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Research Article
Kun Liu
Huai’an First People’s Hospital, Nanjing Medical University
Corresponding Author
License:
This work is licensed under a CC BY 4.0 License. Read Full License
Objectives: Our study was designed to explore the role of Cyclophilin A (CyPA)/CD147 interactions in renal allograft fibrosis and chronic allograft dysfunction (CAD).
Methods and materials: A rat renal transplant model with significant CAD was successfully identified. Renal allograft tissues and blood samples were collected. HE, Masson and immunohistochemistry staining were performed. Then human HK-2 cells were intervened by certain concentrations of CyPA, and total protein and mRNA were extracted. Western blot assay and PCR were performed to explore the protein and mRNA expression of CyPA, CD147 and epithelial-to-mesenchymal transition (EMT)-related biomarkers. CD147 siRNA and specific inhibitor of MAPK were used to explore the involved cellular mechanism.
Results: We have successfully established and identified a 20-weeks renal transplant CAD model. We observed significant distributed and expressed CyPA and CD147 in the renal allograft fibrosis tissues. We also found the significant expression of CD147 and EMT-related markers in the HK-2 cells stimulated by CyPA. The CD147 siRNA confirmed the previous results in vitro. The selective inhibition of MAPK suggested the notable role of MAPK signaling pathway in the CyP/CD147 interactions involved in renal allograft fibrosis.
Conclusions: Our study reported the positive relationship of CyPA/CD147 interactions with the renal allograft dysfunction. In vitro study suggested that CyPA could bind to CD147 and then induce the development of EMT process by MAPK signaling, thus contributing to the renal allograft fibrosis and CAD.
Keywords
Cyclophilin A, CD147, epithelial-to-mesenchymal transition, kidney transplantation, chronic allograft dysfunction
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No competing interests reported.
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This is a preprint. It has not completed peer review.
Research Article
Kun Liu
Huai’an First People’s Hospital, Nanjing Medical University
Corresponding Author
Badges
Prescreen
This manuscript passed our Prescreen assessment
Complete author information
Appropriate declaration statements
Potential risks to human health
Prescreen
History
CURRENT STATUS: Posted
Version 1
Posted 18 Mar, 2021
No community comments so far
Metrics
Comments: 0
PDF Downloads: ...
HTML Views: ...
Subject Areas
Urology & Nephrology
License:
This work is licensed under a CC BY 4.0 License. Read Full License
Objectives: Our study was designed to explore the role of Cyclophilin A (CyPA)/CD147 interactions in renal allograft fibrosis and chronic allograft dysfunction (CAD).
Methods and materials: A rat renal transplant model with significant CAD was successfully identified. Renal allograft tissues and blood samples were collected. HE, Masson and immunohistochemistry staining were performed. Then human HK-2 cells were intervened by certain concentrations of CyPA, and total protein and mRNA were extracted. Western blot assay and PCR were performed to explore the protein and mRNA expression of CyPA, CD147 and epithelial-to-mesenchymal transition (EMT)-related biomarkers. CD147 siRNA and specific inhibitor of MAPK were used to explore the involved cellular mechanism.
Results: We have successfully established and identified a 20-weeks renal transplant CAD model. We observed significant distributed and expressed CyPA and CD147 in the renal allograft fibrosis tissues. We also found the significant expression of CD147 and EMT-related markers in the HK-2 cells stimulated by CyPA. The CD147 siRNA confirmed the previous results in vitro. The selective inhibition of MAPK suggested the notable role of MAPK signaling pathway in the CyP/CD147 interactions involved in renal allograft fibrosis.
Conclusions: Our study reported the positive relationship of CyPA/CD147 interactions with the renal allograft dysfunction. In vitro study suggested that CyPA could bind to CD147 and then induce the development of EMT process by MAPK signaling, thus contributing to the renal allograft fibrosis and CAD.
Figure 1
Figure 2
Figure 3
Figure 4
Figure 5
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