The Novel Application of EUK‐134 in Retinal Degeneration: Preventing Mitochondrial Oxidative Stress‐Triggered Retinal Pigment Epithelial Cell Apoptosis by Suppressing MAPK/p53 Signaling Pathway
ABSTRACT Age‐related macular degeneration (AMD), a leading cause of blindness, is characterized by mitochondrial dysfunction of retinal pigment epithelium (RPE) cells. EUK‐134 is a mimetic of SOD2 and catalase, widely used for its antioxidant properties in models of light‐induced damage or oxidative...
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| Published in | Environmental toxicology Vol. 40; no. 1; pp. 88 - 100 |
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| Main Authors | , , , , , , , , |
| Format | Journal Article |
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John Wiley & Sons, Inc
01.01.2025
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| Abstract | ABSTRACT
Age‐related macular degeneration (AMD), a leading cause of blindness, is characterized by mitochondrial dysfunction of retinal pigment epithelium (RPE) cells. EUK‐134 is a mimetic of SOD2 and catalase, widely used for its antioxidant properties in models of light‐induced damage or oxidative stress. However, its effects on the retina are not yet clear. Here, we investigated the capability of EUK‐134 in averting AMD using sodium iodate (NaIO3)‐induced Balb/c mouse and ARPE‐19 cells (adult RPE cell line). In vivo, EUK‐134 effectively antagonized NaIO3‐induced retinal deformation and prevented outer and inner nuclear layer thinning. In addition, it was found that the EUK‐134‐treated group significantly down‐regulated the expression of cleaved caspase‐3 compared with the group treated with NaIO3 alone. Our results found that EUK‐134 notably improved cell viability by preventing mitochondrial ROS accumulation‐induced membrane potential depolarization‐mediated apoptosis in NaIO3‐inducted ARPE‐19 cells. Furthermore, we found that EUK‐134 could inhibit p‐ERK, p‐p38, p‐JNK, p‐p53, Bax, cleaved caspase‐9, cleaved caspase‐3, and cleaved PARP by increasing Bcl‐2 protein expression. Additionally, we employed MAPK pathway inhibitors by SB203580 (a p38 inhibitor), U0126 (an ERK inhibitor), and SP600125 (a JNK inhibitor) to corroborate the aforementioned observation. The results support that EUK‐134 may effectively prevent mitochondrial oxidative stress‐mediated retinal apoptosis in NaIO3‐induced retinopathy. |
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| AbstractList | Age-related macular degeneration (AMD), a leading cause of blindness, is characterized by mitochondrial dysfunction of retinal pigment epithelium (RPE) cells. EUK-134 is a mimetic of SOD2 and catalase, widely used for its antioxidant properties in models of light-induced damage or oxidative stress. However, its effects on the retina are not yet clear. Here, we investigated the capability of EUK-134 in averting AMD using sodium iodate (NaIO
)-induced Balb/c mouse and ARPE-19 cells (adult RPE cell line). In vivo, EUK-134 effectively antagonized NaIO
-induced retinal deformation and prevented outer and inner nuclear layer thinning. In addition, it was found that the EUK-134-treated group significantly down-regulated the expression of cleaved caspase-3 compared with the group treated with NaIO
alone. Our results found that EUK-134 notably improved cell viability by preventing mitochondrial ROS accumulation-induced membrane potential depolarization-mediated apoptosis in NaIO
-inducted ARPE-19 cells. Furthermore, we found that EUK-134 could inhibit p-ERK, p-p38, p-JNK, p-p53, Bax, cleaved caspase-9, cleaved caspase-3, and cleaved PARP by increasing Bcl-2 protein expression. Additionally, we employed MAPK pathway inhibitors by SB203580 (a p38 inhibitor), U0126 (an ERK inhibitor), and SP600125 (a JNK inhibitor) to corroborate the aforementioned observation. The results support that EUK-134 may effectively prevent mitochondrial oxidative stress-mediated retinal apoptosis in NaIO
