2 edition of role of ACE2 in diabetic kidney injury in mice. found in the catalog.
role of ACE2 in diabetic kidney injury in mice.
Denise W. Wong
Written in English
Diabetes is a leading cause of end-stage renal failure but the mechanisms responsible are not entirely understood. Treatment with angiotensin-converting enzyme (ACE) inhibitors and angiotensin (Ang) II receptor blockers (ARBs) supposedly benefits kidney disease patients by decreasing steady-state Ang II levels; if so, ACE2 may be similarly protective by degrading Ang II, a vasoconstrictor, to Ang-(1-7), a vasodilator. Deletion of the Ace2 gene in diabetic Akita mice (ACE2 KO/Akita) led to an increase in albumin excretion rate (AER), accompanied by greater mesangial matrix expansion and glomerular basement membrane thickening, compared with the Akita mice. Taken together, ACE2 is an important determinant of diabetic kidney injury. Blood glucose levels, blood pressure, and heart function were similar in both diabetic groups. However, treatment with an ARB reduced the AER in ACE2 KO/Akita mice, suggesting that exacerbation of diabetic kidney injury in the ACE2 KO/Akita mice is, in part, Ang II-mediated.
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Monocyte chemoattractant protein-1 promotes the development of diabetic renal injury in streptozotocin-treated mice. Kidney Int 73–80, Crossref PubMed ISI Google Scholar; Chow FY, Nikolic-Paterson DJ, Ozols E, Atkins RC, Tesch GH. Intercellular adhesion molecule-1 deficiency is protective against nephropathy in type 2 Cited by: St. Louis, Feb. 15, -- Scientists at Washington University School of Medicine in St. Louis used genetically modified mice to uncover a potentially important link between diabetes and obesity. Phone , ; Email [email protected]; Website
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We propose that ACE2 ectodomain shedding is associated with reduced renal ACE2 expression in patients with diabetic nephropathy. A recent study demonstrated that insulin treatment reduced ADAM17 and ACE2 shedding in the kidneys of diabetic Akita mice.
The above findings suggest that the urinary ACE2 protein level and ACE2 activity are useful as Cited by: The findings of Bindom et al. that ACE2 overexpression by means of adenoviral gene delivery can improve pancreatic islet β-cell function in db/db mice are exciting and are in keeping with an important role of ACE2 as a therapeutic target for diabetic kidney disease and several other conditions in which overactivity of Ang II is by: Recombinant mouse ACE2 given for 4 weeks by intraperitoneal daily injections in mice with streptozotocin-induced diabetic nephropathy also failed.
Diabetic mice. We conclude that the Diabetic mice develops features of early kidney disease, including albuminuria and a marked increase in GFR. ACE2 activity is increased starting at an early stage in both serum and urine.
Moreover, these alterations can be completely prevented by the chronic administration of insulin. ACE2-deficient mice also show a worse outcome in other inflammation and injury models, such as diabetic and shock-induced kidney injury (,), chronic hepatic injury.
They found, based on urine measurements, that the kidney damage seen in the Akita mice was reversed within two months on the ketogenic diet. In the db/db type 2 diabetes mouse model, the mice developed high blood sugar by 12 weeks of age.
At this time, half of the db/db mice and the non-diabetic mice were placed on the ketogenic diet. Inhibition of kidney proximal tubular glucose reabsorption does not prevent against diabetic nephropathy in type 1 diabetic eNOS knockout mice.
PLoS ONE. 9, Cited by: The organ-specific role of ACE2 has been recently reported in the context of the anatomical restriction of ACE2 expression to the heart and kidneys.
Loss of ACE2 is associated with age-dependent development of glomerulosclerosis and albuminuria as well as exacerbation of diabetic kidney injury in by: 2.
One key feature of diabetic kidney disease in Akita mice is that the severity of renal injury is significantly influenced by genetic background. In this chapter, we describe the Akita model and present some of the experimental studies Cited by: The current pandemic outbreak of COVID originated from Wuhan, China.
It is caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV. Chan J, Lo CS, Shi Y, Chenier I, Zhang SL. Os overexpression of heterogeneous nuclear ribonucleoprotein F prevents systemic hypertension and kidney injury and normalizes renal renin-angiotensin system genes expression in type 2 diabetic Db/db transgenic mice.
J Hypertens. ;34(Suppl 1 - ISH Abstract Book):eCited by: 3. The major clinical associations with the progression of diabetic kidney disease (DKD) are glycemic control and systemic hypertension.
