Ignet

Gene Information

Gene symbol: MIRN155

Gene name: microRNA 155

HGNC ID: 31542

Related Genes

#	Gene Symbol	Number of hits
1	IL17A	1 hits
2	IL6	1 hits
3	MAPK1	1 hits
4	MIRN126	1 hits
5	NPHS1	1 hits
6	SIRT1	1 hits
7	TGFA	1 hits
8	WT1	1 hits

Related Sentences

#	PMID	Sentence
1	24969676	MicroRNA-155 deficiency promotes nephrin acetylation and attenuates renal damage in hyperglycemia-induced nephropathy.
2	24969676	Diabetes also significantly decreased the levels of nephrin and acetylated nephrin, whereas the expression of miR-155 was markedly increased in diabetes group when compared with control.
3	24969676	MiR-155(-/-) mice showed significantly increased expression of nephrin, acetylated nephrin, and Wilm's tumor-1 protein (WT-1) when compared with wild-type control.
4	24969676	MiR-155 deficiency results in significantly decrease in IL-17A expression both in vivo and in vitro.
5	24969676	And the increased expression of WT-1, nephrin, and ac-nephrin was reversed with additional treatment of rmIL-17.
6	24969676	In conclusion, miR-155 deficiency promotes nephrin acetylation and attenuates renal damage in hyperglycemia-induced nephropathy.
7	24969676	This was associated with inhibited IL-17 production through enhancement of SOCS1 expression.
8	24969676	MicroRNA-155 deficiency promotes nephrin acetylation and attenuates renal damage in hyperglycemia-induced nephropathy.
9	24969676	Diabetes also significantly decreased the levels of nephrin and acetylated nephrin, whereas the expression of miR-155 was markedly increased in diabetes group when compared with control.
10	24969676	MiR-155(-/-) mice showed significantly increased expression of nephrin, acetylated nephrin, and Wilm's tumor-1 protein (WT-1) when compared with wild-type control.
11	24969676	MiR-155 deficiency results in significantly decrease in IL-17A expression both in vivo and in vitro.
12	24969676	And the increased expression of WT-1, nephrin, and ac-nephrin was reversed with additional treatment of rmIL-17.
13	24969676	In conclusion, miR-155 deficiency promotes nephrin acetylation and attenuates renal damage in hyperglycemia-induced nephropathy.
14	24969676	This was associated with inhibited IL-17 production through enhancement of SOCS1 expression.
15	24969676	MicroRNA-155 deficiency promotes nephrin acetylation and attenuates renal damage in hyperglycemia-induced nephropathy.
16	24969676	Diabetes also significantly decreased the levels of nephrin and acetylated nephrin, whereas the expression of miR-155 was markedly increased in diabetes group when compared with control.
17	24969676	MiR-155(-/-) mice showed significantly increased expression of nephrin, acetylated nephrin, and Wilm's tumor-1 protein (WT-1) when compared with wild-type control.
18	24969676	MiR-155 deficiency results in significantly decrease in IL-17A expression both in vivo and in vitro.
19	24969676	And the increased expression of WT-1, nephrin, and ac-nephrin was reversed with additional treatment of rmIL-17.
20	24969676	In conclusion, miR-155 deficiency promotes nephrin acetylation and attenuates renal damage in hyperglycemia-induced nephropathy.
21	24969676	This was associated with inhibited IL-17 production through enhancement of SOCS1 expression.
22	24969676	MicroRNA-155 deficiency promotes nephrin acetylation and attenuates renal damage in hyperglycemia-induced nephropathy.
23	24969676	Diabetes also significantly decreased the levels of nephrin and acetylated nephrin, whereas the expression of miR-155 was markedly increased in diabetes group when compared with control.
24	24969676	MiR-155(-/-) mice showed significantly increased expression of nephrin, acetylated nephrin, and Wilm's tumor-1 protein (WT-1) when compared with wild-type control.
25	24969676	MiR-155 deficiency results in significantly decrease in IL-17A expression both in vivo and in vitro.
26	24969676	And the increased expression of WT-1, nephrin, and ac-nephrin was reversed with additional treatment of rmIL-17.
