{"title":"Treating Acquired Optic Disc Pit Maculopathy with an Ocular Hypotensive Agent","authors":"Eric Shrier DO","doi":"10.13188/2334-2838.1000031","DOIUrl":"https://doi.org/10.13188/2334-2838.1000031","url":null,"abstract":"Purpose: To describe a case of glaucomatous optic disc pit maculopathy that resolved after bimatoprost treatment. Observations: A 63-year-old African American female with a history of type 2 diabetes mellitus presented to the clinic after 3 months of blurry vision in the right eye and was found to have an asymmetric cup-to-disc ratio, and right intraretinal and subretinal fluid without leakage on fluorescein angiography concerning for optic disc pit maculopathy. A trial of intravitreal anti-vascular endothelial growth factor (VEGF) injection failed to resolve the fluid. Optical coherence tomography of the ganglion cell complex showed thinning of the ganglion cell complex concerning for previously undiagnosed glaucoma, and the patient was started on bimatoprost. The previously noted fluid resolved, and the patient has been quiescent for 4 years on ocular hypotensive medication. Conclusion: In untreated or poorly controlled glaucoma, progressive cupping of the optic nerve head may lead to the development of an acquired optic disc pit, which can produce maculopathy. This maculopathy can improve under ocular hypotensive treatment.","PeriodicalId":89987,"journal":{"name":"Journal of ocular biology","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"66210042","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Multifocal Polypoidal Choroidal Vasculopathy in Caribbean and African- Americans","authors":"","doi":"10.13188/2334-2838.1000030","DOIUrl":"https://doi.org/10.13188/2334-2838.1000030","url":null,"abstract":"Polypoidal Choroidal Vasculopathy (PCV) is a relatively uncommon form of exudative Age-Related Macular Degeneration (ARMD) first described in 1990 by Yannuzzi et al. [1]. It presents as multiple, branching networks of small, polyp-like clusters, or larger identifiable characteristic polyp-like out-pouchings. Manifestations include lipid exudation, serosanguinous pigment epithelial detachments and sub-retinal hemorrhage. Indocyanine-Green (ICG) angiography has been said to be the necessary for delineating the polypoidal vascular abnormalities, but recently hi-resolution spectral domain Ocular Coherence Tomography (OCT) has been demonstrated to perhaps be diagnostic as well [2]. Recently it has been associated with a pachychoroid [3].","PeriodicalId":89987,"journal":{"name":"Journal of ocular biology","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-12-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43228574","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
N. Broekema, I. Larsen, E. S. Naruzawa, M. Filutowicz, A. Kolb, L. Teixeira, C. Brandt
{"title":"A Mouse Model of Multi-Drug Resistant Staphylococcus aureus-induced Ocular Disease","authors":"N. Broekema, I. Larsen, E. S. Naruzawa, M. Filutowicz, A. Kolb, L. Teixeira, C. Brandt","doi":"10.13188/2334-2838.1000026","DOIUrl":"https://doi.org/10.13188/2334-2838.1000026","url":null,"abstract":"Staphylococcus aureus infection of the cornea is a significant threat to vision. The percentage of bacterial isolates resistant to antibiotics is increasing as is the percentage of infections caused by methicillin resistant isolates. There is a critical need for additional therapeutic approaches and their development will require the use of animal models to test efficacy. Two mouse models of S. aureus keratitis have been described but only quantified stromal keratitis (corneal clouding and perforation). We have extended these models using the methicillin resistant S. aureus USA300 LAC strain and show that eyelid inflammation and swelling (blepharitis) and corneal neovascularization can be quantified. This expanded model should prove useful in assessing additional effects of antibacterial therapies and additional pathological mechanisms involved in bacterial ocular infection.","PeriodicalId":89987,"journal":{"name":"Journal of ocular biology","volume":"4 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2016-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"66210020","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
G. McLellan, Z. Aktaş, Elizabeth A. Hennes-Beean, A. Kolb, I. Larsen, E. J. Schmitz, H. Clausius, Jun Yang, S. Hwang, C. Morisseau, B. Inceoğlu, B. Hammock, C. Brandt
