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  1. AU="Kapphahn, Rebecca J"
  2. AU="Bertuccio, Claudia A"
  3. AU="Jennifer A Gaddy"
  4. AU="Tuccar, Eray"
  5. AU="Koch, Karen E"
  6. AU="Kelly, Allicia P"
  7. AU=Kakinuma Takashi
  8. AU="Nachira, Lorenza"
  9. AU="Wei, Xiang"
  10. AU="Daniell, Esther"
  11. AU="Chou, Chau-Wen"
  12. AU=Kaur Supreet
  13. AU="Yun, Joho"
  14. AU="Tran, Bao G"
  15. AU="Ou Li"
  16. AU="Ting Chen" AU="Ting Chen"
  17. AU="Wilson, Jaymi"
  18. AU="Vane, Christopher H"
  19. AU="Mabbott, Donald"
  20. AU="Martín-Trejo, Jorge Alfonso"
  21. AU=Rieder Hans L

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  1. Artikel ; Online: Dissecting Regulators of Aging and Age-Related Macular Degeneration in the Retinal Pigment Epithelium.

    Karunadharma, Pabalu P / Kapphahn, Rebecca J / Stahl, Madilyn R / Olsen, Timothy W / Ferrington, Deborah A

    Oxidative medicine and cellular longevity

    2022  Band 2022, Seite(n) 6009787

    Abstract: Age-related macular degeneration (AMD), the leading cause of blindness in elderly populations, involves the loss of central vision due to progressive dysfunction of the retinal pigment epithelium (RPE) and subsequent loss of light-sensing photoreceptors. ...

    Abstract Age-related macular degeneration (AMD), the leading cause of blindness in elderly populations, involves the loss of central vision due to progressive dysfunction of the retinal pigment epithelium (RPE) and subsequent loss of light-sensing photoreceptors. While age is a key risk factor, not every aged individual develops AMD. Thus, the critical question is what specific cellular changes tip the balance from healthy aging to disease. To distinguish between changes associated with aging and AMD, we compared the RPE proteome in human eye bank tissue from nondiseased donors during aging (
    Mesh-Begriff(e) Aged ; Humans ; Retinal Pigment Epithelium/metabolism ; Macular Degeneration/metabolism ; Aging ; Oxidative Stress ; Oxidative Phosphorylation
    Sprache Englisch
    Erscheinungsdatum 2022-11-16
    Erscheinungsland United States
    Dokumenttyp Journal Article
    ZDB-ID 2455981-7
    ISSN 1942-0994 ; 1942-0994
    ISSN (online) 1942-0994
    ISSN 1942-0994
    DOI 10.1155/2022/6009787
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  2. Artikel ; Online: Quantitative Proteomics of Human Retinal Pigment Epithelium Reveals Key Regulators for the Pathogenesis of Age-Related Macular Degeneration.

    Shen, Shichen / Kapphahn, Rebecca J / Zhang, Ming / Qian, Shuo / Montezuma, Sandra R / Shang, Peng / Ferrington, Deborah A / Qu, Jun

    International journal of molecular sciences

    2023  Band 24, Heft 4

    Abstract: Age-related macular degeneration (AMD) is the leading cause of blindness in elderly people, with limited treatment options available for most patients. AMD involves the death of retinal pigment epithelium (RPE) and photoreceptor cells, with mitochondria ... ...

    Abstract Age-related macular degeneration (AMD) is the leading cause of blindness in elderly people, with limited treatment options available for most patients. AMD involves the death of retinal pigment epithelium (RPE) and photoreceptor cells, with mitochondria dysfunction being a critical early event. In the current study, we utilized our unique resource of human donor RPE graded for AMD presence and severity to investigate proteome-wide dysregulation involved in early AMD. Organelle-enriched fractions of RPE were isolated from donors with early AMD (
    Mesh-Begriff(e) Humans ; Aged ; Retinal Pigment Epithelium/metabolism ; Proteomics ; Reproducibility of Results ; Macular Degeneration/metabolism ; Oxidative Stress
    Sprache Englisch
    Erscheinungsdatum 2023-02-07
    Erscheinungsland Switzerland
    Dokumenttyp Journal Article
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms24043252
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  3. Artikel: Human iPSC- and Primary-Retinal Pigment Epithelial Cells for Modeling Age-Related Macular Degeneration.