27	24969676	In conclusion, miR-155 deficiency promotes nephrin acetylation and attenuates renal damage in hyperglycemia-induced nephropathy.
28	24969676	This was associated with inhibited IL-17 production through enhancement of SOCS1 expression.
29	24969676	MicroRNA-155 deficiency promotes nephrin acetylation and attenuates renal damage in hyperglycemia-induced nephropathy.
30	24969676	Diabetes also significantly decreased the levels of nephrin and acetylated nephrin, whereas the expression of miR-155 was markedly increased in diabetes group when compared with control.
31	24969676	MiR-155(-/-) mice showed significantly increased expression of nephrin, acetylated nephrin, and Wilm's tumor-1 protein (WT-1) when compared with wild-type control.
32	24969676	MiR-155 deficiency results in significantly decrease in IL-17A expression both in vivo and in vitro.
33	24969676	And the increased expression of WT-1, nephrin, and ac-nephrin was reversed with additional treatment of rmIL-17.
34	24969676	In conclusion, miR-155 deficiency promotes nephrin acetylation and attenuates renal damage in hyperglycemia-induced nephropathy.
35	24969676	This was associated with inhibited IL-17 production through enhancement of SOCS1 expression.
36	28471953	Association of microRNA-155, interleukin 17A, and proteinuria in preeclampsia.
37	29981742	Association of Elevated Urinary miR-126, miR-155, and miR-29b with Diabetic Kidney Disease.
38	29981742	We profiled 754 miRNAs in pooled urine samples from DKD patients (n = 20), detecting significantly increased miR-126, miR-155, and miR-29b compared with controls (n = 20).
39	29981742	These results were confirmed in an independent cohort of 89 DKD patients, 62 diabetic patients without DKD, and 41 controls: miR-126 (2.8-fold increase; P < 0.0001), miR-155 (1.8-fold increase; P < 0.001), and miR-29b (4.6-fold increase; P = 0.024).
40	29981742	Laser-capture microdissection of renal biopsy specimens, followed by quantitative RT-PCR, detected miR-155 in glomeruli and proximal and distal tubules, whereas miR-126 and miR-29b were most abundant in glomerular extracts.
41	29981742	Significantly increased miR-126 and miR-29b were detected in GEnC conditioned medium in response to tumor necrosis factor-α and transforming growth factor-β1, respectively.
42	29981742	Association of Elevated Urinary miR-126, miR-155, and miR-29b with Diabetic Kidney Disease.
43	29981742	We profiled 754 miRNAs in pooled urine samples from DKD patients (n = 20), detecting significantly increased miR-126, miR-155, and miR-29b compared with controls (n = 20).
44	29981742	These results were confirmed in an independent cohort of 89 DKD patients, 62 diabetic patients without DKD, and 41 controls: miR-126 (2.8-fold increase; P < 0.0001), miR-155 (1.8-fold increase; P < 0.001), and miR-29b (4.6-fold increase; P = 0.024).
45	29981742	Laser-capture microdissection of renal biopsy specimens, followed by quantitative RT-PCR, detected miR-155 in glomeruli and proximal and distal tubules, whereas miR-126 and miR-29b were most abundant in glomerular extracts.
46	29981742	Significantly increased miR-126 and miR-29b were detected in GEnC conditioned medium in response to tumor necrosis factor-α and transforming growth factor-β1, respectively.
47	29981742	Association of Elevated Urinary miR-126, miR-155, and miR-29b with Diabetic Kidney Disease.
48	29981742	We profiled 754 miRNAs in pooled urine samples from DKD patients (n = 20), detecting significantly increased miR-126, miR-155, and miR-29b compared with controls (n = 20).
49	29981742	These results were confirmed in an independent cohort of 89 DKD patients, 62 diabetic patients without DKD, and 41 controls: miR-126 (2.8-fold increase; P < 0.0001), miR-155 (1.8-fold increase; P < 0.001), and miR-29b (4.6-fold increase; P = 0.024).
50	29981742	Laser-capture microdissection of renal biopsy specimens, followed by quantitative RT-PCR, detected miR-155 in glomeruli and proximal and distal tubules, whereas miR-126 and miR-29b were most abundant in glomerular extracts.
