The Mechanism of miR-192 in Regulating High Glucose-Induced MCP-1 Expression in Rat Glomerular Mesangial Cells
Copyright© Bentham Science Publishers; For any queries, please email at epubbenthamscience.net..
BACKGROUND: Although the pathogenetic mechanism of Diabetic Kidney Disease (DKD) has not been elucidated, an inflammatory mechanism may be a potential contributor. Monocyte chemotactic protein-1 (MCP-1) is suggested to be implicated in the development of DKD by playing a role in the infiltration of monocyte/macrophage. The aim of this study was to investigate the expression of MCP-1 under high glucose conditions, as well as the effects of microRNA-192 (miR-192) under these conditions, and to study the regulatory mechanism of MCP-1 in DKD.
METHODS: Rat glomerular mesangial cells were cultured in high glucose or isotonic mannitol. The messenger RNA(mRNA) expression of miR-192, miR-200b, miR-200c, E-box-binding homeobox 1 (Zeb1), and MCP-1 was then detected by real-time PCR, and the protein expression of Zeb1 and MCP- 1 was assessed by western blotting. The rat mesangial cells were transfected with an miR-192 inhibitor, NC inhibitor , and transfected with siRNA Zeb1, siNC. The cells were then cultured in high glucose to detect the mRNA expression of miR-192, miR-200b, miR-200c, Zeb1, and MCP-1 using realtime PCR, and Zeb1 and MCP-1 protein expression were determined by western blotting.
RESULTS: MiR-192, miR-200b, miR-200c, and MCP-1 were overexpressed, whereas Zeb1 was downregulated when cultured in high glucose (P < 0.05). After transfection with an miR-192 inhibitor, the expression of miR-192, miR-200b, miR-200c, and MCP-1 was downregulated, whereas Zeb1 was increased, and these differences were statistically significant (P < 0.05). The observed changes in the expression in the NC inhibitor transfection group were similar to that of non-transfected cell lines. Silencing the expression of Zeb1 resulted in a significant increase in the expression of miR-192, miR- 200b, miR-200c, and MCP-1 (P < 0.05). The observed changes in the SiNC transfection group were similar to those of non-transfected cell lines.
CONCLUSIONS: MiR-192 expression was upregulated to increase the expression of inflammatory factor MCP-1 by inhibiting the expression of Zeb1, which was mediated by breaking the regulatory loop of Zeb1 and miR-200b/c in rat mesangial cells cultured in high glucose.
Medienart: |
E-Artikel |
---|
Erscheinungsjahr: |
2019 |
---|---|
Erschienen: |
2019 |
Enthalten in: |
Zur Gesamtaufnahme - volume:19 |
---|---|
Enthalten in: |
Endocrine, metabolic & immune disorders drug targets - 19(2019), 7 vom: 27., Seite 1055-1063 |
Sprache: |
Englisch |
---|
Beteiligte Personen: |
Chen, Fenqin [VerfasserIn] |
---|
Links: |
---|
Themen: |
Ccl2 protein, mouse |
---|
Anmerkungen: |
Date Completed 30.03.2020 Date Revised 30.03.2020 published: Print Citation Status MEDLINE |
---|
doi: |
10.2174/1871530319666190301154640 |
---|
funding: |
|
---|---|
Förderinstitution / Projekttitel: |
|
PPN (Katalog-ID): |
NLM294515569 |
---|
LEADER | 01000naa a22002652 4500 | ||
---|---|---|---|
001 | NLM294515569 | ||
003 | DE-627 | ||
005 | 20231225081641.0 | ||
007 | cr uuu---uuuuu | ||
008 | 231225s2019 xx |||||o 00| ||eng c | ||
024 | 7 | |a 10.2174/1871530319666190301154640 |2 doi | |
028 | 5 | 2 | |a pubmed24n0981.xml |
035 | |a (DE-627)NLM294515569 | ||
035 | |a (NLM)30827272 | ||
040 | |a DE-627 |b ger |c DE-627 |e rakwb | ||
041 | |a eng | ||
100 | 1 | |a Chen, Fenqin |e verfasserin |4 aut | |
245 | 1 | 4 | |a The Mechanism of miR-192 in Regulating High Glucose-Induced MCP-1 Expression in Rat Glomerular Mesangial Cells |
264 | 1 | |c 2019 | |
336 | |a Text |b txt |2 rdacontent | ||
