Label-free LC–MS/MS proteomics analyses reveal proteomic changes in oxidative stress and the SOD antioxidant strategy in TM cells
Background Treatment for glaucoma has traditionally been limited to reducing intraocular pressure (IOP). Inhibiting oxidative stress in the trabecular meshwork (TM) is regarded as a new treatment for glaucoma; however, the effects do not meet expectations. Exploring the mechanism by which oxidative...
Ausführliche Beschreibung
Autor*in: |
Li, Qian [verfasserIn] |
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E-Artikel |
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Sprache: |
Englisch |
Erschienen: |
2022 |
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Anmerkung: |
© The Author(s) 2022 |
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Übergeordnetes Werk: |
Enthalten in: Clinical proteomics - Totowa, NJ : Humana Press, 2004, 19(2022), 1 vom: 14. Mai |
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Übergeordnetes Werk: |
volume:19 ; year:2022 ; number:1 ; day:14 ; month:05 |
Links: |
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DOI / URN: |
10.1186/s12014-022-09350-4 |
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Katalog-ID: |
SPR050707655 |
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520 | |a Background Treatment for glaucoma has traditionally been limited to reducing intraocular pressure (IOP). Inhibiting oxidative stress in the trabecular meshwork (TM) is regarded as a new treatment for glaucoma; however, the effects do not meet expectations. Exploring the mechanism by which oxidative stress and antioxidant stress occur in TM cells will offer clues to aid the development of new treatments. Methods and results In our study, we cultured TM cells and used $ H_{2} %$ O_{2} $ and SOD to induce and inhibit oxidative stress, respectively. Label-free LC–MS/MS quantitative proteomic analysis was conducted to analyze the differentially expressed proteins and relevant signaling pathways. A total of 24 upregulated proteins and 18 downregulated proteins were identified under oxidative stress. PTGS2, TGFβr2 and ICAM-1 are the key proteins. The PTGS2/NF-ĸb pathway, TGF-β/Smad signaling pathway and AGE-RAGE signaling pathway in diabetic complications may be the major signaling pathways under conditions of ROS-induced damage in TM cells. Seventy-eight proteins were upregulated and 73 proteins were downregulated under antioxidant stress in TM cells. The key protein was ICAM-1, which participates in the African trypanosomiasis pathway, one of the most important pathways under antioxidant stress. Combining the results of the Venn diagram with protein–protein interactions (PPIs), ICAM-1 was identified as the major protein. Cell Counting Kit-8 (CCK-8) and western blotting (WB) were used to reveal that suppressing the expression of ICAM-1 would improve the survival of TM cells. Conclusions Key proteins and signaling pathways play important roles in the mechanisms of oxidative stress and antioxidant strategies in TM cells. ICAM-1 knockdown can suppress the apoptosis of TM cells induced by $ H_{2} %$ O_{2,} $ which may reveal new therapeutic targets and biomarkers for glaucoma. | ||
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10.1186/s12014-022-09350-4 doi (DE-627)SPR050707655 (SPR)s12014-022-09350-4-e DE-627 ger DE-627 rakwb eng Li, Qian verfasserin aut Label-free LC–MS/MS proteomics analyses reveal proteomic changes in oxidative stress and the SOD antioxidant strategy in TM cells 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2022 Background Treatment for glaucoma has traditionally been limited to reducing intraocular pressure (IOP). Inhibiting oxidative stress in the trabecular meshwork (TM) is regarded as a new treatment for glaucoma; however, the effects do not meet expectations. Exploring the mechanism by which oxidative stress and antioxidant stress occur in TM cells will offer clues to aid the development of new treatments. Methods and results In our study, we cultured TM cells and used $ H_{2} %$ O_{2} $ and SOD to induce and inhibit oxidative stress, respectively. Label-free LC–MS/MS quantitative proteomic analysis was conducted to analyze the differentially expressed proteins and relevant signaling pathways. A total of 24 upregulated proteins and 18 downregulated proteins were identified under oxidative stress. PTGS2, TGFβr2 and ICAM-1 are the key proteins. The PTGS2/NF-ĸb pathway, TGF-β/Smad signaling pathway and