scholarly journals Nrf2 Deficiency Upregulates Intrarenal Angiotensin-Converting Enzyme-2 and Angiotensin 1-7 Receptor Expression and Attenuates Hypertension and Nephropathy in Diabetic Mice

Endocrinology ◽  
2017 ◽  
Vol 159 (2) ◽  
pp. 836-852 ◽  
Author(s):  
Shuiling Zhao ◽  
Anindya Ghosh ◽  
Chao-Sheng Lo ◽  
Isabelle Chenier ◽  
James W Scholey ◽  
...  
Keyword(s):  
Angiotensin Converting Enzyme ◽  
Receptor Expression ◽  
Converting Enzyme ◽  
Diabetic Mice ◽  
Angiotensin Converting Enzyme 2

Angiotensin-(1–7) prevents systemic hypertension, attenuates oxidative stress and tubulointerstitial fibrosis, and normalizes renal angiotensin-converting enzyme 2 and Mas receptor expression in diabetic mice

2015 ◽  
Vol 128 (10) ◽  
pp. 649-663 ◽  
Author(s):  
Yixuan Shi ◽  
Chao-Sheng Lo ◽  
Ranjit Padda ◽  
Shaaban Abdo ◽  
Isabelle Chenier ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Angiotensin Converting Enzyme ◽  
Renal Injury ◽  
Receptor Expression ◽  
Systemic Hypertension ◽  
Converting Enzyme ◽  
Diabetic Mice ◽  
Angiotensin Converting Enzyme 2 ◽  
Mas Receptor

In summary, our data indicate an important role of Ang-(1–7) in inhibiting intrarenal oxidative stress and subsequent prevention of the development of hypertension and renal injury in diabetic mice.

Angiotensin Converting Enzyme 2 (ACE2) Expression in the Visual System

2021 ◽  
Author(s):  
James M. Hill ◽  
Christian Clement ◽  
L. Arceneaux ◽  
Walter Lukiw
Keyword(s):  
Signal Processing ◽  
Angiotensin Converting Enzyme ◽  
Occipital Lobe ◽  
Cell Types ◽  
Receptor Expression ◽  
Host Cells ◽  
Visual Signal ◽  
Converting Enzyme ◽  
Angiotensin Converting Enzyme 2 ◽  
The Brain

Abstract Background: Multiple lines of evidence currently indicate that the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)gains entry into human host cells via a high-affinity interaction with the angiotensin-converting enzyme 2 (ACE2) transmembrane receptor. Research has further shown the widespread expression of the ACE2 receptor on the surface of many different immune, non-immune and neural host cell types, and that SARS-CoV-2 has there markable capability to attack many different types of human-host cells simultaneously. One principal neuroanatomical region for highACE2 expression patterns occurs in the brainstem, an area of the brain containing regulatory centers for respiration, and this may in part explain the predisposition of many COVID-19 patients to respiratory distress. Early studies also indicated extensive ACE2 expression in the whole eye and the brain’s visual circuitry. In this study we analyzed ACE2 receptor expression at the mRNA and protein level in multiple cell types involved in human vision, including cell types of the external eye and several deep brain regions known to be involved in the processing of visual signals.Methods: ACE2 mRNA and protein analysis; multiple eye and brain cells and tissues; gamma32P-adenosine tri-phosphate ([γ-32P]dATP) radiolabeled probes; Northern analysis; ELISA.Results: The four main findings were: (i)that many different optical and neural cell types of the human visual system provide receptors essential for SARS-CoV-2 invasion; (ii)the remarkable ubiquity of ACE2 presence in cells of the eye and anatomical regions of the brain involved in visual signal processing; (iii)that ACE2 receptor expression in different ocular cell types and visual processing centers of the brain provide multiple compartments for SARS-CoV-2 infiltration; and (iv)a gradient of increasing ACE2 expression from the anterior surface of the eye to the visual signal processing areas of the occipital lobe and the primary visual neocortex.Conclusion: A gradient of ACE2 expression from the eye surface to the occipital lobe provide the SARS-CoV-2 virus a novel pathway from the outer eye into deeper anatomical regions of the brain involved in vision. These findings may explain, in part, the many recently reported neuro-ophthalmic manifestations of SARS-CoV-2infection in COVID-19 affected patients.

scholarly journals ACE2 receptor expression in testes: implications in coronavirus disease 2019 pathogenesis†

2020 ◽  
Vol 103 (3) ◽  
pp. 449-451 ◽  
Author(s):  
Saguna Verma ◽  
Sarini Saksena ◽  
Hooman Sadri-Ardekani
Keyword(s):  
Reproductive Health ◽  
Severe Acute Respiratory Syndrome ◽  
Angiotensin Converting Enzyme ◽  
Receptor Expression ◽  
Converting Enzyme ◽  
Angiotensin Converting Enzyme 2 ◽  
Male Reproductive Health

Expression of angiotensin-converting enzyme 2, receptor of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), is high in the testes, therefore SARS-CoV-2 infection and its association with male reproductive health should be investigated in male coronavirus disease 2019 patients.

scholarly journals Angiotensin‐Converting Enzyme 2 (SARS‐CoV‐2 receptor) expression in human skeletal muscle

2021 ◽  
Author(s):  
Mario Perez‐Valera ◽  
Miriam Martinez‐Canton ◽  
Angel Gallego‐Selles ◽  
Victor Galván‐Alvarez ◽  
Miriam Gelabert‐Rebato ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Angiotensin Converting Enzyme ◽  
Human Skeletal Muscle ◽  
Receptor Expression ◽  
Converting Enzyme ◽  
Angiotensin Converting Enzyme 2

scholarly journals MO626EFFECTS OF RAMIPRIL IN LUNG AND KIDNEY ANGIOTENSIN CONVERTING ENZYME 2 (ACE2) EXPRESSION IN A TYPE 2 DIABETIC MURINE MODEL: LESSONS FOR COVID-19 INFECTION

