Vittorio Porciatti

ORCID: 0000-0002-1592-3532
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About
Contact & Profiles
Research Areas
  • Retinal Development and Disorders
  • Glaucoma and retinal disorders
  • Retinal Diseases and Treatments
  • Photoreceptor and optogenetics research
  • Visual perception and processing mechanisms
  • Neuroscience and Neuropharmacology Research
  • Neural dynamics and brain function
  • Mitochondrial Function and Pathology
  • Retinal Imaging and Analysis
  • Retinal and Optic Conditions
  • Neuroscience and Neural Engineering
  • Retinopathy of Prematurity Studies
  • Virus-based gene therapy research
  • Nerve injury and regeneration
  • Neurological Disorders and Treatments
  • Neurobiology and Insect Physiology Research
  • Ocular and Laser Science Research
  • Receptor Mechanisms and Signaling
  • Multiple Sclerosis Research Studies
  • Corneal surgery and disorders
  • Photosynthetic Processes and Mechanisms
  • Ophthalmology and Visual Impairment Studies
  • Connexins and lens biology
  • Cell death mechanisms and regulation
  • Drug-Induced Ocular Toxicity

University of Miami
2015-2024

University of Miami Health System
2021

Miami Dermatology and Laser Institute
2010-2020

Ospedale Civile di Vittorio Veneto
2020

East Florida Eye Institute
2020

American Academy of Ophthalmology
2017

Ophthalmology Associates (United States)
2010-2014

The California Eye Institute
2005-2013

Research to Prevent Blindness
2010-2011

Elettra-Sincrotrone Trieste S.C.p.A.
2009-2010

Here, we use a mouse model (DBA/2J) to readdress the location of insult(s) retinal ganglion cells (RGCs) in glaucoma. We localize an early sign axon damage astrocyte-rich region optic nerve just posterior retina, analogous lamina cribrosa. In this region, network astrocytes associates intimately with RGC axons. Using BAX-deficient DBA/2J mice, which retain all their RGCs, provide experimental evidence for insult within or very close nerve. show that proximal segments attached cell bodies...

10.1083/jcb.200706181 article EN The Journal of Cell Biology 2007-12-24

Glaucomas are neurodegenerative diseases that cause vision loss, especially in the elderly. The mechanisms initiating glaucoma and driving neuronal vulnerability during normal aging unknown. Studying glaucoma-prone mice, we show mitochondrial abnormalities an early driver of dysfunction, occurring before detectable degeneration. Retinal levels nicotinamide adenine dinucleotide (NAD

10.1126/science.aal0092 article EN Science 2017-02-16

Glaucoma is a common ocular disorder that leading cause of blindness worldwide. It characterized by the dysfunction and loss retinal ganglion cells (RGCs). Although many studies have implicated various molecules in glaucoma, no mechanism has been shown to be responsible for earliest detectable damage RGCs their axons optic nerve. Here, we show leukocyte transendothelial migration pathway activated nerve head at stages disease an inherited mouse model glaucoma. This resulted proinflammatory...

10.1172/jci61135 article EN Journal of Clinical Investigation 2012-03-19

We investigated the effects of photoreceptor degeneration on anatomy and physiology inner retinal neurons in a mouse model retinitis pigmentosa, (rd) mutant mouse. Although there is general assumption that cells do not suffer from death, we confirmed major changes both accompanying after this process. Changes include sprouting horizontal cells, lack development dendrites rod bipolar progressive atrophy cone cells. Electrophysiological recordings demonstrate selective impairment second-order...

10.1523/jneurosci.22-13-05492.2002 article EN Journal of Neuroscience 2002-07-01

In the mammalian visual system formation of eye-specific layers at thalamic level depends on retinal waves spontaneous activity, which rely nicotinic acetylcholine receptor activation. We found that in mutant mice lacking β2 subunit neuronal receptor, but not α4 subunit, retinofugal projections do segregate into areas, both dorso-lateral geniculate nucleus and superior colliculus. Moreover, β2−/− show an expansion binocular subfield primary cortex a decrease acuity cortical retina. conclude...