Recent studies have continued to emphasize vasoactive hormone pathways including aldosterone and endothelin which suggest a key role for vasoconstrictor pathways in promoting renal damage in diabetes. The role of glucose per se. In [italic]db/db[/italic] diabetic mice, there was an age-dependent increase in urinary ACE2 protein expression (45, 65 and 90 KDa) which correlates with the degree of albuminuria.
Thus, it is tempting to speculate that urinary ACE2 is being shed from kidney and could be used as index of intra-renal RAS status. / ACE and ACE2 activity in diabetic mice. In: Diabetes. ; Vol. 55, (STZ)-induced diabetic mice.
In kidney cortex, preparations consisting mainly of proximal tubules and cortical collecting tubules, ACE2 activity had a strong positive correlation with ACE2 protein expression (kDa band) in both knockout models and their respective Cited by: We propose that ACE2 ectodomain shedding is associated with reduced renal ACE2 expression in patients with diabetic nephropathy.
A recent study demonstrated that insulin treatment reduced ADAM17 and ACE2 shedding in the kidneys of diabetic Akita mice. The above findings suggest that the urinary ACE2 protein level and ACE2 activity are useful Cited by: Compared with control mice, diabetic mice developed remarkable renal hypertrophy, which is shown in Fig.
1(a) and was assessed as a kidney weight/body weight ratio as well. Diabetic mice with or without G31P injection maintained higher levels of fasting blood glucose and random blood glucose than nondiabetic mice (P Cited by: 8. p38 mitogen-activated protein kinase (MAPK) signaling promotes diabetic kidney injury.
Apoptosis signal-regulating kinase (ASK)1 is one of the upstream kinases in the p38 MAPK-signaling pathway, which is activated by inflammation and oxidative stress, suggesting a possible role for ASK1 in diabetic by: The diabetic mice, which had abnormal amounts of protein in their urine, indicating poor kidney function, showed improvement in kidney function over eight weeks of being on the ketogenic diet.
In (5/6) Nx mice with or without MLN, kidney cortical ACE2 protein expression was significantly decreased at 4 wk, compared with Sham. Inhibition of ACE2 caused a decrease in renal cortical ACE2 activity. Kidney cortical ACE expression and activity did not differ between groups of mice.
We conclude that ACE2 inhibition in diabetic mice worsens albuminuria and causes mesangial expansion and podocyte alterations. These lesions, moreover, are associated with increased ACE expression in the glomerulus showing that the combination of decreased ACE2 activity and high ACE is injurious to the kidney.
Background: Angiotensin Converting Enzyme (ACE) 2 is an important modulator of the Renin Angiotensin System (RAS) and the RAS plays a central role in renovascular hypertension. Very few studies investigated the role of components of the counterregulatory RAS axis (ACE2, Ang-() and Mas receptor) in renovascular hypertension and the results Cited by: 1.
Rosiglitazone treatment of db/db mice normalized hyperglycemia, attenuated renal injury and decreased urinary ACE2 and renal ADAM17 protein expression.
Urinary excreted ACE2 is enzymatically active. Western blot analysis of urinary ACE2 demonstrated two prominent immunoreactive bands at approximately 70 & 90 kDa. the development of diabetic complications like hypertension and nephropathy.
Our previous work demonstrated role of AT1 receptors (AT1R) in the development of hypertension in db/db diabetic mice. The aim of this study was to test the hypothesis that there is upregulation of renal AT1R and imbalance in renal ACE/ACE2 homeostasis in db/db mice Author: Malav Navinchandra Madhu.
Introduction. Diabetic nephropathy (DN) is a serious microvascular complication that affects a significant proportion of patients suffering from both type 1 and type 2 diabetes, accounting for over 40% of end-stage renal disease (ESRD) cases in North t interventions that target the renin-angiotensin aldosterone system (RAAS) along with strict glycemic control are.
COVID appears to enter the body using the ACE2 receptor (found on the surface of many cells, particularly in the lungs. Also found in high concentrations in the heart and kidneys.
Because of its affinity to ACE2 receptors (and the more widespread Renin Aldosterone Angiotensin System or “RAAS”) COVID is causing upset with the whole.