2021 ◽  
Vol 36 (Supplement_1) ◽  
Author(s):  
Ander Vergara Arana ◽  
Conxita Jacobs Cachá ◽  
Mireia Molina ◽  
Pamela Dominguez ◽  
Begoña Benito ◽  
...  
Keyword(s):  
Angiotensin Converting Enzyme ◽  
Enzymatic Activity ◽  
Mrna Expression ◽  
Renin Angiotensin System ◽  
Converting Enzyme ◽  
Diabetic Mice ◽  
Angiotensin Converting Enzyme 2 ◽  
Ras Blockers ◽  
Activity Decrease

Abstract Background and Aims Angiotensin converting enzyme 2 (ACE2) is one of the components of the renin-angiotensin system (RAS) that mainly degrades angiotensin II to angiotensin-(1-7). ACE2 is predominantly expressed in the kidney and the heart, but it has been evidenced in type 2 alveolar lung cells, where it acts as a receptor for the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). In this context, a controversy arose as to whether the use of RAS blockers could increase ACE2 lung expression and the risk infection by COVID-19. This study aimed to investigate the effect of an ACE inhibitor (Ramipril) on ACE2 expression in experimental diabetes. Method 12 weeks old diabetic db/db mice (n=7) were given ramipril (8 mg/Kg/day) during 8 weeks or the respective vehicle. db/m (n=7) vehicle-treated non-diabetic mice were included as controls. ACE2 mRNA expression and enzymatic activity were studied in kidney, heart and lung samples of these animals to identify if the diabetic condition or treatment with ramipril modulated ACE2 expression. Results In vehicle-treated diabetic db/db animals, ACE2 mRNA expression was significantly increased in the kidney (p<0.001) and ramipril treatment reversed this effect (p=0.026). In the heart, ACE2 expression decreased in db/db when compared to db/m littermates (p=0.035) and ramipril had no effect. We found no differences in ACE2 gene expression in the lung. Besides, ACE2 enzymatic activity was increased in the kidney (29%) and also in the lung (16%) of db/db mice when compared to controls. Ramipril treatment decreased ACE2 activity a 19% in the lung and had no effect in the kidney when compared to untreated db/db (see figure). In the heart, ACE2 activity tended to decrease in db/db mice (29%) when compared to db/m and ramipril increased ACE2 activity (18%) but did not exceed the cardiac ACE2 activity of the db/m. Conclusion ACE2 is increased in the kidney and the lung, and decreased in the heart of diabetic mice. Ramipril treatment restores ACE2 levels. The results suggest that ACE inhibitors do not increase ACE2 expression and the activity decrease exerted in the lung may be protective against COVID-19 infection.

Angiotensin-converting enzyme 2 influences pancreatic and renal function in diabetic mice

2020 ◽  
Vol 100 (9) ◽  
pp. 1169-1183 ◽  
Author(s):  
Heleia Roca-Ho ◽  
Vanesa Palau ◽  
Javier Gimeno ◽  
Julio Pascual ◽  
María José Soler ◽  
...  
Keyword(s):  
Renal Function ◽  
Angiotensin Converting Enzyme ◽  
Converting Enzyme ◽  
Diabetic Mice ◽  
Angiotensin Converting Enzyme 2

scholarly journals Direct renin inhibition prevents cardiac dysfunction in a diabetic mouse model: comparison with an angiotensin receptor antagonist and angiotensin-converting enzyme inhibitor

2013 ◽  
Vol 124 (8) ◽  
pp. 529-545 ◽  
Author(s):  
Candice M. Thomas ◽  
Qian Chen Yong ◽  
Rachid Seqqat ◽  
Niketa Chandel ◽  
David L. Feldman ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Angiotensin Converting Enzyme ◽  
Diabetic Cardiomyopathy ◽  
Angiotensin Receptor Blockers ◽  
Receptor Expression ◽  
Converting Enzyme ◽  
Diabetic Mice ◽  
Angiotensin Receptor ◽  
Prorenin Receptor ◽  
Renin Inhibition

Hyperglycaemia up-regulates intracellular AngII (angiotensin II) production in cardiac myocytes, effects of which are blocked more effectively by renin inhibition than ARBs (angiotensin receptor blockers) or ACEis (angiotensin-converting enzyme inhibitors). In the present study, we determined whether renin inhibition is more effective at preventing diabetic cardiomyopathy than an ARB or ACEi. Diabetes was induced in adult mice for 10 weeks by STZ (streptozotocin). Diabetic mice were treated with insulin, aliskiren (a renin inhibitor), benazeprilat (an ACEi) or valsartan (an ARB) via subcutaneous mini-pumps. Significant impairment in diastolic and systolic cardiac functions was observed in diabetic mice, which was completely prevented by all three RAS (renin–angiotensin system) inhibitors. Hyperglycaemia significantly increased cardiac oxidative stress and circulating inflammatory cytokines, which were blocked by aliskiren and benazeprilat, whereas valsartan was partially effective. Diabetes increased cardiac PRR (prorenin receptor) expression and nuclear translocation of PLZF (promyelocytic zinc finger protein), which was completely prevented by aliskiren and valsartan, and partially by benazeprilat. Renin inhibition provided similar protection of cardiac function to ARBs and ACEis. Activation of PLZF by PRR represented a novel mechanism in diabetic cardiomyopathy. Differential effects of the three agents on oxidative stress, cytokines and PRR expression suggested subtle differences in their mechanisms of action.

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