10.1073/pnas.101120998 article EN Proceedings of the National Academy of Sciences 2001-05-08

To introduce DNA into mitochondria efficiently, we fused adenoassociated virus capsid VP2 with a mitochondrial targeting sequence to carry the gene encoding human NADH ubiquinone oxidoreductase subunit 4 (ND4). Expression of WT ND4 in cells G11778A mutation led restoration defective ATP synthesis. Furthermore, injection rodent eye, levels reached 80% its mouse homolog. The construct expressed most inner retinal neurons, and it also suppressed visual loss optic atrophy induced by mutant...

10.1073/pnas.1119577109 article EN Proceedings of the National Academy of Sciences 2012-04-20

We determined the time lag between loss of retinal ganglion cell function and nerve fiber layer (RNFL) thickness.Glaucoma suspects were followed for at least four years. Patients underwent pattern electroretinography (PERG), optical coherence tomography (OCT) RNFL, standard automated perimetry testing 6-month intervals. Comparisons made changes in all modalities. To compare PERG OCT measurements on a normalized scale, we calculated dynamic range amplitude RNFL thickness. The structure was...

10.1167/iovs.12-11026 article EN Investigative Ophthalmology & Visual Science 2013-02-15

purpose. To compare relative reduction of retinal ganglion cell (RGC) function and nerve fiber layer (RNFL) thickness in early glaucoma by means steady-state pattern electroretinogram (PERG) optical coherence tomography (OCT), respectively. methods. Eighty-four persons with suspected due to disc abnormalities (GS: mean age 56.6 ± 13.8 years, standard automated perimetry [SAP] deviation [MD] −0.58 1.34 dB) 34 patients manifest (EMG, 65.9 10.7 SAP MD −2.7 4.5 were tested PERG OCT. Both GS EMG...

10.1167/iovs.06-0161 article EN Investigative Ophthalmology & Visual Science 2006-08-25

To characterize progressive changes of retinal ganglion cell (RGC) function and intraocular pressure (IOP) in the DBA/2J mouse model spontaneous glaucoma.Serial pattern electroretinograms (PERGs) IOPs measures were obtained from both eyes 32 anesthetized mice over an age range 2 to 12 months at 1-month intervals. Cone-driven flash-ERGs (FERGs) also recorded. The endpoint was defined as which PERG amplitude reached noise level least one eye. At that point, histologically processed evaluate...

10.1167/iovs.07-0483 article EN Investigative Ophthalmology & Visual Science 2007-09-26

10.1007/s10633-007-9059-8 article EN Documenta Ophthalmologica 2007-05-24

To determine the baseline characteristics, reliability, and dynamic range of pattern electroretinogram (PERG) as a tool to monitor progressive RGC dysfunction in DBA/2J mouse model glaucoma with spontaneously elevated intraocular pressure (IOP).PERGs were recorded from 56 undilated eyes 28 anesthetized (ketamine-xylazine-acepromazine) mice different ages (2-4 months, n = 44 eyes; 12-14 12 eyes) response contrast reversal gratings that maximize PERG amplitude (95% contrast, 1-Hz reversal,...

10.1167/iovs.06-0733 article EN Investigative Ophthalmology & Visual Science 2007-01-24

purpose. To characterize the effect of postural IOP elevation and pharmacological lowering on retinal ganglion cell (RGC) function in DBA/2J mouse model glaucoma. methods. Four groups mice (3 months old, n = 7; 5 10 11 8) were anesthetized by intraperitoneal injection (0.6 mL/kg) a mixture ketamine (42.8 mg/mL), xylazine (8.5 acepromazine (1.4 mg/mL). pattern electroretinogram (PERG) sequentially measured with at 0° (horizontal), 60° head-down, again 0°. PERG also before after mannitol 25%...

10.1167/iovs.07-0582 article EN Investigative Ophthalmology & Visual Science 2007-09-26
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