51	29981742	Significantly increased miR-126 and miR-29b were detected in GEnC conditioned medium in response to tumor necrosis factor-α and transforming growth factor-β1, respectively.
52	29981742	Association of Elevated Urinary miR-126, miR-155, and miR-29b with Diabetic Kidney Disease.
53	29981742	We profiled 754 miRNAs in pooled urine samples from DKD patients (n = 20), detecting significantly increased miR-126, miR-155, and miR-29b compared with controls (n = 20).
54	29981742	These results were confirmed in an independent cohort of 89 DKD patients, 62 diabetic patients without DKD, and 41 controls: miR-126 (2.8-fold increase; P < 0.0001), miR-155 (1.8-fold increase; P < 0.001), and miR-29b (4.6-fold increase; P = 0.024).
55	29981742	Laser-capture microdissection of renal biopsy specimens, followed by quantitative RT-PCR, detected miR-155 in glomeruli and proximal and distal tubules, whereas miR-126 and miR-29b were most abundant in glomerular extracts.
56	29981742	Significantly increased miR-126 and miR-29b were detected in GEnC conditioned medium in response to tumor necrosis factor-α and transforming growth factor-β1, respectively.
57	33748285	Inhibition of miRNA-155 Alleviates High Glucose-Induced Podocyte Inflammation by Targeting SIRT1 in Diabetic Mice.
58	33936277	Transforming growth factor-β1-induced podocyte injury is associated with increased microRNA-155 expression, enhanced inflammatory responses and MAPK pathway activation.
59	33936277	Synaptopodin, CD2-associated protein (CD2AP), p38, and extracellular signal-regulated kinase (Erk) 1/2 expressions were detected using western blotting.
60	33936277	Cell supernatants were collected for assaying tumor necrosis factor (TNF)-α and interleukin (IL)-6 concentrations using enzyme-linked immunosorbent assay.
61	33936277	The Pearson correlation analysis was used to analyze the correlation between miR-155 levels and TNF-α or IL-6.
62	33936277	Time- and dose-dependent TGF-β1 treatments downregulated synaptopodin and CD2AP expression levels, and activated the p38 and Erk 1/2 pathway.
63	33936277	Additionally, TNF-α and IL-6 secretions were elevated, and their concentrations were positively correlated with the expression of miR-155 during podocyte injury.
64	33936277	Thus, the present study indicated that miR-155 is a potential biomarker for the diagnosis of EGD, and its expression is associated with the release of pro-inflammatory cytokines and activation of mitogen-activated protein kinase (MAPK) pathway in TGF-β1-induced podocyte injury.
65	33936277	The present study suggests that the TGF-β1/miR-155/MAPK axis is a novel target in the mechanism of EGD.
66	33936277	Transforming growth factor-β1-induced podocyte injury is associated with increased microRNA-155 expression, enhanced inflammatory responses and MAPK pathway activation.
67	33936277	Synaptopodin, CD2-associated protein (CD2AP), p38, and extracellular signal-regulated kinase (Erk) 1/2 expressions were detected using western blotting.
68	33936277	Cell supernatants were collected for assaying tumor necrosis factor (TNF)-α and interleukin (IL)-6 concentrations using enzyme-linked immunosorbent assay.
69	33936277	The Pearson correlation analysis was used to analyze the correlation between miR-155 levels and TNF-α or IL-6.
70	33936277	Time- and dose-dependent TGF-β1 treatments downregulated synaptopodin and CD2AP expression levels, and activated the p38 and Erk 1/2 pathway.
71	33936277	Additionally, TNF-α and IL-6 secretions were elevated, and their concentrations were positively correlated with the expression of miR-155 during podocyte injury.
72	33936277	Thus, the present study indicated that miR-155 is a potential biomarker for the diagnosis of EGD, and its expression is associated with the release of pro-inflammatory cytokines and activation of mitogen-activated protein kinase (MAPK) pathway in TGF-β1-induced podocyte injury.
73	33936277	The present study suggests that the TGF-β1/miR-155/MAPK axis is a novel target in the mechanism of EGD.