AGE-RAGE signaling pathway in diabetic complications may be the major signaling pathways under conditions of ROS-induced damage in TM cells. Seventy-eight proteins were upregulated and 73 proteins were downregulated under antioxidant stress in TM cells. The key protein was ICAM-1, which participates in the African trypanosomiasis pathway, one of the most important pathways under antioxidant stress. Combining the results of the Venn diagram with protein–protein interactions (PPIs), ICAM-1 was identified as the major protein. Cell Counting Kit-8 (CCK-8) and western blotting (WB) were used to reveal that suppressing the expression of ICAM-1 would improve the survival of TM cells. Conclusions Key proteins and signaling pathways play important roles in the mechanisms of oxidative stress and antioxidant strategies in TM cells. ICAM-1 knockdown can suppress the apoptosis of TM cells induced by $ H_{2} %$ O_{2,} $ which may reveal new therapeutic targets and biomarkers for glaucoma. Trabecular meshwork cells (dpeaa)DE-He213 Oxidative stress (dpeaa)DE-He213 Label-free (dpeaa)DE-He213 Proteomic analysis (dpeaa)DE-He213 SOD (dpeaa)DE-He213 Zhang, Liyu aut Xu, Yuxin (orcid)0000-0001-7138-4265 aut Enthalten in Clinical proteomics Totowa, NJ : Humana Press, 2004 19(2022), 1 vom: 14. Mai (DE-627)397618883 (DE-600)2163624-2 1559-0275 nnns volume:19 year:2022 number:1 day:14 month:05 https://dx.doi.org/10.1186/s12014-022-09350-4 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 19 2022 1 14 05 |
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10.1186/s12014-022-09350-4 doi (DE-627)SPR050707655 (SPR)s12014-022-09350-4-e DE-627 ger DE-627 rakwb eng Li, Qian verfasserin aut Label-free LC–MS/MS proteomics analyses reveal proteomic changes in oxidative stress and the SOD antioxidant strategy in TM cells 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2022 Background Treatment for glaucoma has traditionally been limited to reducing intraocular pressure (IOP). Inhibiting oxidative stress in the trabecular meshwork (TM) is regarded as a new treatment for glaucoma; however, the effects do not meet expectations. Exploring the mechanism by which oxidative stress and antioxidant stress occur in TM cells will offer clues to aid the development of new treatments. Methods and results In our study, we cultured TM cells and used $ H_{2} %$ O_{2} $ and SOD to induce and inhibit oxidative stress, respectively. Label-free LC–MS/MS quantitative proteomic analysis was conducted to analyze the differentially expressed proteins and relevant signaling pathways. A total of 24 upregulated proteins and 18 downregulated proteins were identified under oxidative stress. PTGS2, TGFβr2 and ICAM-1 are the key proteins. The PTGS2/NF-ĸb pathway, TGF-β/Smad signaling pathway and AGE-RAGE signaling pathway in diabetic complications may be the major signaling pathways under conditions of ROS-induced damage in TM cells. Seventy-eight proteins were upregulated and 73 proteins were downregulated under antioxidant stress in TM cells. The key protein was ICAM-1, which participates in the African trypanosomiasis pathway, one of the most important pathways under antioxidant stress. Combining the results of the Venn diagram with protein–protein interactions (PPIs), ICAM-1 was identified as the major protein. Cell Counting Kit-8 (CCK-8) and western blotting (WB) were used to reveal that suppressing the expression of ICAM-1 would improve the survival of TM cells. Conclusions Key proteins and signaling pathways play important roles in the mechanisms of oxidative stress and antioxidant strategies in TM cells. ICAM-1 knockdown can suppress the apoptosis of TM cells induced by $ H_{2} %$ O_{2,} $ which may reveal new therapeutic targets and biomarkers for glaucoma. Trabecular meshwork cells (dpeaa)DE-He213 Oxidative stress (dpeaa)DE-He213 Label-free (dpeaa)DE-He213 Proteomic analysis (dpeaa)DE-He213 SOD (dpeaa)DE-He213 Zhang, Liyu aut Xu, Yuxin (orcid)0000-0001-7138-4265 aut Enthalten in Clinical proteomics Totowa, NJ : Humana Press, 2004 19(2022), 1 vom: 14. Mai (DE-627)397618883 (DE-600)2163624-2 1559-0275 nnns volume:19 year:2022 number:1 day:14 month:05 https://dx.doi.org/10.1186/s12014-022-09350-4 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 19 2022 1 14 05 |
allfields_unstemmed |
