Exosomal CCL2 from Tubular Epithelial Cells Is Critical for Albumin-Induced Tubulointerstitial Inflammation

Albuminuria is a key instigator of tubulointerstitial inflammation associated with CKD, but the mechanism through which filtered albumin propagates renal injury remains unclear. In this study, we explored the role in this process of exosome mRNA released from tubular epithelial cells (TECs). Compare...

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Published in:	Journal of the American Society of Nephrology Vol. 29; no. 3; p. 919
Main Authors:	Lv, Lin-Li, Feng, Ye, Wen, Yi, Wu, Wei-Jun, Ni, Hai-Feng, Li, Zuo-Lin, Zhou, Le-Ting, Wang, Bin, Zhang, Jian-Dong, Crowley, Steven D, Liu, Bi-Cheng
Format:	Journal Article
Language:	English
Published:	United States 01.03.2018
Subjects:	albuminuria CCL2 macrophages mRNA exosome extracellular vesicle
ISSN:	1533-3450, 1533-3450
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Abstract	Albuminuria is a key instigator of tubulointerstitial inflammation associated with CKD, but the mechanism through which filtered albumin propagates renal injury remains unclear. In this study, we explored the role in this process of exosome mRNA released from tubular epithelial cells (TECs). Compared with control mice, acute and chronic kidney injury models had more exosomes containing inflammatory cytokine mRNA, particularly the chemokine CCL2, in kidneys and urine. stimulation of TECs with BSA recapitulated this finding. Notably, the internalization of purified TEC exosomes by cultured macrophages increased if TECs were exposed to BSA. Macrophage internalization of exosomes from BSA-treated TECs led to an enhanced inflammatory response and macrophage migration, but CCL2 silencing in TECs prevented these effects. Using a GFP-CCL2 fusion mRNA construct, we observed direct transfer of CCL2 mRNA from TEC exosomes to macrophages. Mice subjected to tail vein injection of purified BSA-treated TEC exosomes developed tubular injury with renal inflammatory cell infiltration. However, injection of exosomes from BSA-treated CCL2-deficient TECs induced less severe kidney inflammation. Finally, in patients with IgA nephropathy, the increase of proteinuria correlated with augmented urinary excretion of exosomes with exaggerated expression of CCL2 mRNA. Moreover, the level of CCL2 mRNA in urinary exosomes correlated closely with levels of renal interstitial macrophage infiltration in these patients. Our studies demonstrate that the increasing release of exosomes that transfer CCL2 mRNA from TECs to macrophages constitutes a critical mechanism of albumin-induced tubulointerstitial inflammation.
AbstractList	Albuminuria is a key instigator of tubulointerstitial inflammation associated with CKD, but the mechanism through which filtered albumin propagates renal injury remains unclear. In this study, we explored the role in this process of exosome mRNA released from tubular epithelial cells (TECs). Compared with control mice, acute and chronic kidney injury models had more exosomes containing inflammatory cytokine mRNA, particularly the chemokine CCL2, in kidneys and urine. stimulation of TECs with BSA recapitulated this finding. Notably, the internalization of purified TEC exosomes by cultured macrophages increased if TECs were exposed to BSA. Macrophage internalization of exosomes from BSA-treated TECs led to an enhanced inflammatory response and macrophage migration, but CCL2 silencing in TECs prevented these effects. Using a GFP-CCL2 fusion mRNA construct, we observed direct transfer of CCL2 mRNA from TEC exosomes to macrophages. Mice subjected to tail vein injection of purified BSA-treated TEC exosomes developed tubular injury with renal inflammatory cell infiltration. However, injection of exosomes from BSA-treated CCL2-deficient TECs induced less severe kidney inflammation. Finally, in patients with IgA nephropathy, the increase of proteinuria correlated with augmented urinary excretion of exosomes with exaggerated expression of CCL2 mRNA. Moreover, the level of CCL2 mRNA in urinary exosomes correlated closely with levels of renal interstitial macrophage infiltration in these patients. Our studies demonstrate that the increasing release of exosomes that transfer CCL2 mRNA from TECs to macrophages constitutes a critical mechanism of albumin-induced tubulointerstitial inflammation. Albuminuria is a key instigator of tubulointerstitial inflammation associated with CKD, but the mechanism through which filtered albumin propagates renal injury remains unclear. In this study, we explored the role in this process of exosome mRNA released from tubular epithelial cells (TECs). Compared with control mice, acute and chronic kidney injury models had more exosomes containing inflammatory cytokine mRNA, particularly the chemokine CCL2, in kidneys and urine. In vitro stimulation of TECs with BSA recapitulated this finding. Notably, the internalization of purified TEC exosomes by cultured macrophages increased if TECs were exposed to BSA. Macrophage internalization of exosomes from BSA-treated TECs led to an enhanced inflammatory response and macrophage