74	33936277	Transforming growth factor-β1-induced podocyte injury is associated with increased microRNA-155 expression, enhanced inflammatory responses and MAPK pathway activation.
75	33936277	Synaptopodin, CD2-associated protein (CD2AP), p38, and extracellular signal-regulated kinase (Erk) 1/2 expressions were detected using western blotting.
76	33936277	Cell supernatants were collected for assaying tumor necrosis factor (TNF)-α and interleukin (IL)-6 concentrations using enzyme-linked immunosorbent assay.
77	33936277	The Pearson correlation analysis was used to analyze the correlation between miR-155 levels and TNF-α or IL-6.
78	33936277	Time- and dose-dependent TGF-β1 treatments downregulated synaptopodin and CD2AP expression levels, and activated the p38 and Erk 1/2 pathway.
79	33936277	Additionally, TNF-α and IL-6 secretions were elevated, and their concentrations were positively correlated with the expression of miR-155 during podocyte injury.
80	33936277	Thus, the present study indicated that miR-155 is a potential biomarker for the diagnosis of EGD, and its expression is associated with the release of pro-inflammatory cytokines and activation of mitogen-activated protein kinase (MAPK) pathway in TGF-β1-induced podocyte injury.
81	33936277	The present study suggests that the TGF-β1/miR-155/MAPK axis is a novel target in the mechanism of EGD.
82	33936277	Transforming growth factor-β1-induced podocyte injury is associated with increased microRNA-155 expression, enhanced inflammatory responses and MAPK pathway activation.
83	33936277	Synaptopodin, CD2-associated protein (CD2AP), p38, and extracellular signal-regulated kinase (Erk) 1/2 expressions were detected using western blotting.
84	33936277	Cell supernatants were collected for assaying tumor necrosis factor (TNF)-α and interleukin (IL)-6 concentrations using enzyme-linked immunosorbent assay.
85	33936277	The Pearson correlation analysis was used to analyze the correlation between miR-155 levels and TNF-α or IL-6.
86	33936277	Time- and dose-dependent TGF-β1 treatments downregulated synaptopodin and CD2AP expression levels, and activated the p38 and Erk 1/2 pathway.
87	33936277	Additionally, TNF-α and IL-6 secretions were elevated, and their concentrations were positively correlated with the expression of miR-155 during podocyte injury.
88	33936277	Thus, the present study indicated that miR-155 is a potential biomarker for the diagnosis of EGD, and its expression is associated with the release of pro-inflammatory cytokines and activation of mitogen-activated protein kinase (MAPK) pathway in TGF-β1-induced podocyte injury.
89	33936277	The present study suggests that the TGF-β1/miR-155/MAPK axis is a novel target in the mechanism of EGD.
90	33936277	Transforming growth factor-β1-induced podocyte injury is associated with increased microRNA-155 expression, enhanced inflammatory responses and MAPK pathway activation.
91	33936277	Synaptopodin, CD2-associated protein (CD2AP), p38, and extracellular signal-regulated kinase (Erk) 1/2 expressions were detected using western blotting.
92	33936277	Cell supernatants were collected for assaying tumor necrosis factor (TNF)-α and interleukin (IL)-6 concentrations using enzyme-linked immunosorbent assay.
93	33936277	The Pearson correlation analysis was used to analyze the correlation between miR-155 levels and TNF-α or IL-6.
94	33936277	Time- and dose-dependent TGF-β1 treatments downregulated synaptopodin and CD2AP expression levels, and activated the p38 and Erk 1/2 pathway.
95	33936277	Additionally, TNF-α and IL-6 secretions were elevated, and their concentrations were positively correlated with the expression of miR-155 during podocyte injury.
96	33936277	Thus, the present study indicated that miR-155 is a potential biomarker for the diagnosis of EGD, and its expression is associated with the release of pro-inflammatory cytokines and activation of mitogen-activated protein kinase (MAPK) pathway in TGF-β1-induced podocyte injury.
97	33936277	The present study suggests that the TGF-β1/miR-155/MAPK axis is a novel target in the mechanism of EGD.