Abstract
Podocyte injury plays an important role in glomerulosclerosis in IgA nephropathy (IgAN), and detachment from the glomerular basement membrane is the main cause of podocyte damage. In a previous study we found that medium from mesangial cells incubated with aggregated IgA1 (aIgA1) isolated from IgAN patients decreased podocyte adhesive capacity. However, the underlying mechanism remains unclear. Podocytes were incubated in medium from mesangial cells incubated with aIgA1 isolated from IgAN patients, enalaprilat (10-5 M) and chymostatin (20 μM), or with enalaprilat and chymostatin separately. Podocyte adhesive capacity was evaluated by cell counting and hexosaminidase assay. Expression of the renin angiotensin system was measured by real-time PCR, Western blot analysis and ELISA. Angiotensinogen, renin and angiotensin II type 1 and 2 receptors mRNA and protein expression, angiotensin-converting enzyme activity, and angiotensin II levels increased in podocyte lysates and conditioned culture media on exposure to mesangial medium containing aIgA1 from IgAN patients (P <0.05). Enalaprilat or chymostatin partly improved the reduced adhesive capacity of podocytes compared to cells exposed to mesangial medium (P <0.05), but it was still lower than for podocytes exposed to mesangial medium containing aIgA1 from healthy controls (P <0.05). Our findings indicate that activation of the renin angiotensin system in podocytes is partly involved in downregulation of adhesive capacity in podocytes by mesangial medium in IgA nephropathy.
Highlights
IgA nephropathy (IgAN) is the most common type of primary glomerular nephritis in China and is the main cause of end-stage renal disease [1]
Podocyte injury plays an important role in glomerulosclerosis in IgA nephropathy (IgAN), and detachment from the glomerular basement membrane is the main cause of podocyte damage
In a previous study we found that medium from mesangial cells incubated with aggregated IgA1 isolated from IgAN patients decreased podocyte adhesive capacity
Summary
IgA nephropathy (IgAN) is the most common type of primary glomerular nephritis in China and is the main cause of end-stage renal disease [1]. Urinary podocyte excretion is related to glomerular sclerosis and interstitial fibrosis, which indicate that podocyturia represents clinical evidence of renal damage [5]. There are two mechanisms that could be suggested for podocyte loss: detachment from the glomerular basement membrane and apoptosis [6]. Interesting experiments have explored whether urinary podocytes are fully viable, can be cultivated and continue to synthesise podocyte-specific proteins in vitro in both experimental and human glomerular disease; the ratio of apoptotic podocytes was
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