Dataset Information

Mice kidney cortex proteome

ABSTRACT: O-GlcNAcylation is a global post translational modification. The purpose of this study is to investigate the role of O-GlcNAcylation in mice kidney proximal tubules. We used drug-inducible proximal tubular cells specific O-GlcNAc transferase (Ogt) KO mice (PTEC-Ogt KO). In this proteomic analysis, we compared kidney cortex from fasted PTEC-Ogt KO and Control mice.

ORGANISM(S): Mus Musculus (mouse)

SUBMITTER: Sho Sugahara

PROVIDER: PXD012456 | JPOST Repository | Fri May 17 00:00:00 BST 2019

REPOSITORIES: jPOST

ACCESS DATA

Dataset's files

Source:

			Action	DRS
	180307_01_SGU_146Cont_500ng_QE.raw	Raw
	180307_02_SGU_168KO_500ng_QE.raw	Raw
	180308_P2017040_MouseKidney.mgf	Mgf
	180309_P2017040_PTEC%20Ogt%20KO%20and%20Control%20mice%20Kidney%20Proteomics_Peptide.csv	Csv
	180309_P2017040_PTEC%20Ogt%20KO%20and%20Control%20mice%20Kidney%20Proteomics_Protein.csv	Csv

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Publications

Protein O-GlcNAcylation Is Essential for the Maintenance of Renal Energy Homeostasis and Function <i>via</i> Lipolysis during Fasting and Diabetes.

Sugahara Sho S Kume Shinji S Chin-Kanasaki Masami M Tomita Issei I Yasuda-Yamahara Mako M Yamahara Kosuke K Takeda Naoko N Osawa Norihisa N Yanagita Motoko M Araki Shin-Ichi SI Maegawa Hiroshi H

Journal of the American Society of Nephrology : JASN 20190501 6

<h4>Background</h4>Energy metabolism in proximal tubular epithelial cells (PTECs) is unique, because ATP production largely depends on lipolysis in both the fed and fasting states. Furthermore, disruption of renal lipolysis is involved in the pathogenesis of diabetic tubulopathy. Emerging evidence suggests that protein O-GlcNAcylation, an intracellular nutrient-sensing system, may regulate a number of metabolic pathways according to changes in nutritional status. Although O-GlcNAcylation in PTEC ...[more]

PMID: 31043434

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Project description:Renal hypoxia is widespread in acute kidney injury (AKI) of various aetiologies. Hypoxia adaptation, conferred through the hypoxia-inducible factor (HIF), appears to be insufficient. Here we show that HIF activation in renal tubules through Pax8-rtTA-based inducible knockout of von Hippel-Lindau protein (VHL-KO) protects from rhabdomyolysis-induced AKI. In this model, histological observations indicate that injury mainly affects proximal convoluted tubules, with 5% necrosis at d1 and 40% necrosis at d2. HIF-1alpha up-regulation in distal tubules reflects renal hypoxia. However, lack of HIF in proximal tubules suggests insufficient adaptation by HIF. AKI in VHL-KO mice leads to prominent HIF activation in all nephron segments, as well as to reduced serum creatinine, serum urea, tubular necrosis, and apoptosis marker caspase-3 protein. At d1 after rhabdomyolysis, when tubular injury is potentially reversible, HIF mediated protection in AKI is associated with activated glycolysis, cellular glucose uptake and utilization, autophagy, vasodilation, and proton removal as demonstrated by qPCR, pathway enrichment analysis and immunohistochemistry. Together, our data provide evidence for a HIF-orchestrated multi-level shift towards glycolysis as a major mechanism for protection against acute tubular injury. All experiments were carried out in transgenic mice in which selective renal tubular VHL knockout (VHL-KO) was inducible by doxycycline (Reference: Mathia S, Paliege A, Koesters R, Peters H, Neumayer HH, Bachmann S, Rosenberger C. Action of hypoxia-inducible factor in liver and kidney from mice with Pax8-rtTA-based deletion of von Hippel-Lindau protein. Acta Physiol (Oxf). 2013; 207(3):565-76.). Four groups of animals were used: 1) controls: untreated mice; 2) VHL-KO: injected with doxycycline (0.1 mg per 10 g body weight SC), 4 days prior to sacrifice; 3) AKI: rhabdomyolysis; 4) VHL-KO/AKI: doxycycline plus rhabdomyolysis. To induce AKI, 50% glycerol (0.05 ml per 10 g body weight) was injected IM into the left hind limb under isoflurane narcosis. Drinking water was withdrawn between 20 h prior and 24 h after glycerol injection.