Effect of Trehalose Supplementation on Autophagy and Cystogenesis in a Mouse Model of Polycystic Kidney Disease.
Li-Fang ChouYa-Lien ChengChun-Yih HsiehChan-Yu LinHuang-Yu YangYung-Chang ChenCheng-Chieh HungYa-Chung TianChih-Wei YangMing-Yang ChangPublished in: Nutrients (2018)
Autophagy impairment has been demonstrated in the pathogenesis of autosomal dominant polycystic kidney disease (ADPKD) and could be a new target of treatment. Trehalose is a natural, nonreducing disaccharide that has been shown to enhance autophagy. Therefore, we investigated whether trehalose treatment reduces renal cyst formation in a Pkd1-hypomorphic mouse model. Pkd1 miRNA transgenic (Pkd1 miR Tg) mice and wild-type littermates were given drinking water supplemented with 2% trehalose from postnatal day 35 to postnatal day 91. The control groups received pure water or 2% sucrose for the control of hyperosmolarity. The effect on kidney weights, cystic indices, renal function, cell proliferation, and autophagic activities was determined. We found that Pkd1 miR Tg mice had a significantly lower renal mRNA expression of autophagy-related genes, including atg5, atg12, ulk1, beclin1, and p62, compared with wild-type control mice. Furthermore, immunohistochemical analysis showed that cystic lining cells had strong positive staining for the p62 protein, indicating impaired degradation of the protein by the autophagy-lysosome pathway. However, trehalose treatment did not improve reduced autophagy activities, nor did it reduce relative kidney weights, plasma blood urea nitrogen levels, or cystatin C levels in Pkd1 miR Tg mice. Histomorphological analysis revealed no significant differences in the renal cyst index, fibrosis score, or proliferative score among trehalose-, sucrose-, and water-treated groups. Our results demonstrate that adding trehalose to drinking water does not modulate autophagy activities and renal cystogenesis in Pkd1-deficient mice, suggesting that an oral supplement of trehalose may not affect the progression of ADPKD.
Keyphrases
- polycystic kidney disease
- wild type
- drinking water
- cell death
- cell proliferation
- endoplasmic reticulum stress
- signaling pathway
- oxidative stress
- mouse model
- induced apoptosis
- cell cycle arrest
- high fat diet induced
- preterm infants
- health risk assessment
- health risk
- type diabetes
- adipose tissue
- cell cycle
- insulin resistance
- single cell
- binding protein
- risk assessment
- smoking cessation
- single molecule
- newly diagnosed