Role of protein kinase C and cyclic AMP/protein kinase A in high glucose-stimulated transcriptional activation of collagen α1 (IV) in glomerular mesangial cells

Ziyadeh, Fuad N.; Fumo, Peter; Rodenberger, Charles H.; Kuncio, Gerald S.

doi:10.1016/1056-8727(95)80016-8

Cited by 36 publications

(33 citation statements)

References 27 publications

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“…5). However, in addition to PKC the possibility that protein kinase A (PKA) may be involved should be considered as well, since PKA has been described to increase the transcription of type-IV collagen, another ECM protein, in MCs induced with HG (63). This transcriptional increase may be related to the phosphorylation of cAMP-responsive element (CRE)-binding protein (CREB) (64).…”

Section: Discussionmentioning

confidence: 99%

High Glucose Stimulates Synthesis of Fibronectin via a Novel Protein Kinase C, Rap1b, and B-Raf Signaling Pathway

Sun¹,

Sahai²,

Chugh³

et al. 2002

Journal of Biological Chemistry

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Section: Discussionmentioning

confidence: 99%

High Glucose Stimulates Synthesis of Fibronectin via a Novel Protein Kinase C, Rap1b, and B-Raf Signaling Pathway

Sun¹,

Sahai²,

Chugh³

et al. 2002

Journal of Biological Chemistry

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“…With the demonstration of a reduced expression of OCTs after 4 weeks of diabetes, this effect is clearly more than just renoprotection. Although aminoguanidine was used in this study as an inhibitor of advanced glycation, aminoguanidine also inhibits the activity of inducible nitric-oxide synthase, which may be activated in early diabetes (Ziyadeh et al, 1995). However, other inhibitors of inducible nitricoxide synthase (N -nitro-L-arginine methyl ester and methylguanidine) are not renoprotective in diabetes (Soulis et al, 1997a), whereas chemically unrelated inhibitors of glycation, such as pyridoxamine, confer some degree of renal protection in diabetes (Degenhardt et al, 2002).…”

Section: Ages and Organic Cation Clearance In Diabetes 461mentioning

confidence: 99%

The Role of Advanced Glycation in Reduced Organic Cation Transport Associated with Experimental Diabetes

Thomas

Tikellis²,

Kantharidis³

et al. 2004

J Pharmacol Exp Ther

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Tubular dysfunction is an important early manifestation of diabetic nephropathy. Reduced renal expression of organic cation transporters (OCTs) potentially contributes to impaired cation clearance in diabetes. This study examines the role of advanced glycation end-products (AGEs) in mediating these changes. Experimental diabetes was induced with streptozotocin (55 mg/kg). Rats were randomly treated with the AGE inhibitor aminoguanidine for 32 weeks. In a second protocol, diabetic rats were followed with and without low-dose insulin therapy (2 U/day) for 4 weeks. Expression of OCTs was determined by real-time RT-PCR (reverse transcription-polymerase chain reaction) and Western blotting. As a marker of cation transport, the fractional clearance of endogenous N-methylnicotinamide (NMN) was determined by high-performance liquid chromatography. Both short-and long-term diabetes was associated with reduced gene and protein expression of the three renal OCT isotypes. This was associated with a reduction in the fractional clearance of NMN compared with control animals by over 50%. These changes correlated with the accumulation of renal and plasma AGEs. Treatment with the AGE inhibitor aminoguanidine restored the expression of OCT-2 and OCT-3 in diabetic animals and normalized renal NMN clearance. NMN clearance was also improved in diabetic animals receiving lowdose insulin, correlating with a reduction in AGEs and improvement in effective renal plasma flow. These studies demonstrate an early impairment of expression of OCTs and cation clearance associated with diabetes. These changes correlate with the accumulation of AGEs and may be partly attenuated by an AGE inhibitor, implicating a role for AGEs in organic cation transport.

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“…Additionally, the signaling cascade of VEGF regulation in response to Ang-II in podocytes is largely unknown. Many studies have demonstrated protein kinase C activation in diabetic glomeruli and mesangial cells cultured under high glucose conditions (Craven & DeRubertis 1989, Williams & Schrier 1993, Ziyadeh et al 1995, Hoshi et al 2002. Increased p38 mitogen activated protein kinase (MAPK) activity has been demonstrated in diabetic glomeruli (Kang et al 2001), and Ang-II also activated p38 MAPK leading to the induction of fibronectin expression and cellular growth in rat mesangial cells (Reddy et al 2002).…”

Section: Introductionmentioning

confidence: 99%

Angiotensin II stimulates the synthesis of vascular endothelial growth factor through the p38 mitogen activated protein kinase pathway in cultured mouse podocytes

Kang¹,

Park²,

Kim³

et al. 2006

Journal of Molecular Endocrinology

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Role of protein kinase C and cyclic AMP/protein kinase A in high glucose-stimulated transcriptional activation of collagen α1 (IV) in glomerular mesangial cells

Cited by 36 publications

References 27 publications

High Glucose Stimulates Synthesis of Fibronectin via a Novel Protein Kinase C, Rap1b, and B-Raf Signaling Pathway

High Glucose Stimulates Synthesis of Fibronectin via a Novel Protein Kinase C, Rap1b, and B-Raf Signaling Pathway

The Role of Advanced Glycation in Reduced Organic Cation Transport Associated with Experimental Diabetes

Angiotensin II stimulates the synthesis of vascular endothelial growth factor through the p38 mitogen activated protein kinase pathway in cultured mouse podocytes

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