migration, but CCL2 silencing in TECs prevented these effects. Using a GFP-CCL2 fusion mRNA construct, we observed direct transfer of CCL2 mRNA from TEC exosomes to macrophages. Mice subjected to tail vein injection of purified BSA-treated TEC exosomes developed tubular injury with renal inflammatory cell infiltration. However, injection of exosomes from BSA-treated CCL2-deficient TECs induced less severe kidney inflammation. Finally, in patients with IgA nephropathy, the increase of proteinuria correlated with augmented urinary excretion of exosomes with exaggerated expression of CCL2 mRNA. Moreover, the level of CCL2 mRNA in urinary exosomes correlated closely with levels of renal interstitial macrophage infiltration in these patients. Our studies demonstrate that the increasing release of exosomes that transfer CCL2 mRNA from TECs to macrophages constitutes a critical mechanism of albumin-induced tubulointerstitial inflammation.Albuminuria is a key instigator of tubulointerstitial inflammation associated with CKD, but the mechanism through which filtered albumin propagates renal injury remains unclear. In this study, we explored the role in this process of exosome mRNA released from tubular epithelial cells (TECs). Compared with control mice, acute and chronic kidney injury models had more exosomes containing inflammatory cytokine mRNA, particularly the chemokine CCL2, in kidneys and urine. In vitro stimulation of TECs with BSA recapitulated this finding. Notably, the internalization of purified TEC exosomes by cultured macrophages increased if TECs were exposed to BSA. Macrophage internalization of exosomes from BSA-treated TECs led to an enhanced inflammatory response and macrophage migration, but CCL2 silencing in TECs prevented these effects. Using a GFP-CCL2 fusion mRNA construct, we observed direct transfer of CCL2 mRNA from TEC exosomes to macrophages. Mice subjected to tail vein injection of purified BSA-treated TEC exosomes developed tubular injury with renal inflammatory cell infiltration. However, injection of exosomes from BSA-treated CCL2-deficient TECs induced less severe kidney inflammation. Finally, in patients with IgA nephropathy, the increase of proteinuria correlated with augmented urinary excretion of exosomes with exaggerated expression of CCL2 mRNA. Moreover, the level of CCL2 mRNA in urinary exosomes correlated closely with levels of renal interstitial macrophage infiltration in these patients. Our studies demonstrate that the increasing release of exosomes that transfer CCL2 mRNA from TECs to macrophages constitutes a critical mechanism of albumin-induced tubulointerstitial inflammation.
Author	Ni, Hai-Feng Li, Zuo-Lin Zhang, Jian-Dong Liu, Bi-Cheng Feng, Ye Crowley, Steven D Lv, Lin-Li Wu, Wei-Jun Zhou, Le-Ting Wen, Yi Wang, Bin
Author_xml	– sequence: 1 givenname: Lin-Li surname: Lv fullname: Lv, Lin-Li organization: Institute of Nephrology, Zhongda Hospitial, Southeast University School of Medicine, Nanjing, China; and – sequence: 2 givenname: Ye surname: Feng fullname: Feng, Ye organization: Institute of Nephrology, Zhongda Hospitial, Southeast University School of Medicine, Nanjing, China; and – sequence: 3 givenname: Yi surname: Wen fullname: Wen, Yi organization: Institute of Nephrology, Zhongda Hospitial, Southeast University School of Medicine, Nanjing, China; and – sequence: 4 givenname: Wei-Jun surname: Wu fullname: Wu, Wei-Jun organization: Institute of Nephrology, Zhongda Hospitial, Southeast University School of Medicine, Nanjing, China; and – sequence: 5 givenname: Hai-Feng surname: Ni fullname: Ni, Hai-Feng organization: Institute of Nephrology, Zhongda Hospitial, Southeast University School of Medicine, Nanjing, China; and – sequence: 6 givenname: Zuo-Lin surname: Li fullname: Li, Zuo-Lin organization: Institute of Nephrology, Zhongda Hospitial, Southeast University School of Medicine, Nanjing, China; and – sequence: 7 givenname: Le-Ting surname: Zhou fullname: Zhou, Le-Ting organization: Institute of Nephrology, Zhongda Hospitial, Southeast University School of Medicine, Nanjing, China; and – sequence: 8 givenname: Bin surname: Wang fullname: Wang, Bin organization: Institute of Nephrology, Zhongda Hospitial, Southeast University School of Medicine, Nanjing, China; and – sequence: 9 givenname: Jian-Dong surname: Zhang fullname: Zhang, Jian-Dong organization: Institute of Nephrology, Zhongda Hospitial, Southeast University School of Medicine, Nanjing, China; and – sequence: 10 givenname: Steven D surname: Crowley fullname: Crowley, Steven D organization: Division of Nephrology, Department of Medicine, Duke University and Durham Veterans Affairs Medical Centers, Durham, North Carolina – sequence: 11 givenname: Bi-Cheng surname: Liu fullname: Liu, Bi-Cheng email: liubc64@163.com organization: Institute of Nephrology, Zhongda Hospitial, Southeast University School of Medicine, Nanjing, China; and liubc64@163.com
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Title	Exosomal CCL2 from Tubular Epithelial Cells Is Critical for Albumin-Induced Tubulointerstitial Inflammation
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