10.1186/s12014-022-09350-4 doi (DE-627)SPR050707655 (SPR)s12014-022-09350-4-e DE-627 ger DE-627 rakwb eng Li, Qian verfasserin aut Label-free LC–MS/MS proteomics analyses reveal proteomic changes in oxidative stress and the SOD antioxidant strategy in TM cells 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2022 Background Treatment for glaucoma has traditionally been limited to reducing intraocular pressure (IOP). Inhibiting oxidative stress in the trabecular meshwork (TM) is regarded as a new treatment for glaucoma; however, the effects do not meet expectations. Exploring the mechanism by which oxidative stress and antioxidant stress occur in TM cells will offer clues to aid the development of new treatments. Methods and results In our study, we cultured TM cells and used $ H_{2} %$ O_{2} $ and SOD to induce and inhibit oxidative stress, respectively. Label-free LC–MS/MS quantitative proteomic analysis was conducted to analyze the differentially expressed proteins and relevant signaling pathways. A total of 24 upregulated proteins and 18 downregulated proteins were identified under oxidative stress. PTGS2, TGFβr2 and ICAM-1 are the key proteins. The PTGS2/NF-ĸb pathway, TGF-β/Smad signaling pathway and AGE-RAGE signaling pathway in diabetic complications may be the major signaling pathways under conditions of ROS-induced damage in TM cells. Seventy-eight proteins were upregulated and 73 proteins were downregulated under antioxidant stress in TM cells. The key protein was ICAM-1, which participates in the African trypanosomiasis pathway, one of the most important pathways under antioxidant stress. Combining the results of the Venn diagram with protein–protein interactions (PPIs), ICAM-1 was identified as the major protein. Cell Counting Kit-8 (CCK-8) and western blotting (WB) were used to reveal that suppressing the expression of ICAM-1 would improve the survival of TM cells. Conclusions Key proteins and signaling pathways play important roles in the mechanisms of oxidative stress and antioxidant strategies in TM cells. ICAM-1 knockdown can suppress the apoptosis of TM cells induced by $ H_{2} %$ O_{2,} $ which may reveal new therapeutic targets and biomarkers for glaucoma. Trabecular meshwork cells (dpeaa)DE-He213 Oxidative stress (dpeaa)DE-He213 Label-free (dpeaa)DE-He213 Proteomic analysis (dpeaa)DE-He213 SOD (dpeaa)DE-He213 Zhang, Liyu aut Xu, Yuxin (orcid)0000-0001-7138-4265 aut Enthalten in Clinical proteomics Totowa, NJ : Humana Press, 2004 19(2022), 1 vom: 14. Mai (DE-627)397618883 (DE-600)2163624-2 1559-0275 nnns volume:19 year:2022 number:1 day:14 month:05 https://dx.doi.org/10.1186/s12014-022-09350-4 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 19 2022 1 14 05 |
allfieldsGer |
10.1186/s12014-022-09350-4 doi (DE-627)SPR050707655 (SPR)s12014-022-09350-4-e DE-627 ger DE-627 rakwb eng Li, Qian verfasserin aut Label-free LC–MS/MS proteomics analyses reveal proteomic changes in oxidative stress and the SOD antioxidant strategy in TM cells 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2022 Background Treatment for glaucoma has traditionally been limited to reducing intraocular pressure (IOP). Inhibiting oxidative stress in the trabecular meshwork (TM) is regarded as a new treatment for glaucoma; however, the effects do not meet expectations. Exploring the mechanism by which oxidative stress and antioxidant stress occur in TM cells will offer clues to aid the development of new treatments. Methods and results In our study, we cultured TM cells and used $ H_{2} %$ O_{2} $ and SOD to induce and inhibit oxidative stress, respectively. Label-free LC–MS/MS quantitative proteomic analysis was conducted to analyze the differentially expressed proteins and relevant signaling pathways. A total of 24 upregulated proteins and 18 downregulated proteins were identified under oxidative stress. PTGS2, TGFβr2 and ICAM-1 are the key proteins. The PTGS2/NF-ĸb pathway, TGF-β/Smad signaling pathway and AGE-RAGE signaling pathway in diabetic complications may be the major signaling pathways under conditions of ROS-induced damage in TM cells. Seventy-eight proteins were upregulated and 73 proteins were downregulated under antioxidant stress in TM cells. The key protein was ICAM-1, which participates in the African trypanosomiasis pathway, one of the most important pathways under antioxidant stress. Combining the results of the Venn diagram with protein–protein interactions (PPIs), ICAM-1 was identified as the major protein. Cell Counting Kit-8 (CCK-8) and western blotting (WB) were used to reveal that suppressing the expression of ICAM-1 would improve the survival