337 | |a ƒaComputermedien |b c |2 rdamedia | ||
338 | |a ƒa Online-Ressource |b cr |2 rdacarrier | ||
500 | |a Date Completed 30.03.2020 | ||
500 | |a Date Revised 30.03.2020 | ||
500 | |a published: Print | ||
500 | |a Citation Status MEDLINE | ||
520 | |a Copyright© Bentham Science Publishers; For any queries, please email at epubbenthamscience.net. | ||
520 | |a BACKGROUND: Although the pathogenetic mechanism of Diabetic Kidney Disease (DKD) has not been elucidated, an inflammatory mechanism may be a potential contributor. Monocyte chemotactic protein-1 (MCP-1) is suggested to be implicated in the development of DKD by playing a role in the infiltration of monocyte/macrophage. The aim of this study was to investigate the expression of MCP-1 under high glucose conditions, as well as the effects of microRNA-192 (miR-192) under these conditions, and to study the regulatory mechanism of MCP-1 in DKD | ||
520 | |a METHODS: Rat glomerular mesangial cells were cultured in high glucose or isotonic mannitol. The messenger RNA(mRNA) expression of miR-192, miR-200b, miR-200c, E-box-binding homeobox 1 (Zeb1), and MCP-1 was then detected by real-time PCR, and the protein expression of Zeb1 and MCP- 1 was assessed by western blotting. The rat mesangial cells were transfected with an miR-192 inhibitor, NC inhibitor , and transfected with siRNA Zeb1, siNC. The cells were then cultured in high glucose to detect the mRNA expression of miR-192, miR-200b, miR-200c, Zeb1, and MCP-1 using realtime PCR, and Zeb1 and MCP-1 protein expression were determined by western blotting | ||
520 | |a RESULTS: MiR-192, miR-200b, miR-200c, and MCP-1 were overexpressed, whereas Zeb1 was downregulated when cultured in high glucose (P < 0.05). After transfection with an miR-192 inhibitor, the expression of miR-192, miR-200b, miR-200c, and MCP-1 was downregulated, whereas Zeb1 was increased, and these differences were statistically significant (P < 0.05). The observed changes in the expression in the NC inhibitor transfection group were similar to that of non-transfected cell lines. Silencing the expression of Zeb1 resulted in a significant increase in the expression of miR-192, miR- 200b, miR-200c, and MCP-1 (P < 0.05). The observed changes in the SiNC transfection group were similar to those of non-transfected cell lines | ||
520 | |a CONCLUSIONS: MiR-192 expression was upregulated to increase the expression of inflammatory factor MCP-1 by inhibiting the expression of Zeb1, which was mediated by breaking the regulatory loop of Zeb1 and miR-200b/c in rat mesangial cells cultured in high glucose | ||
650 | 4 | |a Journal Article | |
650 | 4 | |a High glucose | |
650 | 4 | |a MCP-1 | |
650 | 4 | |a miR-192 | |
650 | 4 | |a miR-200b | |
650 | 4 | |a miR-200c | |
650 | 4 | |a rat glomerular mesangial cells. | |
650 | 7 | |a Ccl2 protein, mouse |2 NLM | |
650 | 7 | |a Chemokine CCL2 |2 NLM | |
650 | 7 | |a MIRN192 microRNA, rat |2 NLM | |
650 | 7 | |a MicroRNAs |2 NLM | |
650 | 7 | |a Glucose |2 NLM | |
650 | 7 | |a IY9XDZ35W2 |2 NLM | |
700 | 1 | |a Wei, Guozhu |e verfasserin |4 aut | |
700 | 1 | |a Zhou, Yang |e verfasserin |4 aut | |
700 | 1 | |a Ma, Xiaoyu |e verfasserin |4 aut | |
700 | 1 | |a Wang, Qiuyue |e verfasserin |4 aut | |
773 | 0 | 8 | |i Enthalten in |t Endocrine, metabolic & immune disorders drug targets |d 2006 |g 19(2019), 7 vom: 27., Seite 1055-1063 |w (DE-627)NLM161976174 |x 2212-3873 |7 nnns |
773 | 1 | 8 | |g volume:19 |g year:2019 |g number:7 |g day:27 |g pages:1055-1063 |
856 | 4 | 0 | |u http://dx.doi.org/10.2174/1871530319666190301154640 |3 Volltext |
912 | |a GBV_USEFLAG_A | ||
912 | |a GBV_NLM | ||
951 | |a AR | ||
952 | |d 19 |j 2019 |e 7 |b 27 |h 1055-1063 |