About Enhancer
| Enhancer ID: | E_02_0332 |
| Species: | human |
| Position : | chr17:34252627-34254627   |
| Biosample name: | |
| Experiment class : | High+Lowthroughput |
| Enhancer type: | Enhancer |
| Disease: | Diabetic retinopathy, inflammation |
| Pubmed ID: | 29678838 |
| Enhancer experiment: | Enzyme-linked immunosorbent assay(ELISA),Western blot,Immunofluorescence, |
| Enhancer experiment description: | Treatment of human retinal Mller cells with high-glucose induced significant upregulation of ROCK-1, VEGF, and MCP-1/CCL2. Fasudil co-treatment normalized the high-glucose-induced upregulation of these mediators. Similarly, fasudil attenuated high-glucose-induced enhanced immunoreactivity for ROCK-1 and VEGF. Diabetes induced upregulation of ROCK-1, p-ERK , p-NF-?B and iNOS expression in retinas of mice. Constant fasudil intake from the onset of diabetes did not affect the metabolic status of diabetic mice but it attenuated diabetes-induced upregulation of these inflammatory signaling pathways.Our finding suggests that Rho-associated protein kinase-1 activation mediates regulation of inflammatory signaling pathways in diabetic retina. |
About Target gene
| Target gene : | CCL2(GDCF-2,HC11,HSMCR30,MCAF,MCP-1,MCP1,SCYA2,SMC-CF),Rho |
| Strong evidence: | qRT-PCR,qPCR,ChIP,3C |
| Less strong evidence: | RNA-Seq |
| Target gene experiment description: | Treatment of human retinal Mller cells with high-glucose induced significant upregulation of ROCK-1, VEGF, and MCP-1/CCL2. Fasudil co-treatment normalized the high-glucose-induced upregulation of these mediators. Similarly, fasudil attenuated high-glucose-induced enhanced immunoreactivity for ROCK-1 and VEGF. Diabetes induced upregulation of ROCK-1, p-ERK , p-NF-?B and iNOS expression in retinas of mice. Constant fasudil intake from the onset of diabetes did not affect the metabolic status of diabetic mice but it attenuated diabetes-induced upregulation of these inflammatory signaling pathways.Our finding suggests that Rho-associated protein kinase-1 activation mediates regulation of inflammatory signaling pathways in diabetic retina.;Treatment of human retinal Mller cells with high-glucose induced significant upregulation of ROCK-1, VEGF, and MCP-1/CCL2. Fasudil co-treatment normalized the high-glucose-induced upregulation of these mediators. Similarly, fasudil attenuated high-glucose-induced enhanced immunoreactivity for ROCK-1 and VEGF. Diabetes induced upregulation of ROCK-1, p-ERK , p-NF-?B and iNOS expression in retinas of mice. Constant fasudil intake from the onset of diabetes did not affect the metabolic status of diabetic mice but it attenuated diabetes-induced upregulation of these inflammatory signaling pathways.Our finding suggests that Rho-associated protein kinase-1 activation mediates regulation of inflammatory signaling pathways in diabetic retina. |
About TF
| TF name : | -- |
| TF experiment: | Enzyme-linked immunosorbent assay(ELISA),Western blot,Immunofluorescence, |
| TF experiment description: | Treatment of human retinal Mller cells with high-glucose induced significant upregulation of ROCK-1, VEGF, and MCP-1/CCL2. Fasudil co-treatment normalized the high-glucose-induced upregulation of these mediators. Similarly, fasudil attenuated high-glucose-induced enhanced immunoreactivity for ROCK-1 and VEGF. Diabetes induced upregulation of ROCK-1, p-ERK , p-NF-?B and iNOS expression in retinas of mice. Constant fasudil intake from the onset of diabetes did not affect the metabolic status of diabetic mice but it attenuated diabetes-induced upregulation of these inflammatory signaling pathways.Our finding suggests that Rho-associated protein kinase-1 activation mediates regulation of inflammatory signaling pathways in diabetic retina.;Treatment of human retinal Mller cells with high-glucose induced significant upregulation of ROCK-1, VEGF, and MCP-1/CCL2. Fasudil co-treatment normalized the high-glucose-induced upregulation of these mediators. Similarly, fasudil attenuated high-glucose-induced enhanced immunoreactivity for ROCK-1 and VEGF. Diabetes induced upregulation of ROCK-1, p-ERK , p-NF-?B and iNOS expression in retinas of mice. Constant fasudil intake from the onset of diabetes did not affect the metabolic status of diabetic mice but it attenuated diabetes-induced upregulation of these inflammatory signaling pathways.Our finding suggests that Rho-associated protein kinase-1 activation mediates regulation of inflammatory signaling pathways in diabetic retina. |
About Function
| Enhancer function : | Treatment of human retinal Mller cells with high-glucose induced significant upregulation of ROCK-1, VEGF, and MCP-1/CCL2. Fasudil co-treatment normalized the high-glucose-induced upregulation of these mediators. Similarly, fasudil attenuated high-glucose-induced enhanced immunoreactivity for ROCK-1 and VEGF. Diabetes induced upregulation of ROCK-1, p-ERK , p-NF-?B and iNOS expression in retinas of mice. Constant fasudil intake from the onset of diabetes did not affect the metabolic status of diabetic mice but it attenuated diabetes-induced upregulation of these inflammatory signaling pathways.Our finding suggests that Rho-associated protein kinase-1 activation mediates regulation of inflammatory signaling pathways in diabetic retina. |
| Enhancer function experiment: | Immunohistochemical staining |
| Enhancer function experiment description: |
Treatment of human retinal Mller cells with high-glucose induced significant upregulation of ROCK-1, VEGF, and MCP-1/CCL2. Fasudil co-treatment normalized the high-glucose-induced upregulation of these mediators. Similarly, fasudil attenuated high-glucose-induced enhanced immunoreactivity for ROCK-1 and VEGF. Diabetes induced upregulation of ROCK-1, p-ERK , p-NF-?B and iNOS expression in retinas of mice. Constant fasudil intake from the onset of diabetes did not affect the metabolic status of diabetic mice but it attenuated diabetes-induced upregulation of these inflammatory signaling pathways.Our finding suggests that Rho-associated protein kinase-1 activation mediates regulation of inflammatory signaling pathways in diabetic retina. |
About SNP
| SNP ID: | -- |
Upstream Pathway Annotation of TF
| GeneName | Pathway Name | Source | Gene Number |
|---|
Enhancer associated network
The number on yellow line represents the distance between enhancer and
target gene