|
| Status |
Public on Apr 10, 2020 |
| Title |
Deficiency of C3a receptor attenuates the development of diabetic nephropathy (Control Group) |
| Organism |
Mus musculus |
| Experiment type |
Expression profiling by array
|
| Summary |
Diabetic nephropathy (DN) is the leading cause of chronic kidney disease and end-stage renal disease. Emerging evidence suggests that complement activation is involved in the pathogenesis of DN. The aim of this study was to investigate the pathogenic role of C3a and C3a receptor (C3aR) in DN. The expression of C3aR was examined in the renal specimen of DN patients. Using a C3aR gene knockout mice (C3aR-/-), we evaluated kidney injury in diabetic mice. The mouse gene expression microarray was performed to further explore the pathogenic role of C3aR. Then the underlying mechanism was investigated in vitro with macrophage treated with C3a. Compared with normal controls, the renal expression of C3aR was significantly increased in DN patients. C3aR-/- diabetic mice developed less severe diabetic renal damage compared with WT diabetic mice, exhibiting significantly lower level of albuminuria and milder renal pathological injury. Microarray profiling uncovered significantly suppressed inflammatory responses and T cell adaptive immunity in C3aR-/- diabetic mice compared with WT diabetic mice and this result was further verified by immunohistochemical staining of renal CD4+, CD8+ T cells and macrophages infiltration. In vitro study demonstrated C3a can enhance macrophages secreted cytokines which could induce inflammatory responses and differentiation of T cell lineage. In conclusion, C3aR deficiency could attenuate diabetic renal damage through suppressing inflammatory responses and T cell adaptive immunity, possibly by influencing macrophages secreted cytokines. Thus, C3aR may be a promising therapeutic target for DN.
|
| |
|
| Overall design |
There were four groups including WT control group, C3aR-/- control group, WT diabetic group, C3aR-/- diabetic group. Total RNA was extracted from three replicate samples per group
This series includes the control samples.
|
| |
|
| Contributor(s) |
Li X, Chang D, Chen M, Zhao M |
| Citation(s) |
31798904 |
| Submission date |
Jul 01, 2019 |
| Last update date |
Apr 10, 2020 |
| Contact name |
Xiao-Qian Li |
| E-mail(s) |
xqli1992@126.com
|
| Organization name |
the First Affiliated Hospital of Zhengzhou University
|
| Department |
Nephrology Hospital
|
| Street address |
No. 1, East of Jianshe Street, Erqi District
|
| City |
Zhengzhou |
| State/province |
Henan |
| ZIP/Postal code |
450052 |
| Country |
China |
| |
|
| Platforms (1) |
| GPL21163 |
Agilent-074809 SurePrint G3 Mouse GE v2 8x60K Microarray [Probe Name version] |
|
| Samples (6)
|
| GSM3912762 |
C3aR-KO-ctrl-1: Renal_C3aR-/- Control_rep1 |
| GSM3912763 |
C3aR-KO-ctrl-2: Renal_C3aR-/- Control_rep2 |
| GSM3912764 |
C3aR-KO-ctrl-3: Renal_C3aR-/- Control_rep3 |
|
| This SubSeries is part of SuperSeries: |
| GSE133598 |
Deficiency of C3a receptor attenuates the development of diabetic nephropathy |
|
| Relations |
| BioProject |
PRJNA552023 |
Less...
More...