ETA Activation Mediates Angiotensin II-Induced Infiltration of Renal Cortical T Cells

Boesen, Erika I.; Krishnan, Karthik R.; Pollock, Jennifer S.; Pollock, David M.

doi:10.1681/asn.2010020193

Cited by 18 publications

(19 citation statements)

References 34 publications

(24 reference statements)

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“…Similarly, ET A receptor blockade in diabetic rats provides anti-inflammatory actions by reducing hyperglycemia-dependent increases in early inflammatory markers such as MCP-1 and ICAM-1 [24]. In addition, ET A receptor activation mediates renal infiltration of T cells in angiotensin II-infused animals [39]. Furthermore, a recent clinical study has uncovered a new interaction between ET-1 and the immune system, with functional autoantibodies against ET A receptors involved in atherosclerotic pathophysiology [40].…”

Section: Role Of Et-1 In the Cardiovascular And Renal Systemsmentioning

confidence: 99%

Role of the endothelin system in sexual dimorphism in cardiovascular and renal diseases

et al. 2016

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Epidemiological studies of blood pressure in men and women and in experimental animal models point to substantial sex differences in the occurrence of arterial hypertension as well as in the various manifestations of arterial hypertension, including myocardial infarction, stroke, retinopathy, chronic kidney failure, as well as hypertension-associated diseases (e.g. diabetes mellitus). Increasing evidence demonstrates that the endothelin (ET) system is a major player in the genesis of sex differences in cardiovascular and renal physiology and diseases. Sex differences in the ET system have been described in the vasculature, heart and kidney of humans and experimental animals. In the current review, we briefly describe the role of the ET system in the cardiovascular and renal systems. We also update information on sex differences at different levels of the ET system including synthesis, circulating and tissue levels, receptors, signaling pathways, ET actions, and responses to antagonists in different organs that contribute to blood pressure regulation. Knowledge of the mechanisms underlying sex differences in arterial hypertension can impact therapeutic strategies. Sex-targeted and/or sex-tailored approaches may improve treatment of cardiovascular and renal diseases.

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Section: Role Of Et-1 In the Cardiovascular And Renal Systemsmentioning

confidence: 99%

Role of the endothelin system in sexual dimorphism in cardiovascular and renal diseases

et al. 2016

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“…TNF-α is one of the most potent inducers of cell death 71 and plays a role in the development of salt-sensitive kidney disease. 75,78,79 We also reported that T cell accumulation in the renal cortex of angiotensin II-induced hypertensive mice was mediated by ET A receptors independent of blood pressure, while T cell accumulation in the medulla was blood pressure dependent. Interestingly, TUDCA failed to decrease the numbers of TUNEL-positive cells in the outer medulla of ET B -deficient rats.…”

Section: Discussionmentioning

confidence: 74%

“…23,70 We demonstrate that loss of ET B function is associated with exaggerated high salt-mediated cell death in the renal cortex. 75 Similar to the ET B deficient rat, this model displays increased ET-1, 76 over-activation of ET A receptors. 72,73 TUDCA significantly attenuated the excretion of TNF-α and also decreased cortical cell death in ET B -deficient rats fed a high salt diet.…”

Section: Discussionmentioning

confidence: 80%

Tauroursodeoxycholic acid (TUDCA) abolishes chronic high salt‐induced renal injury and inflammation

