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Angiotensin-1–7 attenuates kidney injury in experimental Alport syndrome
by
Scholey, James W.
, Kim, Soo Wan
, Choi, Hong Sang
, Kim, Chang Seong
, Bae, Eun Hui
, Kim, In Jin
, Ma, Seong Kwon
in
631/154/555
/ 692/4017
/ ACE2
/ Actin
/ Acute Kidney Injury - drug therapy
/ Acute Kidney Injury - etiology
/ Acute Kidney Injury - pathology
/ Alport syndrome
/ Angiotensin
/ Angiotensin I - pharmacology
/ Angiotensin-converting enzyme 2
/ Animals
/ Antihypertensive Agents - pharmacology
/ Apoptosis
/ Autoantigens - physiology
/ Cell adhesion molecules
/ Collagen
/ Collagen Type IV - physiology
/ Disease Models, Animal
/ Enzymes
/ Fibronectin
/ Heme
/ Heme oxygenase (decyclizing)
/ Humanities and Social Sciences
/ Inflammation
/ Inflammation - etiology
/ Inflammation - pathology
/ Inflammation - prevention & control
/ Kidneys
/ Male
/ Mice
/ Mice, Knockout
/ multidisciplinary
/ Nephritis, Hereditary - complications
/ Nephritis, Hereditary - pathology
/ Nephropathy
/ Oxygenase
/ Peptide Fragments - pharmacology
/ Peptidyl-dipeptidase A
/ Renin
/ Science
/ Science (multidisciplinary)
/ Smad protein
/ Smooth muscle
/ Transforming growth factor-b
/ Tumor necrosis factor-α
2020
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Angiotensin-1–7 attenuates kidney injury in experimental Alport syndrome
by
Scholey, James W.
, Kim, Soo Wan
, Choi, Hong Sang
, Kim, Chang Seong
, Bae, Eun Hui
, Kim, In Jin
, Ma, Seong Kwon
in
631/154/555
/ 692/4017
/ ACE2
/ Actin
/ Acute Kidney Injury - drug therapy
/ Acute Kidney Injury - etiology
/ Acute Kidney Injury - pathology
/ Alport syndrome
/ Angiotensin
/ Angiotensin I - pharmacology
/ Angiotensin-converting enzyme 2
/ Animals
/ Antihypertensive Agents - pharmacology
/ Apoptosis
/ Autoantigens - physiology
/ Cell adhesion molecules
/ Collagen
/ Collagen Type IV - physiology
/ Disease Models, Animal
/ Enzymes
/ Fibronectin
/ Heme
/ Heme oxygenase (decyclizing)
/ Humanities and Social Sciences
/ Inflammation
/ Inflammation - etiology
/ Inflammation - pathology
/ Inflammation - prevention & control
/ Kidneys
/ Male
/ Mice
/ Mice, Knockout
/ multidisciplinary
/ Nephritis, Hereditary - complications
/ Nephritis, Hereditary - pathology
/ Nephropathy
/ Oxygenase
/ Peptide Fragments - pharmacology
/ Peptidyl-dipeptidase A
/ Renin
/ Science
/ Science (multidisciplinary)
/ Smad protein
/ Smooth muscle
/ Transforming growth factor-b
/ Tumor necrosis factor-α
2020
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Angiotensin-1–7 attenuates kidney injury in experimental Alport syndrome
by
Scholey, James W.
, Kim, Soo Wan
, Choi, Hong Sang
, Kim, Chang Seong
, Bae, Eun Hui
, Kim, In Jin
, Ma, Seong Kwon
in
631/154/555
/ 692/4017
/ ACE2
/ Actin
/ Acute Kidney Injury - drug therapy
/ Acute Kidney Injury - etiology
/ Acute Kidney Injury - pathology
/ Alport syndrome
/ Angiotensin
/ Angiotensin I - pharmacology
/ Angiotensin-converting enzyme 2
/ Animals
/ Antihypertensive Agents - pharmacology
/ Apoptosis
/ Autoantigens - physiology
/ Cell adhesion molecules
/ Collagen
/ Collagen Type IV - physiology
/ Disease Models, Animal
/ Enzymes
/ Fibronectin
/ Heme
/ Heme oxygenase (decyclizing)
/ Humanities and Social Sciences
/ Inflammation
/ Inflammation - etiology
/ Inflammation - pathology
/ Inflammation - prevention & control
/ Kidneys
/ Male
/ Mice
/ Mice, Knockout
/ multidisciplinary
/ Nephritis, Hereditary - complications
/ Nephritis, Hereditary - pathology
/ Nephropathy
/ Oxygenase
/ Peptide Fragments - pharmacology
/ Peptidyl-dipeptidase A
/ Renin
/ Science
/ Science (multidisciplinary)
/ Smad protein
/ Smooth muscle
/ Transforming growth factor-b
/ Tumor necrosis factor-α
2020
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Angiotensin-1–7 attenuates kidney injury in experimental Alport syndrome
Journal Article
Angiotensin-1–7 attenuates kidney injury in experimental Alport syndrome
2020
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Overview
Angiotensin-[1–7] (Ang-[1–7]) antagonize the actions of the renin-angiotensin-system via the Mas receptor and thereby exert renoprotective effects. Murine recombinant angiotensin-converting enzyme (ACE)2 was reported to show renoprotective effects in an experimental Alport syndrome model; however, the protective effect of direct administration of Ang-[1–7] is unknown. Here, we used
Col4a3
−/−
mice as a model of Alport syndrome, which were treated with saline or Ang- [1–7]; saline-treated wild-type mice were used as a control group. The mice were continuously infused with saline or Ang-[1–7] (25 μg/kg/h) using osmotic mini-pumps.
Col4a3
−/−
mice showed increased α-smooth muscle actin (SMA), collagen, and fibronectin expression levels, which were attenuated by Ang-[1–7] treatment. Moreover, Ang-[1–7] alleviated activation of transforming growth factor-β/Smad signaling, and attenuated the protein expression of ED-1 and heme oxygenase-1, indicating reduction of renal inflammation. Ang-[1–7] treatment further reduced the expression levels of inflammatory cytokines and adhesion molecules and attenuated apoptosis in human kidney cells. Finally, Ang-[1–7] downregulated TNF-α converting enzyme and upregulated ACE2 expression. Thus, treatment with Ang-[1–7] altered the ACE2-Ang-[1–7]-Mas receptor axis in the kidneys of
Col4a3
−/−
mice to attenuate the nephropathy progression of Alport syndrome.
Publisher
Nature Publishing Group UK,Nature Publishing Group
Subject
/ 692/4017
/ ACE2
/ Actin
/ Acute Kidney Injury - drug therapy
/ Acute Kidney Injury - etiology
/ Acute Kidney Injury - pathology
/ Angiotensin I - pharmacology
/ Angiotensin-converting enzyme 2
/ Animals
/ Antihypertensive Agents - pharmacology
/ Collagen
/ Collagen Type IV - physiology
/ Enzymes
/ Heme
/ Heme oxygenase (decyclizing)
/ Humanities and Social Sciences
/ Inflammation - prevention & control
/ Kidneys
/ Male
/ Mice
/ Nephritis, Hereditary - complications
/ Nephritis, Hereditary - pathology
/ Peptide Fragments - pharmacology
/ Renin
/ Science
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