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Proteomics coupled transcriptomics reveals Slc34a1 and Slc34a3 downregulation as potential features of nephrotoxin-induced acute kidney injury

ABSTRACT: Acute kidney injury (AKI) is a clinically common and severe disease with a significant economic burden worldwide. Although several studies have focused on the pathogenesis of AKI, much remains unknown about its complex molecular regulatory network and pathophysiological mechanisms. This study combines mass spectrometry and RNA sequencing technologies to investigate nephrotoxin-induced AKI mice's protein and RNA expression profiles. The results revealed that Slc34a1 and Slc34a3 were significantly down-regulated in nephrotoxin-induced AKI mice and may be potential diagnostic and therapeutic targets.

ORGANISM(S): Mus musculus

PROVIDER: GSE240304 | GEO | 2023/08/11

REPOSITORIES: GEO

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Proteomics coupled transcriptomics reveals Slc34a1 and Slc34a3 downregulation as potential features of nephrotoxin-induced acute kidney injury

Project description:Acute kidney injury (AKI) is a clinically common and severe disease with a significant economic burden worldwide. Although several studies have focused on the pathogenesis of AKI, much remains unknown about its complex molecular regulatory network and pathophysiological mechanisms. This study combines mass spectrometry and RNA sequencing technologies to investigate nephrotoxin-induced AKI mice's protein and RNA expression profiles. The results revealed that Slc34a1 and Slc34a3 were significantly down-regulated in nephrotoxin-induced AKI mice and may be potential diagnostic and therapeutic targets.

2023-08-03 | PXD044372 |

Proteomics coupled transcriptomics reveals Slc34a1 and Slc34a3 downregulation as potential features of nephrotoxin-induced acute kidney injury

Project description:Proteomics coupled transcriptomics reveals Slc34a1 and Slc34a3 downregulation as potential features of nephrotoxin-induced acute kidney injury

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Project description:Acute kidney injury (AKI) represents a syndrome seldom characterized by a single, distinct pathophysiological cause. Rhabdomyolysis-induced acute kidney injury (RIAKI) constitutes roughly 15% of AKI cases, yet its underlying pathophysiology remains poorly understood. Using a murine model of RIAKI induced by muscular glycerol injection, we aimed to analyse transcriptomic alterations by RNAseq.

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Transcription profiling by array of human renal proximal tubular cell cultures treated with nephrotoxins

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Proteomic Characterization of Acute Kidney Injury in Patients Hospitalized with SARS-CoV2 Infection

Project description:Background: Acute kidney injury (AKI) is a known complication of COVID-19 and is associated with an increased risk of in-hospital mortality. Unbiased proteomics using biological specimens can lead to improved risk stratification and discover pathophysiological mechanisms. Methods: Using measurements of ~4000 plasma proteins in two cohorts of patients hospitalized with COVID-19, we discovered and validated markers of COVID-associated AKI (stage 2 or 3) and long-term kidney dysfunction. In the discovery cohort (N= 437), we identified 413 higher plasma abundances of protein targets and 40 lower plasma abundances of protein targets associated with COVID-AKI (adjusted p <0.05). Of these, 62 proteins were validated in an external cohort (p <0.05, N =261). Results: We demonstrate that COVID-AKI is associated with increased markers of tubular injury (NGAL) and myocardial injury. Using estimated glomerular filtration (eGFR) measurements taken after discharge, we also find that 25 of the 62 AKI-associated proteins are significantly associated with decreased post-discharge eGFR (adjusted p <0.05). Proteins most strongly associated with decreased post-discharge eGFR included desmocollin-2, trefoil factor 3, transmembrane emp24 domain-containing protein 10, and cystatin-C indicating tubular dysfunction and injury. Conclusions: Using clinical and proteomic data, our results suggest that while both acute and long-term COVID-associated kidney dysfunction are associated with markers of tubular dysfunction, AKI is driven by a largely multifactorial process involving hemodynamic instability and myocardial damage.

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Integrated host and viral transcriptome analyses reveal pathology and inflammatory response mechanisms to ALV-J injection in SPF chicken

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Project description:Objective: Cisplatin (CDDP) has been widely used for chemotherapy against tumours. However，the nephrotoxicity has limited its clinical use. Here, we reported a novel compound, Capilliposide A (CPS-A), to exhibit therapeutic effects on CDDP-induced acute kidney injury （AKI）and explored its potential mechanisms via transcriptome and metabolome. Materials and methods: HK-2 cells were treated with CPS-A, after which cell viability, apoptosis and inflammation were investigated. A mouse model of AKI was constructed by single injection of CDDP in vivo. The renal function and morphology and mitochondrial function were assessed by pathological section and transmission electron microscope (TEM). Transcriptomics and metabolomics are used to explore possible mechanisms which was later verified in vitro. Results: CPS-A administration improved the survival rates of HK-2 cells with a significant decrease in the expression of KIM-1, NGAL, IL-6, IL-8 and IL-1β. In vivo results also suggested that CPS-A attenuates CDDP-induced kidney injury by reducing serum creatinine (Cr) and blood urea nitrogen (BUN) levels. Furthermore, TEM also showed the improvement of mitochondrial ultrastructure both in vivo and vitro. Transcriptomics analysis of the mice's renal cortex indicated the expression of ATF4 and CHOP were upregulated, which was further validated by qPCR and Western blotting in vitro. Integrative analysis of transcriptome and metabolome indicated that L-Leucine enriched in Valine, leucine and isoleucine degradation might be potential targets. Conclusions: CPS-A can effectively regulate endogenous metabolites associated with amino acid metabolism and ameliorate apoptosis and oxidative stress in CDDP-induced AKI by reducing endoplasmic reticulum stress.

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Urinary proteomics investigations into contrast-induced acute kidney injury

Project description:The incidence of CI-AKI varies from 5% to 20% among hospitalized patients. However, research on the pathophysiological mechanism and biomarkers of CI-AKI has not been deep so far, especially research with LC-MS/MS methods. MS has brought proteomics research into the modern era and continues to be the best choice for accurate medicine. Thus, we identified the urine proteins of CI-AKI patients with LC-MS/MS methods and compared the differences in urine protein expression between CI-AKI patients and non-CI-AKI patients with bioinformatics analysis. Several DEPs were identified in CI-AKI patients, some of which are related to kidney diseases, including annexin A2 (ANXA2), growth differentiation factor 15 (GDF15) and retinol-binding protein 4 (RBP4). We think that they are likely to be biomarkers of CI-AKI. Among the DEPs, we found that the number and degree of proteins expressed in tubules were more significant than those in glomeruli, which indicated that tubule injury may play a more important role in CI-AKI. Through bioinformatics analysis, we found that the immune response and inflammation were involved in CI-AKI, which indicated that the immune system and inflammatory response may participate in CI-AKI progression. Our study revealed some proteins that are likely to be biomarkers and provided a further understanding of CI-AKI.

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