Rescue of the Congenital Hereditary Endothelial Dystrophy Mouse Model by Adeno-Associated Virus–Mediated Slc4a11 Replacement

[1]  P. Liton,et al.  Mitochondrial ROS Induced Lysosomal Dysfunction and Autophagy Impairment in an Animal Model of Congenital Hereditary Endothelial Dystrophy , 2021, Investigative ophthalmology & visual science.

[2]  Chia-Yang Liu,et al.  Inducible Slc4a11 Knockout Triggers Corneal Edema Through Perturbation of Corneal Endothelial Pump , 2021, Investigative ophthalmology & visual science.

[3]  Rajalekshmy Shyam,et al.  Bicarbonate activates glycolysis and lactate production in corneal endothelial cells by increased pHi. , 2020, Experimental eye research.

[4]  Liujiang Song,et al.  Adeno-Associated Virus Mediated Gene Therapy for Corneal Diseases , 2020, Pharmaceutics.

[5]  J. Mehta,et al.  Prospects and Challenges of Translational Corneal Bioprinting , 2020, Bioengineering.

[6]  J. Ambati,et al.  Start codon disruption with CRISPR/Cas9 prevents murine Fuchs’ endothelial corneal dystrophy , 2020, bioRxiv.

[7]  J. Bonanno,et al.  Corneal Endothelial Pump Coupling to Lactic Acid Efflux in the Rabbit and Mouse , 2020, Investigative ophthalmology & visual science.

[8]  M. Emami,et al.  Observation of nine previously reported and 10 non-reported SLC4A11 mutations among 20 Iranian CHED probands and identification of an MPDZ mutation as possible cause of CHED and FECD in one family , 2019, British Journal of Ophthalmology.

[9]  J. Casey,et al.  Human Corneal Expression of SLC4A11, a Gene Mutated in Endothelial Corneal Dystrophies , 2019, Scientific Reports.

[10]  Rajalekshmy Shyam,et al.  Ammonia sensitive SLC4A11 mitochondrial uncoupling reduces glutamine induced oxidative stress , 2019, Redox biology.

[11]  S. Feizi.  Corneal endothelial cell dysfunction: etiologies and management , 2018, Therapeutic advances in ophthalmology.

[12]  S. Chaurasia,et al.  SLC4A11 depletion impairs NRF2 mediated antioxidant signaling and increases reactive oxygen species in human corneal endothelial cells during oxidative stress , 2017, Scientific Reports.

[13]  C. O'brien,et al.  Therapeutic potential of AAV-mediated MMP-3 secretion from corneal endothelium in treating glaucoma , 2017, Human molecular genetics.

[14]  R. Frausto,et al.  Multifunctional ion transport properties of human SLC4A11: comparison of the SLC4A11-B and SLC4A11-C variants. , 2016, American journal of physiology. Cell physiology.

[15]  H. Khanna,et al.  Advances in Gene Therapy for Diseases of the Eye , 2016, Human gene therapy.

[16]  J. Bonanno,et al.  Fluid transport by the cornea endothelium is dependent on buffering lactic acid efflux. , 2016, American journal of physiology. Cell physiology.

[17]  M. Parker,et al.  SLC4A11 and the Pathophysiology of Congenital Hereditary Endothelial Dystrophy , 2015, BioMed research international.

[18]  J. Bennett,et al.  The Status of RPE65 Gene Therapy Trials: Safety and Efficacy. , 2015, Cold Spring Harbor perspectives in medicine.

[19]  T. Nguyen,et al.  CD147 required for corneal endothelial lactate transport. , 2014, Investigative ophthalmology & visual science.

[20]  J. Mehta,et al.  Mice with a targeted disruption of Slc4a11 model the progressive corneal changes of congenital hereditary endothelial dystrophy. , 2013, Investigative ophthalmology & visual science.

[21]  J. Han,et al.  Genetics of the corneal endothelial dystrophies: an evidence‐based review , 2013, Clinical genetics.

[22]  T. Nguyen,et al.  Lactate-H⁺ transport is a significant component of the in vivo corneal endothelial pump. , 2012, Investigative ophthalmology & visual science.

[23]  J. Bonanno.  Molecular mechanisms underlying the corneal endothelial pump. , 2012, Experimental eye research.

[24]  U. Jurkunas,et al.  Molecular bases of corneal endothelial dystrophies. , 2012, Experimental eye research.

[25]  V. Scorcia,et al.  Descemet-stripping automated endothelial keratoplasty for congenital hereditary endothelial dystrophy. , 2011, Archives of ophthalmology.

[26]  F. Alkuraya,et al.  Mutational spectrum of SLC4A11 in autosomal recessive CHED in Saudi Arabia. , 2009, Investigative ophthalmology & visual science.

[27]  S. E. Barker,et al.  Subretinal delivery of adeno-associated virus serotype 2 results in minimal immune responses that allow repeat vector administration in immunocompetent mice , 2009, The journal of gene medicine.

[28]  T. Dada,et al.  Pediatric keratoplasty. , 2009, Survey of ophthalmology.

[29]  R. Veitia,et al.  Identification of mutations in the SLC4A11 gene in patients with recessive congenital hereditary endothelial dystrophy. , 2008, Archives of ophthalmology.

[30]  M. Salto‐Tellez,et al.  Mutations in sodium-borate cotransporter SLC4A11 cause recessive congenital hereditary endothelial dystrophy (CHED2) , 2006, Nature Genetics.

[31]  V. Choi,et al.  Mechanisms of AAV transduction in glaucoma‐associated human trabecular meshwork cells , 2006, The journal of gene medicine.

[32]  W M Bourne,et al.  Biology of the corneal endothelium in health and disease , 2003, Eye.

[33]  T. D. de By.  Shortage in the face of plenty: improving the allocation of corneas for transplantation. , 2003, Developments in ophthalmology.

[34]  H E Kaufman,et al.  Corneal transplantation. , 1977, Annual review of medicine.