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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

Effects of high glucose on KSC differentiation into epithelial cells.(A) Flow cytometry analysis of CK18 expression (P = 0.045); (B) E-cadherin and AQP-1 gene expression analysis by qRT-PCR. (*P < 0.05, **P < 0.01).
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pone.0139607.g007: Effects of high glucose on KSC differentiation into epithelial cells.(A) Flow cytometry analysis of CK18 expression (P = 0.045); (B) E-cadherin and AQP-1 gene expression analysis by qRT-PCR. (*P < 0.05, **P < 0.01).

Mentions: Normal- or high-glucose medium-pretreated KSCs were co-cultured with hypoxia-injured RTECs in induction medium to investigate their propensity to undergo epithelial differentiation. Notably, after induction, normal-glucose pretreated KSCs showed a significantly higher expression of CK18 than those of high-glucose pretreated KSCs (52.37 ± 1.23 vs. 39.86 ± 7.44%, P < 0.05) (Fig 7A). Moreover, the induction of epithelial E-cadherin and AQP-1 expression in KSCs were markedly increased in co-cultures with injured RTECs when compared to single-culture controls (P < 0.01), while compare with high-glucose medium-pretreated KSCs induced group, E-cadherin and AQP-1 expression levels increased more obviously in normal-glucose medium-pretreated KSCs induced group (P < 0.01) (Fig 7B).


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)

Effects of high glucose on KSC differentiation into epithelial cells.(A) Flow cytometry analysis of CK18 expression (P = 0.045); (B) E-cadherin and AQP-1 gene expression analysis by qRT-PCR. (*P < 0.05, **P < 0.01).
© Copyright Policy
Related In: Results  -  Collection

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

pone.0139607.g007: Effects of high glucose on KSC differentiation into epithelial cells.(A) Flow cytometry analysis of CK18 expression (P = 0.045); (B) E-cadherin and AQP-1 gene expression analysis by qRT-PCR. (*P < 0.05, **P < 0.01).
Mentions: Normal- or high-glucose medium-pretreated KSCs were co-cultured with hypoxia-injured RTECs in induction medium to investigate their propensity to undergo epithelial differentiation. Notably, after induction, normal-glucose pretreated KSCs showed a significantly higher expression of CK18 than those of high-glucose pretreated KSCs (52.37 ± 1.23 vs. 39.86 ± 7.44%, P < 0.05) (Fig 7A). Moreover, the induction of epithelial E-cadherin and AQP-1 expression in KSCs were markedly increased in co-cultures with injured RTECs when compared to single-culture controls (P < 0.01), while compare with high-glucose medium-pretreated KSCs induced group, E-cadherin and AQP-1 expression levels increased more obviously in normal-glucose medium-pretreated KSCs induced group (P < 0.01) (Fig 7B).

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