-induced retinopathy. Age-related macular degeneration (AMD), a leading cause of blindness, is characterized by mitochondrial dysfunction of retinal pigment epithelium (RPE) cells. EUK-134 is a mimetic of SOD2 and catalase, widely used for its antioxidant properties in models of light-induced damage or oxidative stress. However, its effects on the retina are not yet clear. Here, we investigated the capability of EUK-134 in averting AMD using sodium iodate (NaIO3)-induced Balb/c mouse and ARPE-19 cells (adult RPE cell line). In vivo, EUK-134 effectively antagonized NaIO3-induced retinal deformation and prevented outer and inner nuclear layer thinning. In addition, it was found that the EUK-134-treated group significantly down-regulated the expression of cleaved caspase-3 compared with the group treated with NaIO3 alone. Our results found that EUK-134 notably improved cell viability by preventing mitochondrial ROS accumulation-induced membrane potential depolarization-mediated apoptosis in NaIO3-inducted ARPE-19 cells. Furthermore, we found that EUK-134 could inhibit p-ERK, p-p38, p-JNK, p-p53, Bax, cleaved caspase-9, cleaved caspase-3, and cleaved PARP by increasing Bcl-2 protein expression. Additionally, we employed MAPK pathway inhibitors by SB203580 (a p38 inhibitor), U0126 (an ERK inhibitor), and SP600125 (a JNK inhibitor) to corroborate the aforementioned observation. The results support that EUK-134 may effectively prevent mitochondrial oxidative stress-mediated retinal apoptosis in NaIO3-induced retinopathy.Age-related macular degeneration (AMD), a leading cause of blindness, is characterized by mitochondrial dysfunction of retinal pigment epithelium (RPE) cells. EUK-134 is a mimetic of SOD2 and catalase, widely used for its antioxidant properties in models of light-induced damage or oxidative stress. However, its effects on the retina are not yet clear. Here, we investigated the capability of EUK-134 in averting AMD using sodium iodate (NaIO3)-induced Balb/c mouse and ARPE-19 cells (adult RPE cell line). In vivo, EUK-134 effectively antagonized NaIO3-induced retinal deformation and prevented outer and inner nuclear layer thinning. In addition, it was found that the EUK-134-treated group significantly down-regulated the expression of cleaved caspase-3 compared with the group treated with NaIO3 alone. Our results found that EUK-134 notably improved cell viability by preventing mitochondrial ROS accumulation-induced membrane potential depolarization-mediated apoptosis in NaIO3-inducted ARPE-19 cells. Furthermore, we found that EUK-134 could inhibit p-ERK, p-p38, p-JNK, p-p53, Bax, cleaved caspase-9, cleaved caspase-3, and cleaved PARP by increasing Bcl-2 protein expression. Additionally, we employed MAPK pathway inhibitors by SB203580 (a p38 inhibitor), U0126 (an ERK inhibitor), and SP600125 (a JNK inhibitor) to corroborate the aforementioned observation. The results support that EUK-134 may effectively prevent mitochondrial oxidative stress-mediated retinal apoptosis in NaIO3-induced retinopathy. Age‐related macular degeneration (AMD), a leading cause of blindness, is characterized by mitochondrial dysfunction of retinal pigment epithelium (RPE) cells. EUK‐134 is a mimetic of SOD2 and catalase, widely used for its antioxidant properties in models of light‐induced damage or oxidative stress. However, its effects on the retina are not yet clear. Here, we investigated the capability of EUK‐134 in averting AMD using sodium iodate (NaIO 3 )‐induced Balb/c mouse and ARPE‐19 cells (adult RPE cell line). In vivo, EUK‐134 effectively antagonized NaIO 3 ‐induced retinal deformation and prevented outer and inner nuclear layer thinning. In addition, it was found that the EUK‐134‐treated group significantly down‐regulated the expression of cleaved caspase‐3 compared with the group treated with NaIO 3 alone. Our results found that EUK‐134 notably improved cell viability by preventing mitochondrial ROS accumulation‐induced membrane potential depolarization‐mediated apoptosis in NaIO 3 ‐inducted ARPE‐19 cells. Furthermore, we found that EUK‐134 could inhibit p‐ERK, p‐p38, p‐JNK, p‐p53, Bax, cleaved caspase‐9, cleaved caspase‐3, and cleaved PARP by increasing Bcl‐2 protein expression. Additionally, we employed MAPK pathway inhibitors by SB203580 (a p38 inhibitor), U0126 (an ERK inhibitor), and SP600125 (a JNK inhibitor) to corroborate the aforementioned observation. The results support that EUK‐134 may effectively prevent mitochondrial oxidative stress‐mediated retinal apoptosis in NaIO 3 ‐induced retinopathy. Age‐related macular degeneration (AMD), a leading cause of blindness, is characterized by mitochondrial dysfunction of retinal pigment epithelium (RPE) cells. EUK‐134 is a mimetic of SOD2 and catalase, widely