| First Author | Suzuki C | Year | 2019 |
| Journal | Int J Mol Sci | Volume | 20 |
| Issue | 7 | PubMed ID | 30959855 |
| Mgi Jnum | J:290675 | Mgi Id | MGI:6443300 |
| Doi | 10.3390/ijms20071711 | Citation | Suzuki C, et al. (2019) Lack of Cathepsin D in the Renal Proximal Tubular Cells Resulted in Increased Sensitivity against Renal Ischemia/Reperfusion Injury. Int J Mol Sci 20(7):1711 |
| abstractText | Cathepsin D is one of the major lysosomal aspartic proteases that is essential for the normal functioning of the autophagy-lysosomal system. In the kidney, cathepsin D is enriched in renal proximal tubular epithelial cells, and its levels increase during acute kidney injury. To investigate how cathepsin D-deficiency impacts renal proximal tubular cells, we employed a conditional knockout CtsD(flox/-); Spink3(Cre) mouse. Immunohistochemical analyses using anti-cathepsin D antibody revealed that cathepsin D was significantly decreased in tubular epithelial cells of the cortico-medullary region, mainly in renal proximal tubular cells of this mouse. Cathepsin D-deficient renal proximal tubular cells showed an increase of microtubule-associated protein light chain 3 (LC3; a marker for autophagosome/autolysosome)-signals and an accumulation of abnormal autophagic structures. Renal ischemia/reperfusion injury resulted in an increase of early kidney injury marker, Kidney injury molecule 1 (Kim-1), in the cathepsin D-deficient renal tubular epithelial cells of the CtsD(flox/-); Spink3(Cre) mouse. Inflammation marker was also increased in the cortico-medullary region of the CtsD(flox/-); Spink3(Cre) mouse. Our results indicated that lack of cathepsin D in the renal tubular epithelial cells led to an increase of sensitivity against ischemia/reperfusion injury. |
