Next Article in Journal
Safety Assessment of Compounds after In Vitro Metabolic Conversion Using Zebrafish Eleuthero Embryos
Next Article in Special Issue
The Role of Cysteine Cathepsins in Cancer Progression and Drug Resistance
Previous Article in Journal
Gonadal, Not Maternal, Acquisition of Duplicated pax6 Orthologs in Megalobrama Amblycephala
Open AccessArticle

Lack of Cathepsin D in the Renal Proximal Tubular Cells Resulted in Increased Sensitivity against Renal Ischemia/Reperfusion Injury

1
Department of Cellular and Molecular Neuropathology, Juntendo University Graduate School of Medicine, Bunkyo-Ku, Tokyo 113-0033, Japan
2
Department of Cellular and Molecular Pharmacology, Juntendo University Graduate School of Medicine, Bunkyo-Ku, Tokyo 113-0033, Japan
3
Department of Cell Biology and Neuroscience, Juntendo University School of Medicine, Bunkyo-Ku, Tokyo 113-0033, Japan
4
Department of Genetics, Hyogo College of Medicine, Nishinomiya 663-8131, Japan
5
Laboratory of Morphology and Image Analysis, Biomedical Research Center, Juntendo University Graduate School of Medicine, Bunkyo-Ku 113-0033, Japan
*
Authors to whom correspondence should be addressed.
Int. J. Mol. Sci. 2019, 20(7), 1711; https://doi.org/10.3390/ijms20071711
Received: 25 February 2019 / Revised: 29 March 2019 / Accepted: 2 April 2019 / Published: 5 April 2019
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 CtsDflox/−; Spink3Cre 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 CtsDflox/−; Spink3Cre mouse. Inflammation marker was also increased in the cortico-medullary region of the CtsDflox/−; Spink3Cre 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. View Full-Text
Keywords: cathepsin D; renal proximal tubular cells; ischemia/reperfusion injury; gene knockout mouse cathepsin D; renal proximal tubular cells; ischemia/reperfusion injury; gene knockout mouse
Show Figures

Figure 1

MDPI and ACS Style

Suzuki, C.; Tanida, I.; Ohmuraya, M.; Oliva Trejo, J.A.; Kakuta, S.; Sunabori, T.; Uchiyama, Y. Lack of Cathepsin D in the Renal Proximal Tubular Cells Resulted in Increased Sensitivity against Renal Ischemia/Reperfusion Injury. Int. J. Mol. Sci. 2019, 20, 1711.

Show more citation formats Show less citations formats
Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Article Access Map by Country/Region

1
Search more from Scilit
 
Search
Back to TopTop