{"title":"Effect of a Soluble Epoxide Hydrolase Inhibitor, UC1728, on LPS-Induced Uveitis in the Rabbit","authors":"G. McLellan, Z. Aktaş, Elizabeth A. Hennes-Beean, A. Kolb, I. Larsen, E. J. Schmitz, H. Clausius, Jun Yang, S. Hwang, C. Morisseau, B. Inceoğlu, B. Hammock, C. Brandt","doi":"10.13188/2334-2838.1000024","DOIUrl":"https://doi.org/10.13188/2334-2838.1000024","url":null,"abstract":"Cytochrome P450 epoxygenase isozymes convert free arachidonic acid into eicosanoids named epoxyeicosatrienoic acids (EETs) that have roles in regulating inflammation. EETs are rapidly converted to dihydroxyeicosatrienoic acids (DiHETs) by soluble epoxide hydrolase (sEH). Little is known about the potential role of these metabolites in uveitis, but conversion of EETs to DiHETs could contribute to the inflammation. We tested a potent and orally available inhibitor of sEH for its ability to reduce ocular inflammation in a rabbit LPS-induced model of uveitis. Rabbits were treated by subcutaneous injection with the sEH inhibitor (UC1728, 3 mg/kg), or the vehicle control (PEG400) and uveitis was assessed at 6, 24 and 48 h post-intracameral LPS injection using a modified Hackett-McDonald scoring system. Eyes treated by intra-cameral injection of PBS, or by aseptic preparation served as further controls. Signs of inflammation in this model were mild and transient. Treatment with UC1728 did not significantly reduce inflammation compared to animals treated with the PEG400 vehicle. Blood levels of UC1728 were a thousand fold higher than the in vitro determined inhibitory potency (IC50) of the compound suggesting a significant degree of inhibition of sEH in the rabbit. The lack of efficacy suggests that sEH or its substrates the EETs may not be involved in mediating inflammation in this model of uveitis.","PeriodicalId":89987,"journal":{"name":"Journal of ocular biology","volume":"4 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2016-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"66209919","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"The Trabecular Meshwork: A Basic Review of Form and Function.","authors":"Diala W Abu-Hassan, Ted S Acott, Mary J Kelley","doi":"10.13188/2334-2838.1000017","DOIUrl":"https://doi.org/10.13188/2334-2838.1000017","url":null,"abstract":"","PeriodicalId":89987,"journal":{"name":"Journal of ocular biology","volume":"2 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2014-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4209746/pdf/nihms-625016.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"32781412","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Mitochondrial Dynamics in Retinal Ganglion Cell Axon Regeneration and Growth Cone Guidance.","authors":"Kira L Lathrop, Michael B Steketee","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Failed axon regeneration and retinal ganglion cell (RGC) death after trauma or disease, including glaucomatous and mitochondrial optic neuropathies, are increasingly linked to mitochondrial dysfunction. Mitochondria are highly dynamic organelles whose size, organization, and function are regulated by a balance between mitochondrial fission and fusion. Mitochondria are ubiquitous in axonal growth cones both in vitro and in vivo and during development and regeneration. However, the roles that mitochondrial fission and fusion dynamics play in the growth cone during axon regeneration are largely unstudied. Here we discuss recent data suggesting mitochondria in the distal axon and growth cone play a central role in axon growth by integrating intrinsic axon growth states with signaling from extrinsic cues. Mitochondrial fission and fusion are intrinsically regulated in the distal axon in the growth cones of acutely purified embryonic and postnatal RGCs with differing intrinsic axon growth potentials. These differences in fission and fusion correlate with differences in mitochondrial bioenergetics; embryonic RGCs with high intrinsic axon growth potential rely more on glycolysis whereas RGCs with low intrinsic axon growth potential rely more on oxidative phosphorylation. Mitochondrial fission and fusion are also differentially modulated by KLFs that either promote or suppress intrinsic axon growth, and altering the balance between mitochondrial fission and fusion can differentially regulate axon growth rate and growth cone guidance responses to both inhibitory and permissive guidance cues.</p>","PeriodicalId":89987,"journal":{"name":"Journal of ocular biology","volume":"1 2","pages":"9"},"PeriodicalIF":0.0,"publicationDate":"2013-09-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3946936/pdf/nihms530918.