Fast Oscillation of the Corneoretinal Potential in Ischemic Retinopathy

1977 ◽  
Vol 9 (5) ◽  
pp. 324-328 ◽  
Author(s):  
A. Thaler ◽  
P. Heilig ◽  
V. Scheiber
Keyword(s):  
Fast Oscillation ◽  
Ischemic Retinopathy ◽  
Corneoretinal Potential

Retinal macroaneurysm after carotid endarterectomy in patient with chronic ischemic retinopathy associated with hemodynamically significant stenosis of the internal carotid artery (clinical case)

2021 ◽  
pp. 274-277
Author(s):  
V.V. Tuzlaev ◽  
◽  
O.V. Kolenko ◽  
V.V. Egorov ◽  
I.Z. Kravchenko ◽  
...  
Keyword(s):  
Blood Flow ◽  
Carotid Artery ◽  
Internal Carotid Artery ◽  
Carotid Endarterectomy ◽  
Clinical Case ◽  
Internal Carotid ◽  
Significant Stenosis ◽  
Ischemic Retinopathy ◽  
Retinal Macroaneurysm ◽  
Intraretinal Hemorrhages

Purpose. To present a clinical case of development of retinal macroaneurysm after carotid endarterectomy (CE) in patient with chronic ischemic retinopathy (CIR) associated with hemodynamically significant stenosis of the internal carotid artery (ICA). Material and methods. Patient R., 74 years old, diagnosed with CIR of the 1st degree of severity of the right eye. In addition to standard ophthalmic examination methods, Doppler ultrasound with registration of blood flow in the orbital artery and spiral computed tomography of the ICA were performed. Results. Panretinal photocoagulation (PRP) of the retina led to obliteration of the retinal macroaneurysm, resorption of intraretinal hemorrhages, and stabilization of the course of CIR after CE of the ICA. Conclusion. The appearance of retinal macroaneurysm and intraretinal hemorrhages after CE in patient with CIR associated with hemodynamically significant ICA stenosis can be regarded as reperfusion complications after restoration of blood flow in the orbital artery, which requires timely retinal PRP of the retina. Key words: chronic ischemic retinopathy, retinal macroaneurysm, internal carotid artery, carotid endarterectomy.

scholarly journals Voltage-Dependent Calcium Channel CaV1.3 Subunits Regulate the Light Peak of the Electroretinogram

2007 ◽  
Vol 97 (5) ◽  
pp. 3731-3735 ◽  
Author(s):  
Jiang Wu ◽  
Alan D. Marmorstein ◽  
Jörg Striessnig ◽  
Neal S. Peachey
Keyword(s):  
Calcium Channel ◽  
Pigment Epithelium ◽  
Retinal Pigment ◽  
Rod Photoreceptor ◽  
Wild Type ◽  
Fast Oscillation ◽  
Light Peak ◽  
Voltage Dependent Calcium Channel ◽  
Voltage Dependent ◽  
Voltage Dependent Calcium Channels

In response to light, the mouse retinal pigment epithelium (RPE) generates a series of slow changes in potential that are referred to as the c-wave, fast oscillation (FO), and light peak (LP) of the electroretinogram (ERG). The LP is generated by a depolarization of the basolateral RPE plasma membrane by the activation of a calcium-sensitive chloride conductance. We have previously shown that the LP is reduced in both mice and rats by nimodipine, which blocks voltage-dependent calcium channels (VDCCs) and is abnormal in lethargic mice, carrying a null mutation in the calcium channel β4 subunit. To define the α1 subunit involved in this process, we examined mice lacking CaV1.3. In comparison with wild-type (WT) control littermates, LPs were reduced in CaV1.3−/− mice. This pattern matched closely with that previously noted in lethargic mice, confirming a role for VDCCs in regulating the signaling pathway that culminates in LP generation. These abnormalities do not reflect a defect in rod photoreceptor activity, which provides the input to the RPE to generate the c-wave, FO, and LP, because ERG a-waves were comparable in WT and CaV1.3−/− littermates. Our results identify CaV1.3 as the principal pore-forming subunit of VDCCs involved in stimulating the ERG LP.

Attenuation of retinal endothelial cell migration and capillary morphogenesis in the absence of bcl-2

2008 ◽  
Vol 294 (6) ◽  
pp. C1521-C1530 ◽  
Author(s):  
Shuji Kondo ◽  
Yixin Tang ◽  
Elizabeth A. Scheef ◽  
Nader Sheibani ◽  
Christine M. Sorenson
Keyword(s):  
Cell Migration ◽  
Vascular System ◽  
Ex Vivo ◽  
Vascular Development ◽  
Critical Role ◽  
Endothelial Cell Migration ◽  
Cellular Functions ◽  
Capillary Morphogenesis ◽  
Angiogenesis Assay ◽  
Ischemic Retinopathy

