be easily adapted for the isolation of other highly enriched ocular cells and cell compartments that have been difficult to isolate from mouse eyes. The combination of LCM and RNA analysis can contribute to a more comprehensive understanding of the cellular events underlying glaucoma.
- Unique percutaneous direct puncture technique for occlusion of a hypoglossal canal dural arteriovenous fistula. [Journal Article]
- JNJ Neurointerv Surg 2018 Jun 16
- CONCLUSIONS: With guidance and imaging provided by CBCT and syngo iGuide navigational software, an otherwise untreatable DAVF was successfully embolised and obliterated by an aggressive unique percutaneous trans-cranial needle puncture of the dominant outflow vein in the hypoglossal canal.
- 22q11.2 microduplication syndrome and juvenile glaucoma. [Journal Article]
- OGOphthalmic Genet 2018 Jun 14; :1-7
- CONCLUSIONS: 22q11.2 microduplication syndrome can be associated with juvenile glaucoma. Trabeculectomy may be complicated by persistent hypotony. Deep sclerectomy appears to be a better surgical option, although the presence of a thin sclera may result in conversion to trabeculectomy.
- Jnk2 deficiency increases the rate of glaucomatous neurodegeneration in ocular hypertensive DBA/2J mice. [Journal Article]
- CDCell Death Dis 2018 Jun 13; 9(6):705
- The cJun N-terminal kinases (JNKs; JNK1, JNK2, and JNK3) promote degenerative processes after neuronal injury and in disease. JNK2 and JNK3 have been shown to promote retinal ganglion cell (RGC) deat...
The cJun N-terminal kinases (JNKs; JNK1, JNK2, and JNK3) promote degenerative processes after neuronal injury and in disease. JNK2 and JNK3 have been shown to promote retinal ganglion cell (RGC) death after optic nerve injury. In their absence, long-term survival of RGC somas is significantly increased after mechanical optic nerve injury. In glaucoma, because optic nerve damage is thought to be a major cause of RGC death, JNKs are an important potential target for therapeutic intervention. To assess the role of JNK2 and JNK3 in an ocular hypertensive model of glaucoma, null alleles of Jnk2 and Jnk3 were backcrossed into the DBA/2J (D2) mouse. JNK activation occurred in RGCs following increased intraocular pressure in D2 mice. However, deficiency of both Jnk2 and Jnk3 together did not lessen optic nerve damage or RGC death. These results differentiate the molecular pathways controlling cell death in ocular hypertensive glaucoma compared with mechanical optic nerve injury. It is further shown that JUN, a pro-death component of the JNK pathway in RGCs, can be activated in glaucoma in the absence of JNK2 and JNK3. This implicates JNK1 in glaucomatous RGC death. Unexpectedly, at younger ages, Jnk2-deficient mice were more likely to develop features of glaucomatous neurodegeneration than D2 mice expressing Jnk2. This appears to be due to a neuroprotective effect of JNK2 and not due to a change in intraocular pressure. The Jnk2-deficient context also unmasked a lesser role for Jnk3 in glaucoma. Jnk2 and Jnk3 double knockout mice had a modestly increased risk of neurodegeneration compared with mice only deficient in Jnk2. Overall, these findings are consistent with pleiotropic effects of JNK isoforms in glaucoma and suggest caution is warranted when using JNK inhibitors to treat chronic neurodegenerative conditions.
- Macular choroidal thickness in highly myopic women during pregnancy and postpartum: a longitudinal study. [Journal Article]
- BPBMC Pregnancy Childbirth 2018 Jun 08; 18(1):220
- CONCLUSIONS: Our study revealed the presence of a significantly thicker choroid during the third trimester of pregnancy compared with 6-mo postpartum in HM women. Macular CT positively correlated with refractive error and negatively correlated with AL during pregnancy, but did not correlate with gestational age, MOPP, IOP, MAP, or BMI.
- Trabecular meshwork ECM remodeling in glaucoma: could RAS be a target? [Journal Article]
- EOExpert Opin Ther Targets 2018 Jun 14; :1-10
- Disturbances of extracellular matrix (ECM) homeostasis in trabecular meshwork (TM) cause increased aqueous outflow resistance leading to elevated intraocular pressure (IOP) in glaucomatous eyes. Ther...