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40300059","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Mitochondrial Dynamics in Retinal Ganglion Cell Axon Regeneration and Growth Cone Guidance.","authors":"K. Lathrop, M. Steketee","doi":"10.13188/2334-2838.1000010","DOIUrl":"https://doi.org/10.13188/2334-2838.1000010","url":null,"abstract":"Failed axon regeneration and retinal ganglion cell (RGC) death after trauma or disease, including glaucomatous and mitochondrial optic neuropathies, are increasingly linked to mitochondrial dysfunction. Mitochondria are highly dynamic organelles whose size, organization, and function are regulated by a balance between mitochondrial fission and fusion. Mitochondria are ubiquitous in axonal growth cones both in vitro and in vivo and during development and regeneration. However, the roles that mitochondrial fission and fusion dynamics play in the growth cone during axon regeneration are largely unstudied. Here we discuss recent data suggesting mitochondria in the distal axon and growth cone play a central role in axon growth by integrating intrinsic axon growth states with signaling from extrinsic cues. Mitochondrial fission and fusion are intrinsically regulated in the distal axon in the growth cones of acutely purified embryonic and postnatal RGCs with differing intrinsic axon growth potentials. These differences in fission and fusion correlate with differences in mitochondrial bioenergetics; embryonic RGCs with high intrinsic axon growth potential rely more on glycolysis whereas RGCs with low intrinsic axon growth potential rely more on oxidative phosphorylation. Mitochondrial fission and fusion are also differentially modulated by KLFs that either promote or suppress intrinsic axon growth, and altering the balance between mitochondrial fission and fusion can differentially regulate axon growth rate and growth cone guidance responses to both inhibitory and permissive guidance cues.","PeriodicalId":89987,"journal":{"name":"Journal of ocular biology","volume":"1 2 1","pages":"9"},"PeriodicalIF":0.0,"publicationDate":"2013-09-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"66209896","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Padmanabhan P Pattabiraman, David L Epstein, Ponugoti Vasantha Rao
{"title":"Regulation of Adherens Junctions in Trabecular Meshwork Cells by Rac GTPase and their influence on Intraocular Pressure.","authors":"Padmanabhan P Pattabiraman, David L Epstein, Ponugoti Vasantha Rao","doi":"10.13188/2334-2838.1000002","DOIUrl":"https://doi.org/10.13188/2334-2838.1000002","url":null,"abstract":"<p><p>Intercellular adherens junctions and cell-extracellular matrix interactions are presumed to influence aqueous humor (AH) drainage via the conventional route, however, their direct role in modulation of intraocular pressure (IOP) is not well understood. Here, we investigated the role of Rac GTPase signaling in basal and growth factor-induced formation of adherens junctions in human trabecular meshwork (HTM) cells as compared to human umbilical vascular endothelial cells, and evaluated the effects of inhibition of Rac GTPase activity on IOP in rabbits. Expression of a constitutively active Rac1 GTPase or treatment with platelet derived growth factor (PDGF), a known activator of Rac GTPase, induced formation of β-catenin-based adherens junctions, actin cytoskeletal reorganization and membrane ruffle in HTM cells. In contrast, treatment of HTM cells with inhibitors of Rac GTPase caused cell-cell separation, a decrease in adherens junctions, and reorganization of actin stress fibers to the cell cortical regions and focal adhesion to the cell leading edges. Both, constitutively active Rac1 and PDGF stimulated generation of Reactive Oxygen Species (ROS) in HTM cells, and ROS were found to increase adherens junction formation and transendothelial electrical resistance (TEER) in HTM cells. Topical application of Rac GTPase inhibitors (EHT1864 and NSC23766), however, only marginally influenced IOP in rabbit eyes. Taken together, these data reveal that while Rac GTPase signaling plays a significant role in regulation of adherens junctions, ROS production and TEER in cells of the AH outflow pathway, Rac inhibitors showed only a marginal influence on IOP in live rabbits.