Positron emission tomography imaging of renal mitochondria is a powerful tool in the study of acute and progressive kidney disease models

Saeki, Satoshi; Ohba, Hiroyuki; Ube, Yuko; Tanaka, Kayoko; Haruyama, Waka; Uchii, Masako; Kitayama, Tetsuya; Tsukada, Hideo; Shimada, Takashi

doi:10.1016/j.kint.2020.02.024

Cited by 9 publications

(5 citation statements)

References 41 publications

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“…The kidney is rich in mitochondria, which meet its high energy demand through the oxidative phosphorylation process ( 360 ). Several studies have demonstrated that in glomerulonephritis nephropathy rats, the number of mitochondria in tubular epithelial cells is reduced and cristae structure is destroyed.…”

Section: Renal Microenvironmentmentioning

confidence: 99%

A Deep Insight Into Regulatory T Cell Metabolism in Renal Disease: Facts and Perspectives

Han

Tao

et al. 2022

Front. Immunol.

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Kidney disease encompasses a complex set of diseases that can aggravate or start systemic pathophysiological processes through their complex metabolic mechanisms and effects on body homoeostasis. The prevalence of kidney disease has increased dramatically over the last two decades. CD4+CD25+ regulatory T (Treg) cells that express the transcription factor forkhead box protein 3 (Foxp3) are critical for maintaining immune homeostasis and preventing autoimmune disease and tissue damage caused by excessive or unnecessary immune activation, including autoimmune kidney diseases. Recent studies have highlighted the critical role of metabolic reprogramming in controlling the plasticity, stability, and function of Treg cells. They are also likely to play a vital role in limiting kidney transplant rejection and potentially promoting transplant tolerance. Metabolic pathways, such as mitochondrial function, glycolysis, lipid synthesis, glutaminolysis, and mammalian target of rapamycin (mTOR) activation, are involved in the development of renal diseases by modulating the function and proliferation of Treg cells. Targeting metabolic pathways to alter Treg cells can offer a promising method for renal disease therapy. In this review, we provide a new perspective on the role of Treg cell metabolism in renal diseases by presenting the renal microenvironment、relevant metabolites of Treg cell metabolism, and the role of Treg cell metabolism in various kidney diseases.

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Section: Renal Microenvironmentmentioning

confidence: 99%

A Deep Insight Into Regulatory T Cell Metabolism in Renal Disease: Facts and Perspectives

Han

Tao

et al. 2022

Front. Immunol.

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“…25 PET, a reference standard for quantitative cortical perfusion, 26 also allows molecular imaging. 27 PET has been used successfully in patients with renovascular disease, 28 renal allografts, 29 and CKD. 30 The combined PET/CT modality provides detailed morphology in addition to molecular function and is thus particularly powerful for assessments of renal perfusion and metabolism.…”

Section: Renal Perfusionmentioning

confidence: 99%

“…Metabolism. PET-derived uptake of [18F]fluorodeoxyglucose (FDG) is a powerful index of kidney metabolism, 50 and 2-tert-butyl-4-chloro-5-[6-(4-[( 18) F]fluorobutoxy)pyridin-3-ylmethoxy]-2H-pyridazin-3-one ( 18 F-BCPP-BF) uptake detects mitochondrial function in vivo, 27 but both are limited by radioactivity and low spatial resolution. Hyperpolarized-carbon-13 MRI is an emerging technique based on enzymatic conversion of injected hyperpolarized substrates, which provides both chemical and spatial information.…”

Section: I N I R E V I E Wmentioning

confidence: 99%

Basic principles and new advances in kidney imaging

Caroli

Remuzzi

Lerman

2021

Kidney International

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“…Mitochondria are the main source of cellular energy and play essential roles in regulating cell survival, calcium homeostasis, oxidative stress, and several metabolic processes (Abate et al., 2020; Aparicio‐Trejo, Tapia, Sanchez‐Lozada, & Pedraza‐Chaverri, 2018). Consequently, mitochondrial dysfunction is associated with many diseases, including cancers (Anderson, Ghiraldeli, & Pardee, 2018; Missiroli et al., 2020; Scatena, 2012), myopathies (Apostolopoulou, Corsini, & Roden, 2015; Lu & Tarnopolsky, 2021), diabetes (Prasun, 2020; Siasos, Paschou, & Tousoulis, 2020), obesity (Kras et al., 2018; Schottl et al., 2020), neurodegenerative disorders (Kumar, Dhawan, Kadam, & Shinde, 2018; Missiroli et al., 2020), and renal diseases (Gao, Yang, & Sun, 2020; Podrini, Cassina, & Boletta, 2020; Saeki et al., 2020), as well as aging (Giorgi et al., 2018; Rango & Bresolin, 2018). In the kidney, a large number of mitochondria have been found in renal cells, as these require high energy for their activities in regulating ion transport/homeostasis, reabsorption of glucose and nutrients, and hormonal production (Bhargava & Schnellmann, 2017).…”

Section: Introductionmentioning

confidence: 99%

Gel‐Based and Gel‐Free Phosphoproteomics to Measure and Characterize Mitochondrial Phosphoproteins

Thongboonkerd

Chaiyarit

2022

Current Protocols

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The mitochondrion is a key intracellular organelle regulating metabolic processes, oxidative stress, energy production, calcium homeostasis, and cell survival. Protein phosphorylation plays an important role in regulating mitochondrial functions and cellular signaling pathways. Dysregulation of protein phosphorylation status can cause protein malfunction and abnormal signal transduction, leading to organ dysfunction and disease. Investigating the mitochondrial phosphoproteins is therefore crucial to better understand the molecular and pathogenic mechanisms of many metabolic disorders. Conventional analyses of phosphoproteins, for instance, via western blotting, can be done only for proteins for which specific antibodies to their phosphorylated forms are available. Moreover, such an approach is not suitable for large‐scale study of phosphoproteins. Currently, proteomics represents an important tool for large‐scale analysis of proteins and their post‐translational modifications, including phosphorylation. Here, we provide step‐by‐step protocols for the proteomics analysis of mitochondrial phosphoproteins (the phosphoproteome), using renal tubular cells as an example. These protocols include methods to effectively isolate mitochondria and to validate the efficacy of mitochondrial enrichment as well as its purity. We also provide detailed protocols for performing both gel‐based and gel‐free phosphoproteome analyses. The gel‐based analysis involves two‐dimensional gel electrophoresis and phosphoprotein‐specific staining, followed by protein identification via mass spectrometry, whereas the gel‐free approach is based on in‐solution mass spectrometric identification of specific phosphorylation sites and residues. In all, these approaches allow large‐scale analyses of mitochondrial phosphoproteins that can be applied to other cells and tissues of interest. © 2022 Wiley Periodicals LLC. Basic Protocol 1: Mitochondrial isolation/purification from renal tubular cells Support Protocol: Validation of enrichment efficacy and purity of mitochondrial isolation Basic Protocol 2: Gel‐based phosphoproteome analysis Basic Protocol 3: Gel‐free phosphoproteome analysis

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Positron emission tomography imaging of renal mitochondria is a powerful tool in the study of acute and progressive kidney disease models

Cited by 9 publications

References 41 publications

A Deep Insight Into Regulatory T Cell Metabolism in Renal Disease: Facts and Perspectives

A Deep Insight Into Regulatory T Cell Metabolism in Renal Disease: Facts and Perspectives

Basic principles and new advances in kidney imaging

Gel‐Based and Gel‐Free Phosphoproteomics to Measure and Characterize Mitochondrial Phosphoproteins

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