used for its antioxidant properties in models of light‐induced damage or oxidative stress. However, its effects on the retina are not yet clear. Here, we investigated the capability of EUK‐134 in averting AMD using sodium iodate (NaIO₃)‐induced Balb/c mouse and ARPE‐19 cells (adult RPE cell line). In vivo, EUK‐134 effectively antagonized NaIO₃‐induced retinal deformation and prevented outer and inner nuclear layer thinning. In addition, it was found that the EUK‐134‐treated group significantly down‐regulated the expression of cleaved caspase‐3 compared with the group treated with NaIO₃ alone. Our results found that EUK‐134 notably improved cell viability by preventing mitochondrial ROS accumulation‐induced membrane potential depolarization‐mediated apoptosis in NaIO₃‐inducted ARPE‐19 cells. Furthermore, we found that EUK‐134 could inhibit p‐ERK, p‐p38, p‐JNK, p‐p53, Bax, cleaved caspase‐9, cleaved caspase‐3, and cleaved PARP by increasing Bcl‐2 protein expression. Additionally, we employed MAPK pathway inhibitors by SB203580 (a p38 inhibitor), U0126 (an ERK inhibitor), and SP600125 (a JNK inhibitor) to corroborate the aforementioned observation. The results support that EUK‐134 may effectively prevent mitochondrial oxidative stress‐mediated retinal apoptosis in NaIO₃‐induced retinopathy. Age‐related macular degeneration (AMD), a leading cause of blindness, is characterized by mitochondrial dysfunction of retinal pigment epithelium (RPE) cells. EUK‐134 is a mimetic of SOD2 and catalase, widely used for its antioxidant properties in models of light‐induced damage or oxidative stress. However, its effects on the retina are not yet clear. Here, we investigated the capability of EUK‐134 in averting AMD using sodium iodate (NaIO3)‐induced Balb/c mouse and ARPE‐19 cells (adult RPE cell line). In vivo, EUK‐134 effectively antagonized NaIO3‐induced retinal deformation and prevented outer and inner nuclear layer thinning. In addition, it was found that the EUK‐134‐treated group significantly down‐regulated the expression of cleaved caspase‐3 compared with the group treated with NaIO3 alone. Our results found that EUK‐134 notably improved cell viability by preventing mitochondrial ROS accumulation‐induced membrane potential depolarization‐mediated apoptosis in NaIO3‐inducted ARPE‐19 cells. Furthermore, we found that EUK‐134 could inhibit p‐ERK, p‐p38, p‐JNK, p‐p53, Bax, cleaved caspase‐9, cleaved caspase‐3, and cleaved PARP by increasing Bcl‐2 protein expression. Additionally, we employed MAPK pathway inhibitors by SB203580 (a p38 inhibitor), U0126 (an ERK inhibitor), and SP600125 (a JNK inhibitor) to corroborate the aforementioned observation. The results support that EUK‐134 may effectively prevent mitochondrial oxidative stress‐mediated retinal apoptosis in NaIO3‐induced retinopathy. ABSTRACT Age‐related macular degeneration (AMD), a leading cause of blindness, is characterized by mitochondrial dysfunction of retinal pigment epithelium (RPE) cells. EUK‐134 is a mimetic of SOD2 and catalase, widely used for its antioxidant properties in models of light‐induced damage or oxidative stress. However, its effects on the retina are not yet clear. Here, we investigated the capability of EUK‐134 in averting AMD using sodium iodate (NaIO3)‐induced Balb/c mouse and ARPE‐19 cells (adult RPE cell line). In vivo, EUK‐134 effectively antagonized NaIO3‐induced retinal deformation and prevented outer and inner nuclear layer thinning. In addition, it was found that the EUK‐134‐treated group significantly down‐regulated the expression of cleaved caspase‐3 compared with the group treated with NaIO3 alone. Our results found that EUK‐134 notably improved cell viability by preventing mitochondrial ROS accumulation‐induced membrane potential depolarization‐mediated apoptosis in NaIO3‐inducted ARPE‐19 cells. Furthermore, we found that EUK‐134 could inhibit p‐ERK, p‐p38, p‐JNK, p‐p53, Bax, cleaved caspase‐9, cleaved caspase‐3, and cleaved PARP by increasing Bcl‐2 protein expression. Additionally, we employed MAPK pathway inhibitors by SB203580 (a p38 inhibitor), U0126 (an ERK inhibitor), and SP600125 (a JNK inhibitor) to corroborate the aforementioned observation. The results support that EUK‐134 may effectively prevent mitochondrial oxidative stress‐mediated retinal apoptosis in NaIO3‐induced retinopathy. |