    Fisher, Cody R / Ebeling, Mara C / Geng, Zhaohui / Kapphahn, Rebecca J / Roehrich, Heidi / Montezuma, Sandra R / Dutton, James R / Ferrington, Deborah A

    Antioxidants (Basel, Switzerland)

    2022  Band 11, Heft 4

    Abstract: Primary cultures of retinal pigment epithelium (RPE) from human adult donors (haRPE) and induced pluripotent stem cell derived-RPE (iPSC-RPE) are valuable model systems for gaining mechanistic insight and for testing potential therapies for age-related ... ...

    Abstract Primary cultures of retinal pigment epithelium (RPE) from human adult donors (haRPE) and induced pluripotent stem cell derived-RPE (iPSC-RPE) are valuable model systems for gaining mechanistic insight and for testing potential therapies for age-related macular degeneration (AMD). This study evaluated the treatment response of haRPE and iPSC-RPE to oxidative stress and potential therapeutics addressing mitochondrial defects. haRPE and iSPC-RPE were derived from donors with or without AMD. Mitochondrial function was measured after treatment with menadione, AICAR, or trehalose and the response to treatment was compared between cell models and by disease status. In a subset of samples, haRPE and iPSC-RPE were generated from the same human donor to make a side-by-side comparison of the two cell models' response to treatment. Disease-specific responses to all three treatments was observed in the haRPE. In contrast, iPSC-RPE had a similar response to all treatments irrespective of disease status. Analysis of haRPE and iPSC-RPE generated from the same human donor showed a similar response for donors without AMD, but there were significant differences in treatment response between cell models generated from AMD donors. These results support the use of iPSC-RPE and haRPE when investigating AMD mechanisms and new therapeutics but indicates that attention to experimental conditions is required.
    Sprache Englisch
    Erscheinungsdatum 2022-03-22
    Erscheinungsland Switzerland
    Dokumenttyp Journal Article
    ZDB-ID 2704216-9
    ISSN 2076-3921
    ISSN 2076-3921
    DOI 10.3390/antiox11040605
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  4. Artikel: Testing Mitochondrial-Targeted Drugs in iPSC-RPE from Patients with Age-Related Macular Degeneration.

    Ebeling, Mara C / Geng, Zhaohui / Stahl, Madilyn R / Kapphahn, Rebecca J / Roehrich, Heidi / Montezuma, Sandra R / Ferrington, Deborah A / Dutton, James R

    Pharmaceuticals (Basel, Switzerland)

    2022  Band 15, Heft 1

    Abstract: Age-related macular degeneration (AMD) is the leading cause of blindness in the elderly. No universally effective treatments exist for atrophic or "dry" AMD, which results from loss of the retinal pigment epithelium (RPE) and photoreceptors and accounts ... ...

    Abstract Age-related macular degeneration (AMD) is the leading cause of blindness in the elderly. No universally effective treatments exist for atrophic or "dry" AMD, which results from loss of the retinal pigment epithelium (RPE) and photoreceptors and accounts for ≈80% of all AMD patients. Prior studies provide evidence for the involvement of mitochondrial dysfunction in AMD pathology. This study used induced pluripotent stem cell (iPSC) RPE derived from five AMD patients to test the efficacy of three drugs (AICAR (5-Aminoimidazole-4-carboxamide ribonucleotide), Metformin, trehalose) that target key processes in maintaining optimal mitochondrial function. The patient iPSC-RPE lines were used in a proof-of-concept drug screen, utilizing an analysis of RPE mitochondrial function following acute and extended drug exposure. Results show considerable variability in drug response across patient cell lines, supporting the need for a personalized medicine approach for treating AMD. Furthermore, our results demonstrate the feasibility of using iPSC-RPE from AMD patients to develop a personalized drug treatment regime and provide a roadmap for the future clinical management of AMD.
    Sprache Englisch
    Erscheinungsdatum 2022-01-04
    Erscheinungsland Switzerland
    Dokumenttyp Journal Article
    ZDB-ID 2193542-7
    ISSN 1424-8247
    ISSN 1424-8247
    DOI 10.3390/ph15010062
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  5. Artikel ; Online: Inflammasome Activation in Retinal Pigment Epithelium from Human Donors with Age-Related Macular Degeneration.

