Expression of nestin in the podocytes of normal and diseased human kidneys

Su, Wei; Chen, Jing; Yang, Haichun; Li, You; Xu, Linfeng; Wang, Xiang; Li, Ruixi; Gu, Yong; Lin, Shan; Xu, Hong; Breyer, Matthew D.; Hao, Chuan‐Ming

doi:10.1152/ajpregu.00319.2006

Cited by 33 publications

(43 citation statements)

References 20 publications

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“…This may explain that other mutations should be looked for. Indeed, human or animal studies have demonstrated several new mutated proteins that may play a pivotal role in the filtration barrier integrity, including laminin β2 [24], α-actinin-4 [25], CD2AP [26], Neph1 [27], Nck adaptor proteins [28], β-arrestin2 [29], ZHX proteins [30], nestin [31], and TRPC6 [32]. Over the next few years, the addition of clinical studies will be a crucial step forward and will certainly improve the ability to detect and redefine these glomerular renal diseases.…”

Section: Discussionmentioning

confidence: 99%

Genetic forms of nephrotic syndrome: a single-center experience in Brussels

et al. 2009

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The aim of the study was to present our experience in treating children with genetic forms of nephrotic syndrome and diagnosing these diseases. We retrospectively reviewed the clinical data, mutational analyses, histopathological features, treatment modalities, and outcome of 26 consecutive children (20 families) suffering from congenital and/or steroid-resistant nephrotic syndrome who were assessed by genetic analysis. Ten out of 26 children (38%) had congenital nephrotic syndrome, 4/26 (15%) had infantile nephrotic syndrome, 10/26 (38%) had late-onset nephrotic syndrome, and 2/26 (9%) had asymptomatic proteinuria. We detected a mutation in 21/26 (81%) patients and in 15/20 (75%) families. NPHS1 mutation analyses were positive in 4/20 (20%), NPHS2 mutations in 4/20 (20%), WT1 mutations in 4/20 (20%), and PLCE1 mutations in 3/20 (15%) families. NPHS1 and PLCE1 mutations were solely found in patients with the earliest onset. The majority of patients, especially those with early onset of nephrotic syndrome, had serious adverse events related to the nephrotic status, and 19/26 (73%) reached end-stage renal failure at a median age of 27 months. Genetic forms of nephrotic syndrome comprise a heterogeneous group of genetic mutations. The progression toward end-stage renal failure is the rule but is highly variable between patients.

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Section: Discussionmentioning

confidence: 99%

Genetic forms of nephrotic syndrome: a single-center experience in Brussels

et al. 2009

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“…Under normal condition, Nestin is expressed in several glomerular cell types, including mesangial cells and endothelial cells, at the early stage of development and become confined to the podocytes in mature glomeruli [13, 14]. Although Tomioka et al [9] indicated that increased Nestin expression at the tubulointerstitial areas of IgA nephropathy was associated with the deterioration of the renal function, Su et al [10] demonstrated the expression level of Nestin protein and mRNA in the kidneys of patients with IgA nephropathy and proteinuria. The authors also reported that membranous nephropathy and focal segmental glomerular sclerosis with proteinuria were significantly reduced as compared with that in normal kidney, suggesting that Nestin may play an important role in maintaining normal podocyte function.…”

Section: Discussionmentioning

confidence: 99%

Nestin Improves Preeclampsia-Like Symptoms by Inhibiting Activity of Cyclin-Dependent Kinase 5

Yang¹,

Ding²,

Yang³

et al. 2018

Kidney Blood Press Res

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Background/Aims: Preeclampsia (PE) is a pregnancy-specific hypertensive disorder that is characterised by a high incidence of hypertension and proteinuria. Podocytes are involved in the formation of a split membrane, which is the last barrier preventing the leakage of protein into the urine. Nestin, a cytoskeleton protein, is expressed stably in podocytes. However, the association between the Nestin concentration in urine and the progression of PE and the role of Nestin in PE remains unclear. Methods: In the present study, a mouse podocyte cell line, PE-like animal model and PE patients’ urine samples were used. Eilsa kits were used to detect the levels of proteins expression in urine samples from patients and animal models. Western Blotting and immunofluorescence were used to detect proteins expression levels in cell samples and animal tissue samples. Flow cytometry was used to detect the level of apoptosis in cells. Tunel assay was used to detect the levels of apoptosis in animal tissue samples. Results: Nestin levels were significantly increased in PE patients than in hypertensive patients and healthy subjects, and positively correlated with proteinuria and podocalyxin. Ang II treatment decreased the expression of Nestin and Podocin in a time- and dose- dependent manner in podocytes. Restoration of the Nestin levels could reverse Ang II-induced F-actin degradation and attenuate Ang II-mediated podocyte apoptosis, while knockdown of the Nestin level exhibited the opposite. Moreover, the protective role of Nestin on podocytes is mediated by inhibition of the kinase activity of CDK5. In PE-like animal model induced by L-NAME injection, restoration of Nestin lowered the pressure and proteinuria concentration, attenuated the loss of podocytes, and decreased the expression of p35, p53 and the activity of CDK5 kinase, as compared with the control. Conclusions: Our findings suggest that Nestin could improve preeclampsia-like symptoms by inhibiting the activity of CDK5, and Nestin may become a new prognostic factor and a potential therapy target for PE.

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“…Nestin is highly expressed in renal interstitial cells [45,46] or podocytes [47,48] after suffering from tubulointerstitial injury or Glomerular Disease. These evidences suggested that renal Nestin expressing cells may have important roles in kidney homeostasis and tissue repair.…”

Section: Discussionmentioning

confidence: 99%