of TM cells. Conclusions Key proteins and signaling pathways play important roles in the mechanisms of oxidative stress and antioxidant strategies in TM cells. ICAM-1 knockdown can suppress the apoptosis of TM cells induced by $ H_{2} %$ O_{2,} $ which may reveal new therapeutic targets and biomarkers for glaucoma. Trabecular meshwork cells (dpeaa)DE-He213 Oxidative stress (dpeaa)DE-He213 Label-free (dpeaa)DE-He213 Proteomic analysis (dpeaa)DE-He213 SOD (dpeaa)DE-He213 Zhang, Liyu aut Xu, Yuxin (orcid)0000-0001-7138-4265 aut Enthalten in Clinical proteomics Totowa, NJ : Humana Press, 2004 19(2022), 1 vom: 14. Mai (DE-627)397618883 (DE-600)2163624-2 1559-0275 nnns volume:19 year:2022 number:1 day:14 month:05 https://dx.doi.org/10.1186/s12014-022-09350-4 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 19 2022 1 14 05 |
allfieldsSound |
10.1186/s12014-022-09350-4 doi (DE-627)SPR050707655 (SPR)s12014-022-09350-4-e DE-627 ger DE-627 rakwb eng Li, Qian verfasserin aut Label-free LC–MS/MS proteomics analyses reveal proteomic changes in oxidative stress and the SOD antioxidant strategy in TM cells 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2022 Background Treatment for glaucoma has traditionally been limited to reducing intraocular pressure (IOP). Inhibiting oxidative stress in the trabecular meshwork (TM) is regarded as a new treatment for glaucoma; however, the effects do not meet expectations. Exploring the mechanism by which oxidative stress and antioxidant stress occur in TM cells will offer clues to aid the development of new treatments. Methods and results In our study, we cultured TM cells and used $ H_{2} %$ O_{2} $ and SOD to induce and inhibit oxidative stress, respectively. Label-free LC–MS/MS quantitative proteomic analysis was conducted to analyze the differentially expressed proteins and relevant signaling pathways. A total of 24 upregulated proteins and 18 downregulated proteins were identified under oxidative stress. PTGS2, TGFβr2 and ICAM-1 are the key proteins. The PTGS2/NF-ĸb pathway, TGF-β/Smad signaling pathway and AGE-RAGE signaling pathway in diabetic complications may be the major signaling pathways under conditions of ROS-induced damage in TM cells. Seventy-eight proteins were upregulated and 73 proteins were downregulated under antioxidant stress in TM cells. The key protein was ICAM-1, which participates in the African trypanosomiasis pathway, one of the most important pathways under antioxidant stress. Combining the results of the Venn diagram with protein–protein interactions (PPIs), ICAM-1 was identified as the major protein. Cell Counting Kit-8 (CCK-8) and western blotting (WB) were used to reveal that suppressing the expression of ICAM-1 would improve the survival of TM cells. Conclusions Key proteins and signaling pathways play important roles in the mechanisms of oxidative stress and antioxidant strategies in TM cells. ICAM-1 knockdown can suppress the apoptosis of TM cells induced by $ H_{2} %$ O_{2,} $ which may reveal new therapeutic targets and biomarkers for glaucoma. Trabecular meshwork cells (dpeaa)DE-He213 Oxidative stress (dpeaa)DE-He213 Label-free (dpeaa)DE-He213 Proteomic analysis (dpeaa)DE-He213 SOD (dpeaa)DE-He213 Zhang, Liyu aut Xu, Yuxin (orcid)0000-0001-7138-4265 aut Enthalten in Clinical proteomics Totowa, NJ : Humana Press, 2004 19(2022), 1 vom: 14. Mai (DE-627)397618883 (DE-600)2163624-2 1559-0275 nnns volume:19 year:2022 number:1 day:14 month:05 https://dx.doi.org/10.1186/s12014-022-09350-4 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 19 2022 1 14 05 |
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Enthalten in Clinical proteomics 19(2022), 1 vom: 14. Mai volume:19 year:2022 number:1 day:14 month:05 |
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Li, Qian misc Trabecular meshwork cells misc Oxidative stress misc Label-free misc Proteomic analysis misc SOD Label-free LC–MS/MS proteomics analyses reveal proteomic changes in oxidative stress and the SOD antioxidant strategy in TM cells |
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Label-free LC–MS/MS proteomics analyses reveal proteomic changes in oxidative stress and the SOD antioxidant strategy in TM cells Trabecular meshwork cells (dpeaa)DE-He213 Oxidative stress (dpeaa)DE-He213 Label-free (dpeaa)DE-He213 Proteomic analysis (dpeaa)DE-He213 SOD (dpeaa)DE-He213 |
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label-free lc–ms/ms proteomics analyses reveal proteomic changes in oxidative stress and the sod antioxidant strategy in tm cells |
