Cathepsin S Deficiency Mitigated Chronic Stress-Related Neointimal Hyperplasia in Mice.
Animals
Carotid Arteries
/ drug effects
Carotid Artery Injuries
/ genetics
Cathepsins
/ antagonists & inhibitors
Cell Movement
/ genetics
Cell Proliferation
/ drug effects
Elastin
/ metabolism
Hyperplasia
Ligation
Macrophages
Matrix Metalloproteinases
/ genetics
Mice
Mice, Knockout
Myocytes, Smooth Muscle
Neointima
/ genetics
Plaque, Atherosclerotic
/ genetics
RNA, Messenger
/ metabolism
Restraint, Physical
Stress, Psychological
/ genetics
hyperplasia
hypertension
protease
stress
vascular disease
Journal
Journal of the American Heart Association
ISSN: 2047-9980
Titre abrégé: J Am Heart Assoc
Pays: England
ID NLM: 101580524
Informations de publication
Date de publication:
16 07 2019
16 07 2019
Historique:
entrez:
13
7
2019
pubmed:
13
7
2019
medline:
13
11
2020
Statut:
ppublish
Résumé
Background Exposure to chronic psychosocial stress is a risk factor for atherosclerosis-based cardiovascular disease. We previously demonstrated the increased expressions of cathepsin S (CatS) in atherosclerotic lesions. Whether CatS participates directly in stress-related neointimal hyperplasia has been unknown. Methods and Results Male wild-type and CatS-deficient mice that underwent carotid ligation injury were subjected to chronic immobilization stress for morphological and biochemical studies at specific times. On day 14 after stress/surgery, stress enhanced the neointima formation. At the early time points, the stressed mice had increased plaque elastin disruption, cell proliferation, macrophage accumulation, mRNA and/or protein levels of vascular cell adhesion molecule-1, angiotensin II type 1 receptor, monocyte chemoattractant protein-1, gp91
Identifiants
pubmed: 31296090
doi: 10.1161/JAHA.119.011994
pmc: PMC6662117
doi:
Substances chimiques
RNA, Messenger
0
Elastin
9007-58-3
Cathepsins
EC 3.4.-
cathepsin S
EC 3.4.22.27
Matrix Metalloproteinases
EC 3.4.24.-
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
e011994Références
Hypertension. 2011 May;57(5):981-9
pubmed: 21464389
Atherosclerosis. 2012 Jul;223(1):69-77
pubmed: 22304794
Diabetes. 2012 Jun;61(6):1552-61
pubmed: 22396205
Am J Pathol. 2008 Aug;173(2):358-69
pubmed: 18583318
Proc Natl Acad Sci U S A. 2013 Oct 8;110(41):16574-9
pubmed: 24062448
Nat Commun. 2014 Jun 04;5:3838
pubmed: 24894568
J Clin Invest. 2003 Jun;111(11):1733-45
pubmed: 12782676
BMJ. 2006 Mar 4;332(7540):521-5
pubmed: 16428252
Cardiovasc Res. 2012 Dec 1;96(3):401-10
pubmed: 22871592
Lancet. 2004 Sep 11-17;364(9438):953-62
pubmed: 15364186
Circulation. 2012 Mar 27;125(12):1551-62
pubmed: 22451605
Cardiovasc Res. 2013 Oct 1;100(1):84-94
pubmed: 23771947
Nat Med. 2014 Jul;20(7):754-758
pubmed: 24952646
Circ Res. 2003 Mar 21;92(5):493-500
pubmed: 12600886
J Atheroscler Thromb. 2018 Feb 1;25(2):111-123
pubmed: 28978867
Hypertension. 2014 Mar;63(3):607-15
pubmed: 24343118
J Am Coll Cardiol. 2013 Apr 9;61(14):1471-81
pubmed: 23500310
J Mol Cell Cardiol. 2017 Jan;102:10-21
pubmed: 27986445
Sci Rep. 2017 Aug 18;7(1):8703
pubmed: 28821796
Biomark Med. 2012 Feb;6(1):9-11
pubmed: 22296192
J Vasc Surg. 2017 Apr;65(4):1171-1179.e1
pubmed: 26960947
Cardiovasc Res. 2011 Jul 15;91(2):350-7
pubmed: 21421554
Atherosclerosis. 2010 Jun;210(2):430-7
pubmed: 20079903
Am J Pathol. 2006 Feb;168(2):685-94
pubmed: 16436681
J Am Heart Assoc. 2019 Jul 16;8(14):e011994
pubmed: 31296090
Atherosclerosis. 2017 Sep;264:1-10
pubmed: 28734203
Hypertension. 2011 Dec;58(6):978-86
pubmed: 21986502
Arterioscler Thromb Vasc Biol. 2011 Nov;31(11):2500-8
pubmed: 21868704
J Am Heart Assoc. 2017 Sep 28;6(10):
pubmed: 28963101
J Am Heart Assoc. 2017 Jul 14;6(7):
pubmed: 28710180
Circ Res. 2009 Feb 27;104(4):455-65
pubmed: 19122179
Nat Rev Cardiol. 2012 Apr 03;9(6):360-70
pubmed: 22473079
Int J Cardiol. 2015 Mar 15;183:198-208
pubmed: 25668148
Stress. 2012 Mar;15(2):121-9
pubmed: 21790484
Int J Cardiol. 2017 Sep 15;243:413-420
pubmed: 28549747