</p>","PeriodicalId":89987,"journal":{"name":"Journal of ocular biology","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2013-06-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4057051/pdf/nihms518410.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"32427968","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"The Juxtacanalicular Region of Ocular Trabecular Meshwork: A Tissue with a Unique Extracellular Matrix and Specialized Function.","authors":"Kate E. Keller, T. Acott","doi":"10.13188/2334-2838.1000003","DOIUrl":"https://doi.org/10.13188/2334-2838.1000003","url":null,"abstract":"The trabecular meshwork (TM) is a filter-like tissue located in the anterior segment of the eye. It is composed of a series of fenestrated beams through which aqueous humor flows to exit the anterior chamber via Schlemm's canal. The primary function of the TM is to regulate the flow of aqueous humor in order to establish intraocular pressure (IOP). Dysregulated aqueous humor outflow causes elevated IOP, which is a primary risk factor for glaucoma. The region of the TM implicated in establishing IOP lies adjacent to Schlemm's canal and is called the juxtacanalicular tissue (JCT) or cribriform region. Recent advanced light microscopy studies suggest that the JCT can be subdivided into inner and outer zones based on the localization of certain extracellular matrix (ECM) molecules. By comparing the ECM of the JCT to other connectives tissues and disease processes, this review outlines the evidence for two new concepts in TM biology: (1) continuous maintenance ECM remodeling, which may be critical in order to preserve open aqueous humor flow channels by releasing trapped debris and associated ECM fragments from the outflow pathways; (2) the JCT ECM as a barrier to functionally isolate the aqueous outflow channels. The ECM surrounding the outflow channels in the JCT may function to sequester small active regulatory molecules and prevent them from aberrantly modulating outflow resistance. These adaptations point to a distinctive tissue that has evolved transient ECM remodeling processes in order to regulate aqueous humor outflow and maintain rigorous control of IOP.","PeriodicalId":89987,"journal":{"name":"Journal of ocular biology","volume":"1 1 1","pages":"3"},"PeriodicalIF":0.0,"publicationDate":"2013-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"66210161","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"The Juxtacanalicular Region of Ocular Trabecular Meshwork: A Tissue with a Unique Extracellular Matrix and Specialized Function.","authors":"Kate E Keller, Ted S Acott","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The trabecular meshwork (TM) is a filter-like tissue located in the anterior segment of the eye. It is composed of a series of fenestrated beams through which aqueous humor flows to exit the anterior chamber via Schlemm's canal. The primary function of the TM is to regulate the flow of aqueous humor in order to establish intraocular pressure (IOP). Dysregulated aqueous humor outflow causes elevated IOP, which is a primary risk factor for glaucoma. The region of the TM implicated in establishing IOP lies adjacent to Schlemm's canal and is called the juxtacanalicular tissue (JCT) or cribriform region. Recent advanced light microscopy studies suggest that the JCT can be subdivided into inner and outer zones based on the localization of certain extracellular matrix (ECM) molecules. By comparing the ECM of the JCT to other connectives tissues and disease processes, this review outlines the evidence for two new concepts in TM biology: (1) continuous maintenance ECM remodeling, which may be critical in order to preserve open aqueous humor flow channels by releasing trapped debris and associated ECM fragments from the outflow pathways; (2) the JCT ECM as a barrier to functionally isolate the aqueous outflow channels. The ECM surrounding the outflow channels in the JCT may function to sequester small active regulatory molecules and prevent them from aberrantly modulating outflow resistance. These adaptations point to a distinctive tissue that has evolved transient ECM remodeling processes in order to regulate aqueous humor outflow and maintain rigorous control of IOP.</p>","PeriodicalId":89987,"journal":{"name":"Journal of ocular biology","volume":"1 1","pages":"3"},"PeriodicalIF":0.0,"publicationDate":"2013-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3867143/pdf/nihms-520258.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31978043","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}