| Author | Lin, Hui‐Wen Chen, Tzu‐Chun Yeh, Jui‐Hsuan Wang, Inga Wang, Meilin Chang, Yuan‐Yen Hsu, Chin‐Lin Chuang, Chen‐Ju Tsou, Shang‐Chun |
| Author_xml | – sequence: 1 givenname: Shang‐Chun surname: Tsou fullname: Tsou, Shang‐Chun organization: Chung Shan Medical University – sequence: 2 givenname: Chen‐Ju surname: Chuang fullname: Chuang, Chen‐Ju organization: St. Martin De Porres Hospital – sequence: 3 givenname: Chin‐Lin surname: Hsu fullname: Hsu, Chin‐Lin organization: Chung Shan Medical University – sequence: 4 givenname: Tzu‐Chun surname: Chen fullname: Chen, Tzu‐Chun organization: Chung Shan Medical University – sequence: 5 givenname: Jui‐Hsuan surname: Yeh fullname: Yeh, Jui‐Hsuan organization: Chung Shan Medical University – sequence: 6 givenname: Meilin surname: Wang fullname: Wang, Meilin organization: School of Medicine, Chung Shan Medical University – sequence: 7 givenname: Inga surname: Wang fullname: Wang, Inga organization: University of Wisconsin‐Milwaukee – sequence: 8 givenname: Yuan‐Yen orcidid: 0000-0001-6395-4280 surname: Chang fullname: Chang, Yuan‐Yen email: cyy0709@csmu.edu.tw organization: Chung Shan Medical University Hospital – sequence: 9 givenname: Hui‐Wen surname: Lin fullname: Lin, Hui‐Wen email: d9138001@asia.edu.tw organization: Asia University |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/39268877$$D View this record in MEDLINE/PubMed |
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| Keywords | age‐related macular degeneration (AMD) retinal pigment epithelium (RPE) EUK‐134 sodium iodate (NaIO3) MAPK signaling pathway |
| Language | English |
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| Notes | Shang‐Chun Tsou, Chen‐Ju Chuang, and Chin‐Lin Hsu have contributed equally to this work and share the first authorship. Funding The authors would like to thank the Ministry of Science and Technology, Taiwan (project numbers: MOST‐109‐2320‐B‐468‐004‐MY3, MOST 111‐2320‐B‐040 ‐006 ‐MY3, and MOST‐112‐2320‐B‐468‐002‐MY3) for financially supporting this research. ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 |
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| Snippet | ABSTRACT
Age‐related macular degeneration (AMD), a leading cause of blindness, is characterized by mitochondrial dysfunction of retinal pigment epithelium... Age‐related macular degeneration (AMD), a leading cause of blindness, is characterized by mitochondrial dysfunction of retinal pigment epithelium (RPE) cells.... Age-related macular degeneration (AMD), a leading cause of blindness, is characterized by mitochondrial dysfunction of retinal pigment epithelium (RPE) cells.... |
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| SubjectTerms | adults age‐related macular degeneration (AMD) Animals Antioxidant properties antioxidants Antioxidants - pharmacology Apoptosis Apoptosis - drug effects blindness Caspase caspase-3 caspase-9 Catalase Cell Line cell lines Cell viability Deformation Deformation effects Degeneration Depolarization ecotoxicology epithelial cells Epithelium EUK‐134 Eye diseases Humans In vivo methods and tests Inhibitors Iodates Iodates - toxicity Macular degeneration Male MAP kinase MAP Kinase Signaling System - drug effects MAPK signaling pathway Membrane potential Mice Mice, Inbred BALB C Mitochondria Mitochondria - drug effects Organometallic Compounds - pharmacology Oxidative stress Oxidative Stress - drug effects p53 Protein Pigments protein synthesis Retina Retinal degeneration Retinal Degeneration - drug therapy Retinal Degeneration - pathology Retinal Degeneration - prevention & control Retinal pigment epithelium retinal pigment epithelium (RPE) Retinal Pigment Epithelium - drug effects Retinal Pigment Epithelium - pathology Retinopathy Salicylates - pharmacology Signal transduction Signal Transduction - drug effects Sodium sodium iodate (NaIO3) Tumor Suppressor Protein p53 - metabolism |
| Title | The Novel Application of EUK‐134 in Retinal Degeneration: Preventing Mitochondrial Oxidative Stress‐Triggered Retinal Pigment Epithelial Cell Apoptosis by Suppressing MAPK/p53 Signaling Pathway |
| URI | https://onlinelibrary.wiley.com/doi/abs/10.1002%2Ftox.24416 https://www.ncbi.nlm.nih.gov/pubmed/39268877 https://www.proquest.com/docview/3142382608 https://www.proquest.com/docview/3104528577 https://www.proquest.com/docview/3154244774 |
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