Project description:The objective of this study was to understand the impact of losing cadherin-11 (CDH11) on kidney injury. CDH11 has previously been demonstrated to be associated with a number of fibrotic diseases, but its role in kidney injury remains unknown. In vivo models of kidney injury demonstrated improved renal function and reduced tubulointerstitial fibrosis with CDH11 inhibition. However, the mechanism by which CDH11 inhibition mitigates kidney injury is unknown. RNAseq analysis showed altered expression of over 50 genes in two models of kidney injury when CDH11-/- mice were compared with CDH11+/+ mice. These results together indicate that CDH11 deletion alters many genes and pathways that could contribute to kidney injury, including alpha-1 antitrypsin, which is increased in CDH11-/- mice and has been shown to be beneficial in kidney injury.
Project description:The objective of this study was to understand the impact of losing cadherin-11 (CDH11) on kidney injury. CDH11 has previously been demonstrated to be associated with a number of fibrotic diseases, but its role in kidney injury remains unknown. In vivo models of kidney injury demonstrated improved renal function and reduced tubulointerstitial fibrosis with CDH11 inhibition. However, the mechanism by which CDH11 inhibition mitigates kidney injury is unknown. RNAseq analysis showed altered expression of over 50 genes in two models of kidney injury when CDH11-/- mice were compared with CDH11+/+ mice. These results together indicate that CDH11 deletion alters many genes and pathways that could contribute to kidney injury, including alpha-1 antitrypsin, which is increased in CDH11-/- mice and has been shown to be beneficial in kidney injury.