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Label-free LC–MS/MS proteomics analyses reveal proteomic changes in oxidative stress and the SOD antioxidant strategy in TM cells |
abstract |
Background Treatment for glaucoma has traditionally been limited to reducing intraocular pressure (IOP). Inhibiting oxidative stress in the trabecular meshwork (TM) is regarded as a new treatment for glaucoma; however, the effects do not meet expectations. Exploring the mechanism by which oxidative stress and antioxidant stress occur in TM cells will offer clues to aid the development of new treatments. Methods and results In our study, we cultured TM cells and used $ H_{2} %$ O_{2} $ and SOD to induce and inhibit oxidative stress, respectively. Label-free LC–MS/MS quantitative proteomic analysis was conducted to analyze the differentially expressed proteins and relevant signaling pathways. A total of 24 upregulated proteins and 18 downregulated proteins were identified under oxidative stress. PTGS2, TGFβr2 and ICAM-1 are the key proteins. The PTGS2/NF-ĸb pathway, TGF-β/Smad signaling pathway and AGE-RAGE signaling pathway in diabetic complications may be the major signaling pathways under conditions of ROS-induced damage in TM cells. Seventy-eight proteins were upregulated and 73 proteins were downregulated under antioxidant stress in TM cells. The key protein was ICAM-1, which participates in the African trypanosomiasis pathway, one of the most important pathways under antioxidant stress. Combining the results of the Venn diagram with protein–protein interactions (PPIs), ICAM-1 was identified as the major protein. Cell Counting Kit-8 (CCK-8) and western blotting (WB) were used to reveal that suppressing the expression of ICAM-1 would improve the survival of TM cells. Conclusions Key proteins and signaling pathways play important roles in the mechanisms of oxidative stress and antioxidant strategies in TM cells. ICAM-1 knockdown can suppress the apoptosis of TM cells induced by $ H_{2} %$ O_{2,} $ which may reveal new therapeutic targets and biomarkers for glaucoma. © The Author(s) 2022 |
abstractGer |
Background Treatment for glaucoma has traditionally been limited to reducing intraocular pressure (IOP). Inhibiting oxidative stress in the trabecular meshwork (TM) is regarded as a new treatment for glaucoma; however, the effects do not meet expectations. Exploring the mechanism by which oxidative stress and antioxidant stress occur in TM cells will offer clues to aid the development of new treatments. Methods and results In our study, we cultured TM cells and used $ H_{2} %$ O_{2} $ and SOD to induce and inhibit oxidative stress, respectively. Label-free LC–MS/MS quantitative proteomic analysis was conducted to analyze the differentially expressed proteins and relevant signaling pathways. A total of 24 upregulated proteins and 18 downregulated proteins were identified under oxidative stress. PTGS2, TGFβr2 and ICAM-1 are the key proteins. The PTGS2/NF-ĸb pathway, TGF-β/Smad signaling pathway and AGE-RAGE signaling pathway in diabetic complications may be the major signaling pathways under conditions of ROS-induced damage in TM cells. Seventy-eight proteins were upregulated and 73 proteins were downregulated under antioxidant stress in TM cells. The key protein was ICAM-1, which participates in the African trypanosomiasis pathway, one of the most important pathways under antioxidant stress. Combining the results of the Venn diagram with protein–protein interactions (PPIs), ICAM-1 was identified as the major protein. Cell Counting Kit-8 (CCK-8) and western blotting (WB) were used to reveal that suppressing the expression of ICAM-1 would improve the survival of TM cells. Conclusions Key proteins and signaling pathways play important roles in the mechanisms of oxidative stress and antioxidant strategies in TM cells. ICAM-1 knockdown can suppress the apoptosis of TM cells induced by $ H_{2} %$ O_{2,} $ which may reveal new therapeutic targets and biomarkers for glaucoma. © The Author(s) 2022 |
abstract_unstemmed |
