Inhibition of the Renin-Angiotensin System Fails to Suppress β-Aminopropionitrile-Induced Thoracic Aortopathy in Mice-Brief Report.


Journal

Arteriosclerosis, thrombosis, and vascular biology
ISSN: 1524-4636
Titre abrégé: Arterioscler Thromb Vasc Biol
Pays: United States
ID NLM: 9505803

Informations de publication

Date de publication:
10 2022
Historique:
pubmed: 26 8 2022
medline: 24 9 2022
entrez: 25 8 2022
Statut: ppublish

Résumé

Cross-linking of lysine residues in elastic and collagen fibers is a vital process in aortic development. Inhibition of lysyl oxidase by BAPN (β-aminopropionitrile) leads to thoracic aortopathies in mice. Although the renin-angiotensin system contributes to several types of thoracic aortopathies, it remains unclear whether inhibition of the renin-angiotensin system protects against aortopathy caused by the impairment of elastic fiber/collagen crosslinking. BAPN (0.5% wt/vol) was started in drinking water to induce aortopathies in male C57BL/6J mice at 4 weeks of age for 4 weeks. Five approaches were used to investigate the impact of the renin-angiotensin system. Bulk RNA sequencing was performed to explore potential molecular mechanisms of BAPN-induced thoracic aortopathies. Losartan increased plasma renin concentrations significantly, compared with vehicle-infused mice, indicating effective angiotensin II type 1 receptor inhibition. However, losartan did not suppress BAPN-induced aortic rupture and dilatation. Since losartan is a surmountable inhibitor of the renin-angiotensin system, irbesartan, an insurmountable inhibitor, was also tested. Although increased plasma renin concentrations indicated effective inhibition, irbesartan did not ameliorate aortic rupture and dilatation in BAPN-administered mice. Thus, BAPN-induced thoracic aortopathies were refractory to angiotensin II type 1 receptor blockade. Next, we inhibited angiotensin II production by pharmacological or genetic depletion of AGT (angiotensinogen), the unique precursor of angiotensin II. However, neither suppressed BAPN-induced thoracic aortic rupture and dilatation. Aortic RNA sequencing revealed molecular changes during BAPN administration that were distinct from other types of aortopathies in which angiotensin II type 1 receptor inhibition protects against aneurysm formation. Inhibition of either angiotensin II action or production of the renin-angiotensin system does not attenuate BAPN-induced thoracic aortopathies in mice.

Sections du résumé

BACKGROUND
Cross-linking of lysine residues in elastic and collagen fibers is a vital process in aortic development. Inhibition of lysyl oxidase by BAPN (β-aminopropionitrile) leads to thoracic aortopathies in mice. Although the renin-angiotensin system contributes to several types of thoracic aortopathies, it remains unclear whether inhibition of the renin-angiotensin system protects against aortopathy caused by the impairment of elastic fiber/collagen crosslinking.
METHODS
BAPN (0.5% wt/vol) was started in drinking water to induce aortopathies in male C57BL/6J mice at 4 weeks of age for 4 weeks. Five approaches were used to investigate the impact of the renin-angiotensin system. Bulk RNA sequencing was performed to explore potential molecular mechanisms of BAPN-induced thoracic aortopathies.
RESULTS
Losartan increased plasma renin concentrations significantly, compared with vehicle-infused mice, indicating effective angiotensin II type 1 receptor inhibition. However, losartan did not suppress BAPN-induced aortic rupture and dilatation. Since losartan is a surmountable inhibitor of the renin-angiotensin system, irbesartan, an insurmountable inhibitor, was also tested. Although increased plasma renin concentrations indicated effective inhibition, irbesartan did not ameliorate aortic rupture and dilatation in BAPN-administered mice. Thus, BAPN-induced thoracic aortopathies were refractory to angiotensin II type 1 receptor blockade. Next, we inhibited angiotensin II production by pharmacological or genetic depletion of AGT (angiotensinogen), the unique precursor of angiotensin II. However, neither suppressed BAPN-induced thoracic aortic rupture and dilatation. Aortic RNA sequencing revealed molecular changes during BAPN administration that were distinct from other types of aortopathies in which angiotensin II type 1 receptor inhibition protects against aneurysm formation.
CONCLUSIONS
Inhibition of either angiotensin II action or production of the renin-angiotensin system does not attenuate BAPN-induced thoracic aortopathies in mice.

Identifiants

pubmed: 36004642
doi: 10.1161/ATVBAHA.122.317712
pmc: PMC9492637
mid: NIHMS1830687
doi:

Substances chimiques

Receptor, Angiotensin, Type 1 0
Angiotensinogen 11002-13-4
Angiotensin II 11128-99-7
Aminopropionitrile 151-18-8
Protein-Lysine 6-Oxidase EC 1.4.3.13
Renin EC 3.4.23.15
Irbesartan J0E2756Z7N
Losartan JMS50MPO89
Lysine K3Z4F929H6

Types de publication

Journal Article Research Support, Non-U.S. Gov't Research Support, N.I.H., Extramural

Langues

eng

Sous-ensembles de citation

IM

Pagination

1254-1261

Subventions

Organisme : NHLBI NIH HHS
ID : R35 HL155649
Pays : United States

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Auteurs

Hisashi Sawada (H)

Saha Cardiovascular Research Center (H.S., S.O.-U., D.Y., M.K.F., J.J.M., D.A.H., A.D., H.S.L.), University of Kentucky, Lexington.
Saha Aortic Center (H.S., A.D., H.S.L.), University of Kentucky, Lexington.
Department of Physiology (H.S., A.D., H.S.L.), University of Kentucky, Lexington.

Satoko Ohno-Urabe (S)

Saha Cardiovascular Research Center (H.S., S.O.-U., D.Y., M.K.F., J.J.M., D.A.H., A.D., H.S.L.), University of Kentucky, Lexington.

Dien Ye (D)

Saha Cardiovascular Research Center (H.S., S.O.-U., D.Y., M.K.F., J.J.M., D.A.H., A.D., H.S.L.), University of Kentucky, Lexington.

Michael K Franklin (MK)

Saha Cardiovascular Research Center (H.S., S.O.-U., D.Y., M.K.F., J.J.M., D.A.H., A.D., H.S.L.), University of Kentucky, Lexington.

Jessica J Moorleghen (JJ)

Saha Cardiovascular Research Center (H.S., S.O.-U., D.Y., M.K.F., J.J.M., D.A.H., A.D., H.S.L.), University of Kentucky, Lexington.

Deborah A Howatt (DA)

Saha Cardiovascular Research Center (H.S., S.O.-U., D.Y., M.K.F., J.J.M., D.A.H., A.D., H.S.L.), University of Kentucky, Lexington.

Adam E Mullick (AE)

Ionis Pharmaceuticals, Carlsbad, CA (A.E.M.).

Alan Daugherty (A)

Saha Cardiovascular Research Center (H.S., S.O.-U., D.Y., M.K.F., J.J.M., D.A.H., A.D., H.S.L.), University of Kentucky, Lexington.
Saha Aortic Center (H.S., A.D., H.S.L.), University of Kentucky, Lexington.
Department of Physiology (H.S., A.D., H.S.L.), University of Kentucky, Lexington.

Hong S Lu (HS)

Saha Cardiovascular Research Center (H.S., S.O.-U., D.Y., M.K.F., J.J.M., D.A.H., A.D., H.S.L.), University of Kentucky, Lexington.
Saha Aortic Center (H.S., A.D., H.S.L.), University of Kentucky, Lexington.
Department of Physiology (H.S., A.D., H.S.L.), University of Kentucky, Lexington.

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Classifications MeSH