Captopril reverses high glucose‐induced effects on LLC‐PK1 cells partly by enhancing facilitative glucose transporter messenger RNA expressions

Yang, Mei‐Li; Guh, Jinn‐Yuh; Yang, Yu‐Lin; Chang, Chun-Chang; Chuang, Li‐Yeh

doi:10.1080/15216549700201531

Cited by 8 publications

(10 citation statements)

References 18 publications

(22 reference statements)

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“…Consistent with our findings, a similar G1 phase arrest has been observed in other studies using different types of renal tubular cells [8]. Together, these findings suggest that tubular renal cell hypertrophy occurs in cell cycle-dependent manner [8, 32, 51]. …”

Section: Discussionsupporting

confidence: 93%

Renoprotective Effects of Aldose Reductase Inhibitor Epalrestat against High Glucose-Induced Cellular Injury

Gamal

Eid

Munusamy

2017

BioMed Research International

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Diabetic nephropathy (DN) is the leading cause of end stage renal disease worldwide. Increased glucose flux into the aldose reductase (AR) pathway during diabetes was reported to exert deleterious effects on the kidney. The objective of this study was to investigate the renoprotective effects of AR inhibition in high glucose milieu in vitro. Rat renal tubular (NRK-52E) cells were exposed to high glucose (30 mM) or normal glucose (5 mM) media for 24 to 48 hours with or without the AR inhibitor epalrestat (1 μM) and assessed for changes in Akt and ERK1/2 signaling, AR expression (using western blotting), and alterations in mitochondrial membrane potential (using JC-1 staining), cell viability (using MTT assay), and cell cycle. Exposure of NRK-52E cells to high glucose media caused acute activation of Akt and ERK pathways and depolarization of mitochondrial membrane at 24 hours. Prolonged high glucose exposure (for 48 hours) induced AR expression and G1 cell cycle arrest and decreased cell viability (84% compared to control) in NRK-52E cells. Coincubation of cells with epalrestat prevented the signaling changes and renal cell injury induced by high glucose. Thus, AR inhibition represents a potential therapeutic strategy to prevent DN.

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Section: Discussionsupporting

confidence: 93%

Renoprotective Effects of Aldose Reductase Inhibitor Epalrestat against High Glucose-Induced Cellular Injury

Gamal

Eid

Munusamy

2017

BioMed Research International

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“…Total RNA was extracted as described in our previous study [Yang et al, 1997]. As described in our previous study [Lee et al, 2004], CTGF cDNA probe was obtained from a PCR fragment (558 bp, derived from forward primer: 5 0 -GAG TGG GTG TGT GAC GAG CCC AAG G-3 0 and reverse primer: 5 0 -ATG TCT CCG TAC ATC TTC CTG TAG T-3 0 ) of HK-2 cDNA.…”

Section: Northern Blotting Of Ctgf Mrnamentioning

confidence: 99%

“…GAPDH cDNA probe was obtained from American Type Culture Collection (Manassas, VA). CTGF mRNA was determined by Northern blotting modified from our previous study [Yang et al, 1997]. Briefly, 100 mg of RNA were separated on 1% agarose, 1M formaldehyde gel, transferred onto nylon filters (Hybond-N, Amersham Co., Buckinghamshier, UK) and fixed by ultraviolet irradiation.…”

Section: Northern Blotting Of Ctgf Mrnamentioning

confidence: 99%

Advanced glycation end‐product‐induced mitogenesis and collagen production are dependent on angiotensin II and connective tissue growth factor in NRK‐49F cells

Lee

Guh

Chen

et al. 2005

J of Cellular Biochemistry

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Diabetic nephropathy (DN) is characterized by glomerulopathy and tubulointerstitial expansion followed by renal fibrosis. Angiotensin II (Ang II) and connective tissue growth factor (CTGF) are involved in the pathogenesis of DN, while Janus kinase 2 (JAK2) is important in advanced glycation end-product (AGE)-induced effects in renal interstitial (NRK-49F) fibroblasts. Thus, we studied the role of Ang II, CTGF, and JAK2 in AGE-induced effects in NRK-49F cells. We found that AGE (150 microg/ml) increased mitogenesis and type I collagen production at 7 days while Ang II (10(-7)M) increased mitogenesis and type I collagen production at 3 days. We also found that AGE (150 microg/ml) increased angiotensinogen protein at 2 days, which was attenuated by AG-490 (a JAK2 inhibitor). AGE (150 microg/ml) increased CTGF mRNA and protein expression at 3 and 5 days, respectively. Ang II (10(-7)M) increased CTGF mRNA and protein expression at 1 and 2 days, respectively, which were attenuated by AG-490. Moreover, losartan (a type I angiotensin receptor blocker) and captopril (an angiotensin converting enzyme inhibitor) attenuated AGE-induced CTGF mRNA/protein expression while attenuating AGE-induced mitogenesis and type I collagen production. AG-490 and CTGF antisense (but not sense) oligodeoxynucleotide (ODN) attenuated Ang II (10(-7)M) and AGE-induced mitogenesis and type I collagen production at 3 and 7 days, respectively. We concluded that AGE (150 microg/ml)-induced mitogenesis and type I collagen production are dependent on the Ang II-JAK2-CTGF pathway in NRK-49F cells. Moreover, Ang II-induced mitogenesis and type I collagen production are dependent on the JAK2-CTGF pathway.

