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Hyperglycemic Stress Impairs the Stemness Capacity of Kidney Stem Cells in Rats.

Yang G, Jia Y, Li C, Cheng Q, Yue W, Pei X - PLoS ONE (2015)

Bottom Line: However, KSC proliferation, differentiation ability and tolerance to hypoxia were decreased in high-glucose cultures.Taken together, these results suggest the high-glucose microenvironment can damage the reparative ability of KSCs.It may result in a decreased of recovery capability of renal tubules from injury.

View Article: PubMed Central - PubMed

Affiliation: Department of Geriatric Nephrology, Chinese PLA General Hospital, State Key Laboratory of Kidney Disease, Beijing, China.

ABSTRACT
The incidence of acute kidney injury in patients with diabetes is significantly higher than that of patients without diabetes, and may be associated with the poor stemness capacity of kidney stem cells (KSCs) and limited recovery of injured renal tubules. To investigate the effects of hyperglycemic stress on KSC stemness, KSCs were isolated from the rat renal papilla and analyzed for their self-renewal and differentiation abilities. Our results showed that isolated KSCs expressed the mesenchymal stem cell markers N-cadherin, Nestin, CD133, CD29, CD90, and CD73. Moreover, KSCs co-cultured with hypoxia-injured renal tubular epithelial cell (RTECs) induced the expression of the mature epithelial cell marker CK18, suggesting that the KSCs could differentiate into RTECs in vitro. However, KSC proliferation, differentiation ability and tolerance to hypoxia were decreased in high-glucose cultures. Taken together, these results suggest the high-glucose microenvironment can damage the reparative ability of KSCs. It may result in a decreased of recovery capability of renal tubules from injury.

No MeSH data available.


Related in: MedlinePlus

Embryonic stem (ES) cell marker expression in KSCs.(A) Nanog, Oct4/Pou5f1, and Sox2 gene expression in KSCs and RTECs. Data represents the mean fold change ± standard error of the mean (SEM) when comparing KSCs to RTECs. All values were normalized to Gapdh expression. (**P < 0.01). B: Western blot analysis of ES markers in KSCs and RTECs. β-actin was used as an internal control.
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pone.0139607.g005: Embryonic stem (ES) cell marker expression in KSCs.(A) Nanog, Oct4/Pou5f1, and Sox2 gene expression in KSCs and RTECs. Data represents the mean fold change ± standard error of the mean (SEM) when comparing KSCs to RTECs. All values were normalized to Gapdh expression. (**P < 0.01). B: Western blot analysis of ES markers in KSCs and RTECs. β-actin was used as an internal control.

Mentions: Evaluation of embryonic stem (ES) cell marker gene expression—including that of Nanog, Oct4/Pou5f1, and Sox2—revealed higher levels in the KSCs when compared to RTEC counterparts (Fig 5A). This was consistent with data from Sox2 and Oct4 protein expression analysis (Fig 5B).


Hyperglycemic Stress Impairs the Stemness Capacity of Kidney Stem Cells in Rats.

Yang G, Jia Y, Li C, Cheng Q, Yue W, Pei X - PLoS ONE (2015)

Embryonic stem (ES) cell marker expression in KSCs.(A) Nanog, Oct4/Pou5f1, and Sox2 gene expression in KSCs and RTECs. Data represents the mean fold change ± standard error of the mean (SEM) when comparing KSCs to RTECs. All values were normalized to Gapdh expression. (**P < 0.01). B: Western blot analysis of ES markers in KSCs and RTECs. β-actin was used as an internal control.
© Copyright Policy
Related In: Results  -  Collection

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Show All Figures
getmorefigures.php?uid=PMC4592017&req=5

pone.0139607.g005: Embryonic stem (ES) cell marker expression in KSCs.(A) Nanog, Oct4/Pou5f1, and Sox2 gene expression in KSCs and RTECs. Data represents the mean fold change ± standard error of the mean (SEM) when comparing KSCs to RTECs. All values were normalized to Gapdh expression. (**P < 0.01). B: Western blot analysis of ES markers in KSCs and RTECs. β-actin was used as an internal control.
Mentions: Evaluation of embryonic stem (ES) cell marker gene expression—including that of Nanog, Oct4/Pou5f1, and Sox2—revealed higher levels in the KSCs when compared to RTEC counterparts (Fig 5A). This was consistent with data from Sox2 and Oct4 protein expression analysis (Fig 5B).

Bottom Line: However, KSC proliferation, differentiation ability and tolerance to hypoxia were decreased in high-glucose cultures.Taken together, these results suggest the high-glucose microenvironment can damage the reparative ability of KSCs.It may result in a decreased of recovery capability of renal tubules from injury.

View Article: PubMed Central - PubMed

Affiliation: Department of Geriatric Nephrology, Chinese PLA General Hospital, State Key Laboratory of Kidney Disease, Beijing, China.

ABSTRACT
The incidence of acute kidney injury in patients with diabetes is significantly higher than that of patients without diabetes, and may be associated with the poor stemness capacity of kidney stem cells (KSCs) and limited recovery of injured renal tubules. To investigate the effects of hyperglycemic stress on KSC stemness, KSCs were isolated from the rat renal papilla and analyzed for their self-renewal and differentiation abilities. Our results showed that isolated KSCs expressed the mesenchymal stem cell markers N-cadherin, Nestin, CD133, CD29, CD90, and CD73. Moreover, KSCs co-cultured with hypoxia-injured renal tubular epithelial cell (RTECs) induced the expression of the mature epithelial cell marker CK18, suggesting that the KSCs could differentiate into RTECs in vitro. However, KSC proliferation, differentiation ability and tolerance to hypoxia were decreased in high-glucose cultures. Taken together, these results suggest the high-glucose microenvironment can damage the reparative ability of KSCs. It may result in a decreased of recovery capability of renal tubules from injury.

No MeSH data available.


Related in: MedlinePlus