et al. 2018

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Aim: Chronic high salt intake exaggerates renal injury and inflammation, especially with the loss of functional ET B receptors. Tauroursodeoxycholic acid (TUDCA) is a chemical chaperone and bile salt that is approved for the treatment of hepatic diseases. Our aim was to determine whether TUDCA is reno-protective in a model of ET B receptor deficiency with chronic high salt-induced renal injury and inflammation. Methods: ET B -deficient and transgenic control rats were placed on normal (0.8% NaCl) or high salt (8% NaCl) diet for 3 weeks, receiving TUDCA (400 mg/kg/d; ip) or vehicle. Histological and biochemical markers of kidney injury, renal cell death and renal inflammation were assessed. Results: In ET B -deficient rats, high salt diet significantly increased glomerular and proximal tubular histological injury, proteinuria, albuminuria, excretion of tubular injury markers KIM-1 and NGAL, renal cortical cell death and renal CD4 + T cell numbers. TUDCA treatment increased proximal tubule megalin expression as well as prevented high salt diet-induced glomerular and tubular damage in ET B -deficient rats, as indicated by reduced kidney injury markers, decreased glomerular permeability and proximal tubule brush border restoration, as well as reduced renal inflammation. However, TUDCA had no significant effect on blood pressure. Conclusions: TUDCA protects against the development of glomerular and proximal tubular damage, decreases renal cell death and inflammation in the renal cortex in rats with ET B receptor dysfunction on a chronic high salt diet. These results highlight the potential use of TUDCA as a preventive tool against chronic high salt induced renal damage. K E Y W O R D SCD4 + T cells, cell death, ET B receptors, high salt diet, renal injury

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“…Chen and colleagues (11) also provided confirmation of P-selectin upregulation ex vivo in their study via immunohistochemical methods. Together, these studies indicate that this methodology could also prove useful in assessing progression or treatment of renal injury due to other causes, since renal inflammation occurs in a variety of disease states, including chronic renal failure (33), hypertension (7,13), diabetes (15), glomerulonephritis (39), and autoimmune diseases such as systemic lupus erythematosus (22). In addition, ultrasound in conjunction with specialized contrast agent destruction has been used as an efficient means of gene transfer in the kidney (21,23).…”

Section: Discussionmentioning

confidence: 99%

Use of ultrasound to assess renal reperfusion and P-selectin expression following unilateral renal ischemia

Boesen

Crislip

Sullivan

2012

American Journal of Physiology-Renal Physiology

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Renal ischemia-reperfusion injury is a major cause of acute kidney injury that carries a high mortality rate and increases the risk of later development of hypertension and chronic kidney disease. Although mouse models have contributed much to our understanding of the mechanisms involved, studying aspects of the injury process in vivo remains technically challenging. This study validates the use of noninvasive ultrasound imaging to assess both renal perfusion and vascular adhesion molecule expression following 1-h unilateral renal ischemia in male and female mice. Pulsed-wave Doppler measurements of renal arterial blood velocity revealed renal perfusion recoveries of 56 ± 9% in male and 69 ± 10% in female mice 1 h after the commencing of reperfusion, which is similar to what we have previously published using conventional invasive methodology. At 24 h postischemia, renal perfusion was 40 ± 8% in male and 46 ± 7% in female mice, representing a further significant reduction of perfusion (P(Time) < 0.001). Using ultrasound imaging of a P-selectin-targeted contrast agent, a significant increase in vascular P-selectin protein expression was observed after 1-h reperfusion in the cortex of the postischemic compared with contralateral kidney in both male and female mice (18 ± 5 vs. 3 ± 3 intensity units in male and 30 ± 6 vs. 0 ± 4 in female mice, P(Ischemia) < 0.01). An approximately sixfold increase in P-selectin mRNA was observed ex vivo in the renal vasculature of male and female mice at this time point (P < 0.01). In conclusion, ultrasound represents an effective and noninvasive method for the measurement of both renal perfusion and vascular adhesion molecule expression in mice.

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ETA Activation Mediates Angiotensin II-Induced Infiltration of Renal Cortical T Cells

Cited by 18 publications

References 34 publications

Role of the endothelin system in sexual dimorphism in cardiovascular and renal diseases

Role of the endothelin system in sexual dimorphism in cardiovascular and renal diseases

Tauroursodeoxycholic acid (TUDCA) abolishes chronic high salt‐induced renal injury and inflammation

Use of ultrasound to assess renal reperfusion and P-selectin expression following unilateral renal ischemia

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