Disturbances of extracellular matrix (ECM) homeostasis in trabecular meshwork (TM) cause increased aqueous outflow resistance leading to elevated intraocular pressure (IOP) in glaucomatous eyes. Therefore, restoration of ECM homeostasis is a rational approach to prevent disease progression. Since renin-angiotensin system (RAS) inhibition positively alters ECM homeostasis in cardiovascular pathologies involving pressure and volume overload, it is likely that RAS inhibitors reduce IOP primarily by restoring ECM homeostasis. Areas covered: Current evidence showing the presence of RAS components in ocular tissue and its role in regulating aqueous humor dynamics is briefly summarized. The role of RAS in ECM remodeling is discussed both in terms of its effects on ECM synthesis and its breakdown. The mechanisms of ECM remodeling involving interactions of RAS with transforming growth factor-β, Wnt/β-catenin signaling, bone morphogenic proteins, connective tissue growth factor, and matrix metalloproteinases in ocular tissue are discussed. Expert opinion: Current literature strongly indicates a significant role of RAS in ECM remodeling in TM of hypertensive eyes. Hence, IOP-lowering effect of RAS inhibitors may primarily be attributed to restoration of ECM homeostasis in aqueous outflow pathways rather than its vascular effects. However, the mechanistic targets for RAS inhibitors have much wider distribution and consequences, which remain relatively unexplored in TM.
- Carbohydrate ingestion induces differential autonomic dysregulation in normal-tension glaucoma and primary open angle glaucoma. [Journal Article]
- PlosPLoS One 2018; 13(6):e0198432
- CONCLUSIONS: NTG and POAG both manifest some systemic autonomic cardiovascular dysregulation. However, the two forms of glaucoma respond differentially to carbohydrate ingestion, irrespective of insulin resistance.
- Real-time intraocular pressure measurements in the vitreous chamber of rabbit eyes during small incision lenticule extraction (SMILE). [Journal Article]
- CECurr Eye Res 2018 Jun 06
- CONCLUSIONS: The IOP fluctuations in the vitreous cavity using an OFPS in a rabbit model during SMILE showed that real-time IOP significantly was increased during Pre-suction, Suction on, Cutting, Suction off and lenticule separation/extraction compared to baseline IOP, although, peaked at Suction on. Neither the degree of myopic correction nor central corneal thickness significantly affected these changes in IOP.
- Biomechanical assessment of healthy and keratoconic corneas (with/without crosslinking) using dynamic ultrahigh-speed Scheimpflug technology and the relevance of the parameter (A1L-A2L). [Journal Article]
- BJBr J Ophthalmol 2018 Jun 05
- CONCLUSIONS: Both A2V and A2L are viable parameters to discriminate healthy from keratoconic but also crosslinked from non-crosslinked keratoconic corneas. The difference of A1L-A2L could reliably discriminate crosslinked from non-crosslinked and healthy corneas. Follow-up examination in a small cohort allows distinction between crosslinked and untreated keratoconus in follow-up examinations. The difference of A1L-A2L could reliably discriminate crosslinked from non-crosslinked and healthy corneas. Measurements of corneal deformation using dynamic ultrahigh-speed Scheimpflug technology are reproducible and provide useful information about keratoconus assessment and biomechanics. Therefore, the Corvis ST seems to provide useful technology to monitor therapeutic success of crosslinking treatment.
New Search Next
- Accumulation of perfluorobutane sulfonate (PFBS) and impairment of visual function in the eyes of marine medaka after a life-cycle exposure. [Journal Article]
- ATAquat Toxicol 2018 May 25; 201:1-10
- As an alternative to perfluorooctane sulfonate (PFOS), increasing usage of perfluorobutane sulfonate (PFBS) has led to ubiquitous presence in the environment. PFBS is also shown to potently disrupt t...
As an alternative to perfluorooctane sulfonate (PFOS), increasing usage of perfluorobutane sulfonate (PFBS) has led to ubiquitous presence in the environment. PFBS is also shown to potently disrupt the thyroid endocrine system. Considering the regulation of thyroid hormones in visual development, PFBS is likely to adversely affect the development and function of visual systems, which is a sensitive target of environmental pollutants. Therefore, the present study exposed marine medaka embryos to environmentally realistic concentrations of PFBS (0, 1.0, 2.9 and 9.5 μg/L) for an entire life-cycle. After exposure until sexual maturity, eyes of adult medaka were dissected to directly investigate the ocular accumulation and toxicity of PFBS. For the first time, substantial accumulation of an environmental pollutant (i.e., PFBS) was observed in the eye tissue. PFBS exposure was also found to impair the visual development and function in a sex-dependent manner. In female medaka, weight of eyes was significantly decreased, while content of water was increased, probably resulting in higher intraocular pressure. Multiple neural signaling processes were also disturbed by PFBS life-cycle exposure, including cholinergic, glutamatergic, GABAergic and monoaminergic systems. Increased levels of norepinephrine and epinephrine neurotransmitters may adaptively decrease the intraocular hypertension in female eyes. In addition, proteomic profiling identified the visual proteins of differential expressions (e.g., beta and gamma crystallins, arrestin and lumican), which were significantly associated with visual perception and motor activity of eyes. Overall, this study found that PFBS was able to accumulate in the eyes and induce ocular toxicities. The susceptibility and sex-specific responses of visual systems to environmental pollutants warrants more works for a comprehensive risk assessment.