    Ebeling, Mara C / Fisher, Cody R / Kapphahn, Rebecca J / Stahl, Madilyn R / Shen, Shichen / Qu, Jun / Montezuma, Sandra R / Ferrington, Deborah A

    Cells

    2022  Band 11, Heft 13

    Abstract: Age-related macular degeneration (AMD), the leading cause of blindness in the elderly, is characterized by the death of retinal pigment epithelium (RPE) and photoreceptors. One of the risk factors associated with developing AMD is the single nucleotide ... ...

    Abstract Age-related macular degeneration (AMD), the leading cause of blindness in the elderly, is characterized by the death of retinal pigment epithelium (RPE) and photoreceptors. One of the risk factors associated with developing AMD is the single nucleotide polymorphism (SNP) found within the gene encoding complement factor H (CFH). Part of the innate immune system, CFH inhibits alternative complement pathway activation. Multi-protein complexes called inflammasomes also play a role in the innate immune response. Previous studies reported that inflammasome activation may contribute to AMD pathology. In this study, we used primary human adult RPE cell cultures from multiple donors, with and without AMD, that were genotyped for the Y402H CFH risk allele. We found complement and inflammasome-related genes and proteins at basal levels in RPE tissue and cell cultures. Additionally, treatment with rotenone, bafilomycin A, and ATP led to inflammasome activation. Overall, the response to priming and activation was similar, irrespective of disease state or CFH genotype. While these data show that the inflammasome is present and active in RPE, our results suggest that inflammasome activation may not contribute to early AMD pathology.
    Mesh-Begriff(e) Aged ; Genotype ; Humans ; Inflammasomes/metabolism ; Macular Degeneration/metabolism ; Polymorphism, Single Nucleotide ; Retinal Pigment Epithelium/metabolism
    Chemische Substanzen Inflammasomes
    Sprache Englisch
    Erscheinungsdatum 2022-06-30
    Erscheinungsland Switzerland
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2661518-6
    ISSN 2073-4409 ; 2073-4409
    ISSN (online) 2073-4409
    ISSN 2073-4409
    DOI 10.3390/cells11132075
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  6. Artikel ; Online: Investigating AKT activation and autophagy in immunoproteasome-deficient retinal cells.

    Karim, Md Razaul / Fisher, Cody R / Kapphahn, Rebecca J / Polanco, Jorge R / Ferrington, Deborah A

    PloS one

    2020  Band 15, Heft 4, Seite(n) e0231212

    Abstract: Two major proteolytic systems, the proteasome and the autophagy pathway, are key components of the proteostasis network. The immunoproteasome, a proteasome subtype, and autophagy are upregulated under stress conditions, forming a coordinated unit ... ...