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“…GAPDH cDNA probe was obtained from ATCC. CTGF mRNA was determined by Northern blotting modified from our previous study [Yang et al, 1997]. Briefly, one hundred micrograms of RNA were separated on 1% agarose, 1 M formaldehyde gel, transferred onto nylon filters (Hybond-N, Amersham Co., Buckinghamshier, UK) and fixed by ultraviolet irradiation.…”

Section: Northern Blotting Of Ctgf Mrnamentioning

confidence: 99%

“…Total RNA was extracted as described in our previous study [Yang et al, 1997]. CTGF cDNA probe was obtained from a PCR fragment (558 bp, derived from forward primer: 5 0 -GAG TGG GTG TGT GAC GAG CCC AAG G-3 0 and reverse primer: 5 0 -ATG TCT CCG TAC ATC TTC CTG TAG T-3 0 ) of HK-2 cDNA.…”

Section: Northern Blotting Of Ctgf Mrnamentioning

confidence: 99%

Leptin and connective tissue growth factor in advanced glycation end‐product‐induced effects in NRK‐49F cells

Lee

Guh

Chen

et al. 2004

J of Cellular Biochemistry

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Previously, we showed that Janus kinase 2 (JAK2) is important in advanced glycation end-product (AGE)-induced effects in renal interstitial (NRK-49F) fibroblasts. Leptin is a JAK2-activating cytokine via the long form leptin receptor (Ob-Rb). Leptin and connective tissue growth factor (CTGF) may be involved in renal fibrosis. However, the relationship between leptin and CTGF in terms of AGE-induced effects remains unknown. Thus, the effects of AGE (150 microg/ml) and leptin on mitogenesis, CTGF and collagen expression in NRK-49F cells were determined. We found that leptin and AGE increased mitogenesis and type I collagen protein expression at 3 and 7 days, respectively. AGE increased leptin mRNA and protein expression at 2-3 days. AGE increased CTGF mRNA and protein expression at 3-5 days. AG-490 (JAK2 inhibitor) abrogated AGE-induced leptin mRNA and protein expression at 2-3 days. AG-490 and Ob-Rb anti-sense oligodeoxynucleotides (ODN) abrogated AGE-induced CTGF mRNA and protein expression at 3-5 days. AG-490 and CTGF anti-sense ODN abrogated AGE-induced mitogenesis and collagen protein expression at 7 days. Additionally, leptin dose (0.2-1 microg/ml) and time (1-2 days)-dependently increased CTGF protein expression. AG-490 abrogated leptin (1 microg/ml)-induced CTGF protein expression at 2 days. AG-490 and CTGF anti-sense ODN abrogated leptin-induced mitogenesis and collagen protein expression at 3 days. We concluded that AGE induced JAK2 to increase leptin while leptin induced JAK2 to increase CTGF-induced mitogenesis and type I collagen protein expression in NRK-49F cells. Additionally, AGE-induced mitogenesis and type I collagen protein expression were dependent on leptin-induced CTGF.

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Captopril reverses high glucose‐induced effects on LLC‐PK1 cells partly by enhancing facilitative glucose transporter messenger RNA expressions

Cited by 8 publications

References 18 publications

Renoprotective Effects of Aldose Reductase Inhibitor Epalrestat against High Glucose-Induced Cellular Injury

Renoprotective Effects of Aldose Reductase Inhibitor Epalrestat against High Glucose-Induced Cellular Injury

Advanced glycation end‐product‐induced mitogenesis and collagen production are dependent on angiotensin II and connective tissue growth factor in NRK‐49F cells

Leptin and connective tissue growth factor in advanced glycation end‐product‐induced effects in NRK‐49F cells

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