Angiotensin-converting enzyme-2 (ACE2) enhances the degradation of ANG II and its expression is altered in diabetic kidneys, but the regulation of this enzyme in the urine is unknCited by: The following changes occur in db/db mice in the early phase of type 2 diabetes: (1) tyrosine phosphorylation of renal cortical proteins is increased; (2) activities of PI 3-kinase, Akt/PKB, and ERK are stimulated; (3) the insulin receptor is activated in the renal cortex of diabetic mice; (4) similar to the kidney, PI 3-kinase and Akt/PKB Cited by: Irbesartan ( mg/day) reduced the risk of progression to overt diabetic nephropathy by 70% in a 2-year follow-up study of hypertensive microalbuminuric type 2 diabetic patients.
Sulforaphane prevents the development of cardiomyopathy in type 2 diabetic mice probably by reversing oxidative stress-induced inhibition of LKB1/AMPK pathway. J Mol Cell Cardiol. ; – doi: / The unique features of kidney dendritic cells are also examined, as well as their role in various acute and chronic types of kidney disease.
Christian Kurts, Florent Ginhoux. New strategy may help prevent kidney failure in patients with diabetes: Investigational compound slows kidney disease progression in mice.
ScienceDaily. Retrieved Febru from www. Accumulating evidence supports intrinsic genetic susceptibility as an important variable in the progression of diabetic nephropathy in people. Mice provide an experimental platform of unparalleled power for dissecting the genetics of mammalian diseases; however, phenotypic analysis of diabetic mice lags behind that already established for by: Specific kidney cell could be key in the treatment of kidney failure in diabetes More information: Protein tyrosine phosphatase 1B deficiency in podocytes mitigates hyperglycemia-induced renal injury.
BioTek Citations, Jun, ACE2 inhibition worsens glomerular injury in association with increased ACE expression in streptozotocin-induced diabetic mice.
podo-gpcr2-a novel podocyte target plays a pathogenic role in the development of diabetic nephropathy: xiaojie ma the long term effect of stem cell transplantation in mice model of acute kidney injury: eljka veceric-haler from angii() is largely independent of ace2 and prcp: peter daniel serofzo: received sp diferencies in.
Repetitive exposure of diabetic mice to low-dose radiation (LDR) at 25 mGy could significantly attenuate diabetes-induced renal inflammation, oxidative damage, remodeling, and dysfunction, for which, however, the underlying mechanism remained unknown.
The present study explored the effects of LDR on the expression and function of Akt and Nrf2 in the kidney of diabetic by: human diabetic nephropathy. This in vivo approach has thus established the functional importance of the AGE-RAGE system in the development of diabetic nephropathy, and the RAGE-overexpressing IDDM mice are regarded as the first single animal model in which the process of diabetes-induced kidney changes leading to ESRD can be followed.
The AGE. . ACE2, an ACE homolog, can convert Ang II to Ang (1e7) [2,3], and this enzyme is thought to play an essen-tial role in heart functions .
Ang II is the central biological effector of the RAS. Systemic Ang II plays a central role in the regulation of blood pressure (Fig. Ang II is the most potent vasoconstrictor. We previously demonstrated that treatment of diabetic peripheral neuropathy with the short (4 hours) half-life phosphodiesterase 5 (PDE5) inhibitor, sildenafil, improved functional outcome in diabetic db/db mice.
To further examine the effect of PDE5 inhibition on diabetic peripheral neuropathy, we investigated the effect of another potent PDE5 inhibitor, tadalafil, on diabetic Cited by: 8. Angiotensin type 2 receptor null mice express reduced levels of renal angiotensin converting enzyme-2/angiotensin ()/Mas receptor and exhibit greater high-fat diet-induced kidney injury.
J Renin Angiotensin Aldosterone Syst. Aug 5;17(3). pii: doi: /. Bone and heart health in chronic kidney disease: Role of dentin matrix protein 1 Martin, A., Jul 1In: Current opinion in nephrology and hypertension.
28, 4, p. 7 p. Research output: Contribution to journal › Review article.Publications Obesity and Diabetic Kidney Disease: Role of Oxidant Stress and Redox Balance. Sharma K, Antioxid Redox Signal.
Mar [Epub ahead of print] Metabolomics Reveals a Key Role for Fumarate in Mediating NOX4 Activity in Diabetic Kidney Disease.The American Journal of Physiology-Renal Physiology publishes original manuscripts on timely topics in both basic science and clinical research.
Published articles address a broad range of subjects relating to the kidney and urinary tract, and may involve human or animal models, individual cell types, and isolated membrane systems.