    Abstract Two major proteolytic systems, the proteasome and the autophagy pathway, are key components of the proteostasis network. The immunoproteasome, a proteasome subtype, and autophagy are upregulated under stress conditions, forming a coordinated unit designed to minimize the effect of cell stress. We investigated how genetic ablation of the LMP2 immunoproteasome subunit affects autophagy in retinal pigment epithelium (RPE) from WT and LMP2 knockout mice. We monitored autophagy regulation by measuring LC3, phosphorylation of AKT (S473), and phosphorylation of S6, a downstream readout of AKT (mTOR) pathway activation. We also evaluated transcription factor EB (TFEB) nuclear translocation, a transcription factor that controls expression of autophagy and lysosome genes. WT and LMP2 KO cells were monitored after treatment with EBSS to stimulate autophagy, insulin to stimulate AKT, or an AKT inhibitor (trehalose or MK-2206). Under basal conditions, we observed hyper-phosphorylation of AKT and S6, as well as lower nuclear-TFEB content in LMP2 KO RPE compared with WT. AKT inhibitors MK-2206 and trehalose significantly inhibited AKT phosphorylation and stimulated nuclear translocation of TFEB. Starvation and AKT inhibition upregulated autophagy, albeit to a lesser extent in LMP2 KO RPE. These data support the idea that AKT hyper-activation is an underlying cause of defective autophagy regulation in LMP2 KO RPE, revealing a unique link between two proteolytic systems and a previously unknown function in autophagy regulation by the immunoproteasome.
    Mesh-Begriff(e) Animals ; Autophagy/drug effects ; Basic Helix-Loop-Helix Leucine Zipper Transcription Factors/metabolism ; Cells, Cultured ; Cysteine Endopeptidases/metabolism ; Enzyme Activation/drug effects ; HEK293 Cells ; Humans ; Insulin/pharmacology ; Mice, Knockout ; Phosphorylation/drug effects ; Proteasome Endopeptidase Complex/immunology ; Protein Transport/drug effects ; Proto-Oncogene Proteins c-akt/antagonists & inhibitors ; Proto-Oncogene Proteins c-akt/metabolism ; Retina/cytology ; Retinal Pigment Epithelium/cytology ; Signal Transduction/drug effects
    Chemische Substanzen Basic Helix-Loop-Helix Leucine Zipper Transcription Factors ; Insulin ; Tcfeb protein, mouse ; LMP-2 protein (144416-78-4) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; Cysteine Endopeptidases (EC 3.4.22.-) ; Proteasome Endopeptidase Complex (EC 3.4.25.1)
    Sprache Englisch
    Erscheinungsdatum 2020-04-10
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2267670-3
    ISSN 1932-6203 ; 1932-6203
    ISSN (online) 1932-6203
    ISSN 1932-6203
    DOI 10.1371/journal.pone.0231212
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  7. Artikel ; Online: Lipid-derived and other oxidative modifications of retinal proteins in a rat model of Smith-Lemli-Opitz syndrome.

    Kapphahn, Rebecca J / Richards, Michael J / Ferrington, Deborah A / Fliesler, Steven J

    Experimental eye research

    2018  Band 178, Seite(n) 247–254

    Abstract: Oxidative modification of proteins can perturb their structure and function, often compromising cellular viability. Such modifications include lipid-derived adducts (e.g., 4-hydroxynonenal (HNE) and carboxyethylpyrrole (CEP)) as well as nitrotyrosine ( ... ...

    Abstract Oxidative modification of proteins can perturb their structure and function, often compromising cellular viability. Such modifications include lipid-derived adducts (e.g., 4-hydroxynonenal (HNE) and carboxyethylpyrrole (CEP)) as well as nitrotyrosine (NTyr). We compared the retinal proteome and levels of such modifications in the AY9944-treated rat model of Smith-Lemli-Opitz syndrome (SLOS), in comparison to age-matched controls. Retinas harvested at 3 months of age were either subjected to proteomic analysis or to immuno-slot blot analysis, the latter probing blots with antibodies raised against HNE, CEP, and NTyr, followed by quantitative densitometry. HNE modification of retinal proteins was markedly (>9-fold) higher in AY9944-treated rats compared to controls, whereas CEP modification was only modestly (≤2-fold) greater, and NTyr modification was minimal and exhibited no difference as a function of AY9944 treatment. Anti-HNE immunoreactivity was greatest in the plexiform and ganglion cell layers, but also present in the RPE, choroid, and photoreceptor outer segment layer in AY9944-treated rats; control retinas showed minimal HNE labeling. 1D-PAGE/Western blot analysis of rod outer segment (ROS) membranes revealed HNE modification of both opsin and β-transducin. Proteomic analysis revealed the differential expression of several retinal proteins as a consequence of AY9944 treatment. Upregulated proteins included those involved in chaperone/protein folding, oxidative and cellular stress responses, transcriptional regulation, and energy production. βA3/A1 Crystallin, which has a role in regulation of lysosomal acidification, was down-regulated. Hence, oxidative modification of retinal proteins occurs in the SLOS rat model, in addition to the previously described oxidation of lipids. The results are discussed in the context of the histological and physiological changes that occur in the retina in the SLOS rat model.
    Mesh-Begriff(e) Aldehydes/metabolism ; Animals ; Blotting, Western ; Disease Models, Animal ; Electrophoresis, Polyacrylamide Gel ; Enzyme Inhibitors/pharmacology ; Female ; Opsins/metabolism ; Oxidative Stress ; Pregnancy ; Proteomics ; Rats ; Rats, Sprague-Dawley ; Retina/metabolism ; Smith-Lemli-Opitz Syndrome/metabolism ; Transducin/metabolism ; trans-1,4-Bis(2-chlorobenzaminomethyl)cyclohexane Dihydrochloride/pharmacology
    Chemische Substanzen Aldehydes ; Enzyme Inhibitors ; Opsins ; trans-1,4-Bis(2-chlorobenzaminomethyl)cyclohexane Dihydrochloride (366-93-8) ; Transducin (EC 3.6.5.1) ; 4-hydroxy-2-nonenal (K1CVM13F96)
    Sprache Englisch
    Erscheinungsdatum 2018-08-14
    Erscheinungsland England
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 80122-7
    ISSN 1096-0007 ; 0014-4835
    ISSN (online) 1096-0007
    ISSN 0014-4835
    DOI 10.1016/j.exer.2018.08.006
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  8. Artikel ; Online: No association between cataract surgery and mitochondrial DNA damage with age-related macular degeneration in human donor eyes.

