Data from: TNFAIP9 protects against the development of the early stage of chronic kidney disease: Focus on inflammation and fibrosis
Data files
Dec 31, 2024 version files 197.21 KB
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Original_Data.pptx
194.72 KB
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README.md
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Abstract
Tumor necrosis factor alpha-induced protein 9 (TNFAIP9) is a crucial effector molecule that protects cells from inflammatory and metabolic damage. This study focuses on investigating the role and regulatory mechanisms of TNFAIP9 in the progression of chronic kidney disease (CKD). By analyzing CKD-related datasets from the GEO database, we discovered that TNFAIP9 was upregulated in CKD patients and CKD mice compared to their normal controls. To elucidate the functional role of TNFAIP9, we established a mouse model of CKD through a two-step 5/6 nephrectomy (Nx). The experimental mice were transduced with an adenoviral vector to express TNFAIP9. The results showed that mice undergoing 5/6-Nx developed evident renal impairment, inflammation, and fibrosis. Overexpression of TNFAIP9 resulted in the remission of renal impairment, a decreased inflammatory response, and a reduced expression of fibrotic markers. In vitro, human renal tubular epithelial human kidney-2 (HK-2) cells were exposed to tumor necrosis factor-alpha (TNF-α) or transforming growth factor-beta (TGF-β) to simulate inflammatory and fibrotic conditions, respectively. Then, the overexpression plasmid or small interfering RNA (siRNA) targeting TNFAIP9 was transfected into HK-2 cells to either overexpress or knock down the target protein. Overexpression of TNFAIP9 reduced the TNF-α-induced inflammatory response, while its knockdown amplified it. Likewise, overexpression of TNFAIP9 decreased the TGF-β-induced fibrosis, whereas its knockdown heightened it. In summary, it is suggested that TNFAIP9 plays a protective role against the early stage of CKD by suppressing renal inflammation and fibrosis. Therefore, targeting TNFAIP9 could be a promising therapeutic approach for CKD.
README: Data from: TNFAIP9 protects against the development of the early stage of chronic kidney disease: focus on inflammation and fibrosis
Introduction
This dataset includes raw data that can be used to form the histogram, including quantitative results of immunofluorescence/immunohistochemistry/pathology scores, kit results, and normalized quantitative results of PCR and Western blot to support the study “TNFAIP9 protects against the development of the early stage of chronic kidney disease: focus on inflammation and fibrosis”, which is currently in press.
File list
Original Data, in pptx format.
Author Information
Name: Ying Chen
Institution: First Hospital of China Medical University, Shenyang, China
Co-investigator 1
Name: Yanqiu Li
Institution: First Hospital of China Medical University, Shenyang, China
Corresponding author
Name: Dr. Deyu Zhang
Institution: Shengjing Hospital of China Medical University, Shenyang, China
Description of the data and file structure
The data presented in this dataset underpins the quantitative statistics for each graph featured in the publication, thereby ensuring that the dataset is derived from the figures reported in the publication. The included data encompasses the following quantitative results: Kit tests yielded serum levels of creatinine and urea nitrogen; Masson’s trichrome staining quantified the percentage of fibrotic areas relative to the total area. ELISA assays determined concentrations of TNF-α, IL-6, and MCP-1 within kidney tissue or cell supernatants. Western blot analysis provided relative quantification values based on grayscale measurements for α-SMA, Fibronectin, TNFAIP9, iNOS, COX-2, p-p65ser536, and Collagen III. The percentage of positively stained areas for TNFAIP9, Collagen III, and NGAL was assessed through immunohistochemistry. Real-time PCR facilitated measurement of relative mRNA content for TNFAIP9. Biochemical assays recorded arterial pressure as well as 24-hour urinary protein excretion from the animals involved in this study. Hematoxylin-eosin (HE) staining offered a quantitative score reflecting tissue injury severity. Additionally, immunofluorescence techniques were employed to quantify the percentage of positively stained cells.
Acknowledgments
This study was funded by the Postdoctoral Science Foundation of China (2021M703608). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
Methods
The current dataset provides raw data that can be used to form the histogram, including quantitative results of immunofluorescence/immunohistochemistry/pathology scores, kit results, and normalized quantitative results of PCR and Western blot.