Background Treatment for glaucoma has traditionally been limited to reducing intraocular pressure (IOP). Inhibiting oxidative stress in the trabecular meshwork (TM) is regarded as a new treatment for glaucoma; however, the effects do not meet expectations. Exploring the mechanism by which oxidative stress and antioxidant stress occur in TM cells will offer clues to aid the development of new treatments. Methods and results In our study, we cultured TM cells and used $ H_{2} %$ O_{2} $ and SOD to induce and inhibit oxidative stress, respectively. Label-free LC–MS/MS quantitative proteomic analysis was conducted to analyze the differentially expressed proteins and relevant signaling pathways. A total of 24 upregulated proteins and 18 downregulated proteins were identified under oxidative stress. PTGS2, TGFβr2 and ICAM-1 are the key proteins. The PTGS2/NF-ĸb pathway, TGF-β/Smad signaling pathway and AGE-RAGE signaling pathway in diabetic complications may be the major signaling pathways under conditions of ROS-induced damage in TM cells. Seventy-eight proteins were upregulated and 73 proteins were downregulated under antioxidant stress in TM cells. The key protein was ICAM-1, which participates in the African trypanosomiasis pathway, one of the most important pathways under antioxidant stress. Combining the results of the Venn diagram with protein–protein interactions (PPIs), ICAM-1 was identified as the major protein. Cell Counting Kit-8 (CCK-8) and western blotting (WB) were used to reveal that suppressing the expression of ICAM-1 would improve the survival of TM cells. Conclusions Key proteins and signaling pathways play important roles in the mechanisms of oxidative stress and antioxidant strategies in TM cells. ICAM-1 knockdown can suppress the apoptosis of TM cells induced by $ H_{2} %$ O_{2,} $ which may reveal new therapeutic targets and biomarkers for glaucoma. © The Author(s) 2022 |
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Label-free LC–MS/MS proteomics analyses reveal proteomic changes in oxidative stress and the SOD antioxidant strategy in TM cells |
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Inhibiting oxidative stress in the trabecular meshwork (TM) is regarded as a new treatment for glaucoma; however, the effects do not meet expectations. Exploring the mechanism by which oxidative stress and antioxidant stress occur in TM cells will offer clues to aid the development of new treatments. Methods and results In our study, we cultured TM cells and used $ H_{2} %$ O_{2} $ and SOD to induce and inhibit oxidative stress, respectively. Label-free LC–MS/MS quantitative proteomic analysis was conducted to analyze the differentially expressed proteins and relevant signaling pathways. A total of 24 upregulated proteins and 18 downregulated proteins were identified under oxidative stress. PTGS2, TGFβr2 and ICAM-1 are the key proteins. The PTGS2/NF-ĸb pathway, TGF-β/Smad signaling pathway and AGE-RAGE signaling pathway in diabetic complications may be the major signaling pathways under conditions of ROS-induced damage in TM cells. Seventy-eight proteins were upregulated and 73 proteins were downregulated under antioxidant stress in TM cells. The key protein was ICAM-1, which participates in the African trypanosomiasis pathway, one of the most important pathways under antioxidant stress. Combining the results of the Venn diagram with protein–protein interactions (PPIs), ICAM-1 was identified as the major protein. Cell Counting Kit-8 (CCK-8) and western blotting (WB) were used to reveal that suppressing the expression of ICAM-1 would improve the survival of TM cells. Conclusions Key proteins and signaling pathways play important roles in the mechanisms of oxidative stress and antioxidant strategies in TM cells. ICAM-1 knockdown can suppress the apoptosis of TM cells induced by $ H_{2} %$ O_{2,} $ which may reveal new therapeutic targets and biomarkers for glaucoma.</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Trabecular meshwork cells</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Oxidative stress</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Label-free</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Proteomic analysis</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">SOD</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Zhang, Liyu</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Xu, Yuxin</subfield><subfield code="0">(orcid)0000-0001-7138-4265</subfield><subfield code="4">aut</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">Enthalten in</subfield><subfield code="t">Clinical proteomics</subfield><subfield code="d">Totowa, NJ : Humana Press, 2004</subfield><subfield code="g">19(2022), 1 vom: 14. 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