    Armbrust, Karen R / Karunadharma, Pabalu P / Terluk, Marcia R / Kapphahn, Rebecca J / Olsen, Timothy W / Ferrington, Deborah A / Montezuma, Sandra R

    PloS one

    2021  Band 16, Heft 10, Seite(n) e0258803

    Abstract: Purpose: To determine whether age-related macular degeneration (AMD) severity or the frequency of retinal pigment epithelium mitochondrial DNA lesions differ in human donor eyes that have undergone cataract surgery compared to phakic eyes.: Methods: ... ...

    Abstract Purpose: To determine whether age-related macular degeneration (AMD) severity or the frequency of retinal pigment epithelium mitochondrial DNA lesions differ in human donor eyes that have undergone cataract surgery compared to phakic eyes.
    Methods: Eyes from human donors aged ≥ 55 years were obtained from the Minnesota Lions Eye Bank. Cataract surgery status was obtained from history provided to Eye Bank personnel by family members at the time of tissue procurement. Donor eyes were graded for AMD severity using the Minnesota Grading System. Quantitative PCR was performed on DNA isolated from macular punches of retinal pigment epithelium to quantitate the frequency of mitochondrial DNA lesions in the donor tissue. Univariable and multivariable analyses were performed to evaluate for associations between (1) cataract surgery and AMD severity and (2) cataract surgery and mitochondrial DNA lesion frequency.
    Results: A total of 157 subjects qualified for study inclusion. Multivariable analysis with age, sex, smoking status, and cataract surgery status showed that only age was associated with AMD grade. Multivariable analysis with age, sex, smoking status, and cataract surgery status showed that none of these factors were associated with retinal pigment epithelium mitochondrial DNA lesion frequency.
    Conclusions: In this study of human donor eyes, neither retinal pigment epithelium mitochondrial DNA damage nor the stage of AMD severity are independently associated with cataract surgery after adjusting for other AMD risk factors. These new pathologic and molecular findings provide evidence against a relationship between cataract surgery and AMD progression and support the idea that cataract surgery is safe in the setting of AMD.
    Mesh-Begriff(e) Aged ; Aged, 80 and over ; Biological Specimen Banks ; Cataract Extraction/adverse effects ; Cataract Extraction/statistics & numerical data ; DNA Damage ; DNA, Mitochondrial/genetics ; Disease Progression ; Female ; Humans ; Macular Degeneration/etiology ; Macular Degeneration/genetics ; Male ; Middle Aged ; Multivariate Analysis ; Retinal Pigment Epithelium/chemistry ; Tissue Donors
    Chemische Substanzen DNA, Mitochondrial
    Sprache Englisch
    Erscheinungsdatum 2021-10-19
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ISSN 1932-6203
    ISSN (online) 1932-6203
    DOI 10.1371/journal.pone.0258803
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  9. Artikel ; Online: Impaired Mitochondrial Function in iPSC-Retinal Pigment Epithelium with the Complement Factor H Polymorphism for Age-Related Macular Degeneration.

    Ebeling, Mara C / Geng, Zhaohui / Kapphahn, Rebecca J / Roehrich, Heidi / Montezuma, Sandra R / Dutton, James R / Ferrington, Deborah A

    Cells

    2021  Band 10, Heft 4

    Abstract: Age-related macular degeneration (AMD), the leading cause of vision loss in the elderly, is characterized by loss of the retinal pigment epithelium (RPE). While the disease mechanism remains unclear, prior studies have linked AMD with RPE mitochondrial ... ...

