PubMed:26555588 / 559-1771
Annnotations
GoldHamster
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of ex vivo rabbit corneas showed that NM exposure increased apoptotic cell death, epithelial thickness, epithelial-stromal separation, and levels of vascular endothelial growth factor, cyclooxygenase 2, and matrix metalloproteinase-9. In HCE cells, NM exposure resulted in a dose-dependent decrease in cell viability and proliferation, which was associated with DNA damage in terms of an increase in p53 ser15, total p53, and H2A.X ser139 levels. NM exposure also induced caspase-3 and poly ADP ribose polymerase cleavage, suggesting their involvement in NM-induced apoptotic death in the rabbit cornea and HCE cells. Similar to rabbit cornea, NM exposure caused an increase in cyclooxygenase 2, matrix metalloproteinase-9, and vascular endothelial growth factor levels in HCE cells, indicating a role of these molecules and related pathways in NM-induced corneal inflammation, epithelial-stromal separation, and neovascularization. NM exposure also induced activation of activator protein 1 transcription factor proteins and upstream signaling pathways including mitogen-activated protein kinases and Akt protein kinase, suggesting that these could be key factors involved in NM-induced corneal injury."}
PubMed_Structured_Abstracts
{"project":"PubMed_Structured_Abstracts","denotations":[{"id":"T3","span":{"begin":0,"end":1212},"obj":"RESULTS"}],"text":"Analysis of ex vivo rabbit corneas showed that NM exposure increased apoptotic cell death, epithelial thickness, epithelial-stromal separation, and levels of vascular endothelial growth factor, cyclooxygenase 2, and matrix metalloproteinase-9. In HCE cells, NM exposure resulted in a dose-dependent decrease in cell viability and proliferation, which was associated with DNA damage in terms of an increase in p53 ser15, total p53, and H2A.X ser139 levels. NM exposure also induced caspase-3 and poly ADP ribose polymerase cleavage, suggesting their involvement in NM-induced apoptotic death in the rabbit cornea and HCE cells. Similar to rabbit cornea, NM exposure caused an increase in cyclooxygenase 2, matrix metalloproteinase-9, and vascular endothelial growth factor levels in HCE cells, indicating a role of these molecules and related pathways in NM-induced corneal inflammation, epithelial-stromal separation, and neovascularization. NM exposure also induced activation of activator protein 1 transcription factor proteins and upstream signaling pathways including mitogen-activated protein kinases and Akt protein kinase, suggesting that these could be key factors involved in NM-induced corneal injury."}
Goldhamster2_Cellosaurus
{"project":"Goldhamster2_Cellosaurus","denotations":[{"id":"T4","span":{"begin":247,"end":250},"obj":"CVCL_1272|Transformed_cell_line|Homo sapiens"},{"id":"T5","span":{"begin":247,"end":250},"obj":"CVCL_M619|Cancer_cell_line|Homo sapiens"},{"id":"T6","span":{"begin":282,"end":283},"obj":"CVCL_6479|Finite_cell_line|Mus musculus"},{"id":"T7","span":{"begin":394,"end":396},"obj":"CVCL_8754|Cancer_cell_line|Homo sapiens"},{"id":"T8","span":{"begin":394,"end":396},"obj":"CVCL_H241|Cancer_cell_line|Homo sapiens"},{"id":"T9","span":{"begin":616,"end":619},"obj":"CVCL_1272|Transformed_cell_line|Homo sapiens"},{"id":"T10","span":{"begin":616,"end":619},"obj":"CVCL_M619|Cancer_cell_line|Homo sapiens"},{"id":"T11","span":{"begin":672,"end":674},"obj":"CVCL_8754|Cancer_cell_line|Homo sapiens"},{"id":"T12","span":{"begin":672,"end":674},"obj":"CVCL_H241|Cancer_cell_line|Homo