Angiotensin II blockade prevents hyperglycemia-induced activation of JAK and STAT proteins in diabetic rat kidney glomeruli.

@article{Banes2004AngiotensinIB,
  title={Angiotensin II blockade prevents hyperglycemia-induced activation of JAK and STAT proteins in diabetic rat kidney glomeruli.},
  author={Amy K.L. Banes and Se{\'a}n M Shaw and John M Jenkins and Heather Redd and Farhad Amiri and David M. Pollock and Mario B. Marrero},
  journal={American journal of physiology. Renal physiology},
  year={2004},
  volume={286 4},
  pages={
          F653-9
        },
  url={https://api.semanticscholar.org/CorpusID:23025980}
}
  • A. BanesS. Shaw M. Marrero
  • Published in AJP - Renal Physiology 1 April 2004
  • Medicine
  • American journal of physiology. Renal physiology
It is demonstrated that hyperglycemia induces activation of JAK2 and the STATs in vivo via an ANG II-dependent mechanism and that these proteins may be involved in the early kidney damage associated with diabetes.
View on PubMed
ajprenal.physiology.org
110 Citations
Highly Influential Citations
7
Background Citations
40
Methods Citations
6
Results Citations
2

Figures and Tables from this paper

110 Citations

Angiotensin II and endothelin-1 augment the vascular complications of diabetes via JAK2 activation.

It is demonstrated that JAK2 activation in vivo participates in the development of vascular complications associated with STZ-induced diabetes.

Effect of simvastatin on high glucose- and angiotensin II-induced activation of the JAK/STAT pathway in mesangial cells.

It is demonstrated that simvastatin blocks ANG II-induced activation of the JAK/STAT pathway in the diabetic environment, in vitro and in vivo, and provides new insights into the molecular mechanisms underlying early diabetic nephropathy.

Angiotensin II-induced JNK activation is mediated by NAD(P)H oxidase in isolated rat pancreatic islets

Angiotensin III Induces JAK2/STAT3 Leading to IL-6 Production in Rat Vascular Smooth Muscle Cells

It is suggested that Ang III acts on AT1Rs to induce JAK2/STAT3, leading to an increase in IL-6 in cultured VSMCs, important in establishing Ang III as an important physiologically relevant peptide inVSMCs.

Suppressors of cytokine signaling abrogate diabetic nephropathy.

Results provide direct evidence for a link between the JAK/STAT/SOCS axis and hyperglycemia-induced cell responses in the kidney and suppressors of cytokine signaling by increasing intracellular SOCS proteins may have therapeutic potential in diabetic nephropathy.

Angiotensin II and endothelin-1 augment the vascular complications of diabetes via JAK 2 activation

It is demonstrated that JAK2 activation in vivo participates in the development of vascular complications associated with STZinduced diabetes.

Macrophage-derived IL-6 contributes to ANG II-mediated angiotensinogen stimulation in renal proximal tubular cells.

It is demonstrated that ANG II-induced IL-6 elevation in MΦ enhances activation of the JAK-STAT pathway and consequent AGT upregulation in PTCs, suggesting involvement of an immune response in driving intrarenal RAS activity.

Fluvastatin inhibits activation of JAK and STAT proteins in diabetic rat glomeruli and mesangial cells under high glucose conditions

The regulation of the phosphorylation of JAK/STAT by fluvastatin may be responsible for its renal protective effects on diabetic nephropathy.

Role of the JAK/STAT signaling pathway in diabetic nephropathy.

This review focuses on some of the key elements in the diabetic microenvironment, especially high glucose and the accumulation of advanced glycoxidation end products and considers their impact on ANG II and other vasoactive peptide-mediated signaling events in vitro and in vivo.

Interleukin 6 Knockout Prevents Angiotensin II Hypertension: Role of Renal Vasoconstriction and Janus Kinase 2/Signal Transducer and Activator of Transcription 3 Activation

It is suggested that IL-6-dependent activation of the renal janus kinase 2/signal transducer and activator of transcription 3 pathway plays a role in Ang II hypertension but not by mediating the effect of Ang II to decrease total RBF.
...

19 References

Renal angiotensin II receptors and protein kinase C in diabetic rats: effects of insulin and ACE inhibition.

It is concluded that in STZ-diabetic rats ANG II receptors and PKC isoforms on preglomerular vessels and glomeruli are differentially regulated by treatment with insulin and/or captopril.

Hyperglycemia Enhances Angiotensin II-induced Janus-activated Kinase/STAT Signaling in Vascular Smooth Muscle Cells*

The effects of hyperglycemia (HG) is examined to suggest that HG augments Ang II induction of VSMC proliferation by increasing signal transduction through the JAK/STAT pathway.

Angiotensin II activation of the JAK/STAT pathway in mesangial cells is altered by high glucose.

Evidence is provided that activation of the JAK/STAT pathway by HG or/and Ang II may be of importance in the increased GMC cell growth and collagen IV synthesis that is seen in diabetic nephropathy.

Renoprotective effects of angiotensin II receptor blockade in type 1 diabetic patients with diabetic nephropathy.

The results indicate that the reduction in albuminuria and blood pressure during ACE inhibition is primarily caused by interference in the renin-angiotensin system and suggests that losartan represents a valuable new drug in the treatment of hypertension and proteinuria in type 1 diabetic patients with diabetic nephropathy.

Direct stimulation of Jak/STAT pathway by the angiotensin II AT1 receptor

It is shown here that angiotensin II induces the rapid phosphorylation of tyrosine in the intracellular kinases Jak2 and Tyk2 in rat aortic smooth-muscle cells and that thisosphorylation is associated with increased activity of Jak2.

The functional role of the JAK-STAT pathway in post-infarction remodeling.

Regulation of angiotensin II-induced JAK2 tyrosine phosphorylation: roles of SHP-1 and SHP-2.

Angiotensin II (ANG II) exerts its effects on vascular smooth muscle cells through G protein-coupled AT1 receptors. ANG II stimulation activates the Janus kinase/signal transducers and activators of…

Inhibition of the JAK/STAT Signaling Pathway Prevents the High Glucose-Induced Increase in TGF-β and Fibronectin Synthesis in Mesangial Cells

Results provide direct evidence for linkages between JAK2, STAT1, and the glucose-induced overproduction of TGF-β and fibronectin in GMC.

ETA receptor blockade attenuates the hypertension but not renal dysfunction in DOCA-salt rats.

ETA receptors appear to play a role in the maintenance and development of DOCA-salt hypertension but not in the accompanying reduction of renal function.

Angiotensin II receptors.

This review examines the recent progress in the field of angiotensin receptors. Multiplicity of these receptors was demonstrated initially on the basis of pharmacologic differences and then confirmed…

Related Papers

Showing 1 through 3 of 0 Related Papers