    Abstract Age-related macular degeneration (AMD), the leading cause of vision loss in the elderly, is characterized by loss of the retinal pigment epithelium (RPE). While the disease mechanism remains unclear, prior studies have linked AMD with RPE mitochondrial defects and genetic polymorphisms in the complement pathway. This study used RPE generated from induced pluripotent stem cells (iPSC-RPE), which were derived from human donors with or without AMD and genotyped for the complement factor H (CFH) AMD high-risk allele (rs1061170, Y402H) to investigate whether donor disease state or genotype had a detrimental effect on mitochondrial function and inflammation. Results show that cells derived from donors with AMD display decreased mitochondrial function under conditions of stress and elevated expression of inflammatory markers compared to iPSC-RPE from individuals without AMD. A more pronounced reduction in mitochondrial function and increased inflammatory markers was observed in CFH high-risk cells, irrespective of disease state. These results provide evidence for a previously unrecognized link between CFH and mitochondrial function that could contribute to RPE loss in AMD patients harboring the CFH high-risk genotype.
    Mesh-Begriff(e) Aged ; Aged, 80 and over ; Biomarkers/metabolism ; Cell Line ; Complement Factor H/genetics ; Complement System Proteins/metabolism ; Epithelial Cells/pathology ; Female ; Humans ; Induced Pluripotent Stem Cells/pathology ; Inflammation/pathology ; Macular Degeneration/genetics ; Male ; Middle Aged ; Mitochondria/metabolism ; Mitochondria/pathology ; Mitochondrial Proteins/metabolism ; Models, Biological ; Polymorphism, Genetic ; Retinal Pigment Epithelium/pathology ; Risk ; Tissue Donors
    Chemische Substanzen Biomarkers ; Mitochondrial Proteins ; Complement Factor H (80295-65-4) ; Complement System Proteins (9007-36-7)
    Sprache Englisch
    Erscheinungsdatum 2021-04-02
    Erscheinungsland Switzerland
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2661518-6
    ISSN 2073-4409 ; 2073-4409
    ISSN (online) 2073-4409
    ISSN 2073-4409
    DOI 10.3390/cells10040789
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  10. Artikel ; Online: N-Acetyl-L-cysteine Protects Human Retinal Pigment Epithelial Cells from Oxidative Damage: Implications for Age-Related Macular Degeneration.

    Terluk, Marcia R / Ebeling, Mara C / Fisher, Cody R / Kapphahn, Rebecca J / Yuan, Ching / Kartha, Reena V / Montezuma, Sandra R / Ferrington, Deborah A

    Oxidative medicine and cellular longevity

    2019  Band 2019, Seite(n) 5174957

    Abstract: Age-related macular degeneration (AMD) involves the loss of retinal pigment epithelium (RPE) and photoreceptors and is one of the leading causes of blindness in the elderly. Oxidative damage to proteins, lipids, and DNA has been associated with RPE ... ...

    Abstract Age-related macular degeneration (AMD) involves the loss of retinal pigment epithelium (RPE) and photoreceptors and is one of the leading causes of blindness in the elderly. Oxidative damage to proteins, lipids, and DNA has been associated with RPE dysfunction and AMD. In this study, we evaluated oxidative stress in AMD and the efficacy of antioxidant, N-acetyl-L-cysteine (NAC), in protecting RPE from oxidative damage. To test this idea, primary cultures of RPE from human donors with AMD (
    Mesh-Begriff(e) Acetylcysteine/pharmacology ; Acetylcysteine/therapeutic use ; Epithelial Cells/metabolism ; Humans ; Macular Degeneration/genetics ; Macular Degeneration/pathology ; Retinal Pigment Epithelium/metabolism
    Chemische Substanzen Acetylcysteine (WYQ7N0BPYC)
    Sprache Englisch
    Erscheinungsdatum 2019-08-14
    Erscheinungsland United States
    Dokumenttyp Journal Article
    ZDB-ID 2455981-7
    ISSN 1942-0994 ; 1942-0994
    ISSN (online) 1942-0994
    ISSN 1942-0994
    DOI 10.1155/2019/5174957
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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