Metabolic rates of 4-hydroxynonenal in tubular and mesangial cells of the kidney.

Exp Nephrol

Clinics of Physical Medicine and Rehabilitation, Medical Faculty (Charité), Humboldt University, Berlin.

Published: March 1999

The degradation of the lipid peroxidation product 4-hydroxynonenal (HNE) in primary cultures of kidney tubular and mesangial cells was determined. Using various initial concentrations of the aldehyde a decline of cellular viability was found. Mesangial cells were more susceptible to the toxic effects of HNE. In consumption studies of HNE the decline of the exogenously added aldehyde was comparable in both cell types after addition of 10 and 1 micromol HNE/l. After addition of 100 micromol/l aldehyde a drastically lower HNE degrading capacity was found in mesangial cells as compared to tubular cells. The loss in the HNE degrading capacity was accompanied by an increased formation of HNE-protein aggregates as demonstrated by immunoblots. Therefore, we concluded that the low ability of mesangial cells to degrade HNE may be a factor of the toxicity of free radicals on the kidney.

Download full-text PDF

Source
http://dx.doi.org/10.1159/000020585DOI Listing

Publication Analysis

Top Keywords

mesangial cells
20
tubular mesangial
8
hne degrading
8
degrading capacity
8
cells
6
hne
6
mesangial
5
metabolic rates
4
rates 4-hydroxynonenal
4
4-hydroxynonenal tubular
4

Similar Publications

Mechanical forces such as glomerular hyperfiltration are crucial in the pathogenesis and progression of diabetic kidney disease. Piezo2 is a mechanosensitive cation channel and plays a major role in various biological and pathophysiological phenomena. We previously reported Piezo2 expression in mouse and rat kidneys and its alteration by dehydration and hypertension.

View Article and Find Full Text PDF

Purpose: This study seeks to investigate the fundamental molecular processes through which histone deacetylase 9 (HDAC9) governs the proliferation of glomerular mesangial cells in the context of immunoglobulin A nephropathy (IgAN) and to identify novel targets for clinical research on IgAN.

Methods: Data from high-throughput RNA sequencing for IgAN were procured from the Gene Expression Omnibus database to assess the expression profiles and clinical diagnostic significance of histone deacetylase family proteins (HDACs). Blood samples from 20 IgAN patients were employed in RT-qPCR analysis, and the spearman linear regression method was utilized to analyze the clinical correlation.

View Article and Find Full Text PDF

Background: Mizagliflozin (MIZ) is a specific inhibitor of sodium-glucose cotransport protein 1 (SGLT1) originally developed as a medication for diabetes.

Aim: To explore the impact of MIZ on diabetic nephropathy (DN).

Methods: Diabetic mice were created using db/db mice.

View Article and Find Full Text PDF

The maintenance of a healthy epithelial-endothelial juxtaposition requires cross-talk within glomerular cellular niches. We sought to understand the spatially-anchored regulation and transition of endothelial and mesangial cells from health to injury in DKD. From 74 human kidney samples, an integrated multi-omics approach was leveraged to identify cellular niches, cell-cell communication, cell injury trajectories, and regulatory transcription factor (TF) networks in glomerular capillary endothelial (EC-GC) and mesangial cells.

View Article and Find Full Text PDF

Regulatory role of the mTOR signaling pathway in autophagy and mesangial proliferation in IgA nephropathy.

Zhong Nan Da Xue Xue Bao Yi Xue Ban

August 2024

Department of Nephrology, Second Xiangya Hospital, Central South University, Changsha 410011.

Objectives: IgA nephropathy (IgAN) is the most common primary glomerular disease in China, but its pathogenesis remains unclear. This study aims to explore the regulatory role of the mammalian target of rapamycin (mTOR) signaling pathway in autophagy and mesangial proliferation during renal injury in IgA.

Methods: The activity of mTOR and autophagy was evaluated in kidney samples from IgAN patients and in an IgAN mouse model induced by oral bovine serum albumin and carbon tetrachloride (CCl4) injection.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!