sapiens"},{"id":"T13","span":{"begin":782,"end":785},"obj":"CVCL_1272|Transformed_cell_line|Homo sapiens"},{"id":"T14","span":{"begin":782,"end":785},"obj":"CVCL_M619|Cancer_cell_line|Homo sapiens"},{"id":"T15","span":{"begin":804,"end":805},"obj":"CVCL_6479|Finite_cell_line|Mus musculus"},{"id":"T16","span":{"begin":967,"end":977},"obj":"CVCL_C410|Hybridoma|Mus musculus"},{"id":"T17","span":{"begin":981,"end":990},"obj":"CVCL_C410|Hybridoma|Mus musculus"},{"id":"T18","span":{"begin":1081,"end":1090},"obj":"CVCL_C410|Hybridoma|Mus musculus"}],"text":"Analysis of ex vivo rabbit corneas showed that NM exposure increased apoptotic cell death, epithelial thickness, epithelial-stromal separation, and levels of vascular endothelial growth factor, cyclooxygenase 2, and matrix metalloproteinase-9. In HCE cells, NM exposure resulted in a dose-dependent decrease in cell viability and proliferation, which was associated with DNA damage in terms of an increase in p53 ser15, total p53, and H2A.X ser139 levels. NM exposure also induced caspase-3 and poly ADP ribose polymerase cleavage, suggesting their involvement in NM-induced apoptotic death in the rabbit cornea and HCE cells. Similar to rabbit cornea, NM exposure caused an increase in cyclooxygenase 2, matrix metalloproteinase-9, and vascular endothelial growth factor levels in HCE cells, indicating a role of these molecules and related pathways in NM-induced corneal inflammation, epithelial-stromal separation, and neovascularization. NM exposure also induced activation of activator protein 1 transcription factor proteins and upstream signaling pathways including mitogen-activated protein kinases and Akt protein kinase, suggesting that these could be key factors involved in NM-induced corneal injury."}
Inflammaging
{"project":"Inflammaging","denotations":[{"id":"T7","span":{"begin":0,"end":243},"obj":"Sentence"},{"id":"T8","span":{"begin":244,"end":455},"obj":"Sentence"},{"id":"T9","span":{"begin":456,"end":626},"obj":"Sentence"},{"id":"T10","span":{"begin":627,"end":941},"obj":"Sentence"},{"id":"T11","span":{"begin":942,"end":1212},"obj":"Sentence"},{"id":"T7","span":{"begin":0,"end":243},"obj":"Sentence"},{"id":"T8","span":{"begin":244,"end":455},"obj":"Sentence"},{"id":"T9","span":{"begin":456,"end":626},"obj":"Sentence"},{"id":"T10","span":{"begin":627,"end":941},"obj":"Sentence"},{"id":"T11","span":{"begin":942,"end":1212},"obj":"Sentence"}],"text":"Analysis of ex vivo rabbit corneas showed that NM exposure increased apoptotic cell death, epithelial thickness, epithelial-stromal separation, and levels of vascular endothelial growth factor, cyclooxygenase 2, and matrix metalloproteinase-9. In HCE cells, NM exposure resulted in a dose-dependent decrease in cell viability and proliferation, which was associated with DNA damage in terms of an increase in p53 ser15, total p53, and H2A.X ser139 levels. NM exposure also induced caspase-3 and poly ADP ribose polymerase cleavage, suggesting their involvement in NM-induced apoptotic death in the rabbit cornea and HCE cells. Similar to rabbit cornea, NM exposure caused an increase in cyclooxygenase 2, matrix metalloproteinase-9, and vascular endothelial growth factor levels in HCE cells, indicating a role of these molecules and related pathways in NM-induced corneal inflammation, epithelial-stromal separation, and neovascularization. NM exposure also induced activation of activator protein 1 transcription factor proteins and upstream signaling pathways including mitogen-activated protein kinases and Akt protein kinase, suggesting that these could be key factors involved in NM-induced corneal injury."}