Apoptosis plays a critical role during development and in the maintenance of the vascular system. B-cell leukemia lymphoma 2 (bcl-2) protects endothelial cells (EC) from apoptosis in response to a variety of stimuli. Previous work from this laboratory demonstrated attenuation of postnatal retinal vascular development and retinal neovascularization during oxygen-induced ischemic retinopathy in bcl-2-deficient (bcl-2−/−) mice. To gain further insight into the function of bcl-2 in the endothelium, we isolated retinal EC from bcl-2+/+ and bcl-2−/− mice. Retinal EC lacking bcl-2 demonstrated reduced cell migration, tenascin-C expression, and adhesion to vitronectin and fibronectin. The bcl-2−/− retinal EC also failed to undergo capillary morphogenesis in Matrigel. In addition, using an ex vivo angiogenesis assay, we observed reduced sprouting from aortic rings grown in culture from bcl-2−/− mice compared with bcl-2+/+ mice. Furthermore, reexpression of bcl-2 was sufficient to restore migration and capillary morphogenesis defects observed in bcl-2−/− retinal EC. Mechanistically, bcl-2−/− cells expressed significantly less endothelial nitric oxide synthase, an important downstream effecter of proangiogenic signaling. This may be attributed to increased oxidative stress in the absence of bcl-2. In fact, incubation of retinal EC or aortic rings from bcl-2−/− mice with the antioxidant N-acetylcysteine rescued their capillary morphogenesis and sprouting defects. Thus, bcl-2-mediated cellular functions play important roles not only in survival but also in proangiogenic phenotype of EC with a significant impact on vascular development and angiogenesis.

Therapies targeting Frizzled‐7/β‐catenin pathway prevent the development of pathological angiogenesis in an ischemic retinopathy model

2019 ◽  
Vol 34 (1) ◽  
pp. 1288-1303 ◽  
Author(s):  
Marie‐Lise Bats ◽  
Pauline Bougaran ◽  
Claire Peghaire ◽  
Florian Gueniot ◽  
Alice Abelanet ◽  
...  
Keyword(s):  
Pathological Angiogenesis ◽  
Ischemic Retinopathy

ISCHEMIC RETINOPATHY IN NEUROFIBROMATOSIS TYPE 1

2015 ◽  
Vol 9 (4) ◽  
pp. 290-294 ◽  
Author(s):  
Kunal K. Dansingani ◽  
Jesse J. Jung ◽  
Irina Belinsky ◽  
Brian P. Marr ◽  
K. Bailey Freund
Keyword(s):  
Neurofibromatosis Type 1 ◽  
Neurofibromatosis Type ◽  
Ischemic Retinopathy

scholarly journals CYP1B1 expression promotes the proangiogenic phenotype of endothelium through decreased intracellular oxidative stress and thrombospondin-2 expression

Blood ◽  
2009 ◽  
Vol 113 (3) ◽  
pp. 744-754 ◽  
Author(s):  
Yixin Tang ◽  
Elizabeth A. Scheef ◽  
Shoujian Wang ◽  
Christine M. Sorenson ◽  
Craig B. Marcus ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Endothelial Cells ◽  
Retinopathy Of Prematurity ◽  
Cellular Responses ◽  
Retinal Endothelial Cells ◽  
Capillary Morphogenesis ◽  
Ischemic Retinopathy ◽  
Intracellular Oxidative Stress

Abstract Reactive species derived from cell oxygenation processes play an important role in vascular homeostasis and the pathogenesis of many diseases including retinopathy of prematurity. We show that CYP1B1-deficient (CYP1B1−/−) mice fail to elicit a neovascular response during oxygen-induced ischemic retinopathy. In addition, the retinal endothelial cells (ECs) prepared from CYP1B1−/− mice are less adherent, less migratory, and fail to undergo capillary morphogenesis. These aberrant cellular responses were completely reversed when oxygen levels were lowered or an antioxidant added. CYP1B1−/− ECs exhibited increased oxidative stress and expressed increased amounts of the antiangiogenic factor thrombospondin-2 (TSP2). Increased lipid peroxidation and TSP2 were both observed in retinas from CYP1B1−/− mice and were reversed by administration of an antioxidant. Reexpression of CYP1B1 in CYP1B1−/− ECs resulted in down-regulation of TSP2 expression and restoration of capillary morphogenesis. A TSP2 knockdown in CYP1B1−/− ECs also restored capillary morphogenesis. Thus, CYP1B1 metabolizes cell products that modulate intracellular oxidative stress, which enhances production of TSP2, an inhibitor of EC migration and capillary morphogenesis. Evidence is presented that similar changes occur in retinal endothelium in vivo to limit neovascularization.

scholarly journals Retinal vascular repair and neovascularization are not dependent on CX3CR1 signaling in a model of ischemic retinopathy

2009 ◽  
Vol 88 (6) ◽  
pp. 1004-1013 ◽  
Author(s):  
Lian Zhao ◽  
Wenxin Ma ◽  
Robert N. Fariss ◽  
Wai T. Wong
Keyword(s):  
Vascular Repair ◽  
Ischemic Retinopathy
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