Effect of sex differences in treatment response to angioplasty in a murine arteriovenous fistula model.
Actins
/ genetics
Angioplasty
Animals
Antigens, CD
/ genetics
Antigens, Differentiation, Myelomonocytic
/ genetics
Arginase
/ genetics
Arteriovenous Fistula
/ pathology
Female
Gene Expression Regulation
Male
Mice, Inbred C57BL
Myosin Heavy Chains
/ genetics
Platelet Endothelial Cell Adhesion Molecule-1
/ genetics
Receptor, Transforming Growth Factor-beta Type I
/ genetics
S100 Calcium-Binding Protein A4
/ genetics
Sex Factors
Transforming Growth Factor beta1
/ genetics
Up-Regulation
angioplasty
arteriovenous fistula
murine model
restenosis
sexual disparity
Journal
American journal of physiology. Renal physiology
ISSN: 1522-1466
Titre abrégé: Am J Physiol Renal Physiol
Pays: United States
ID NLM: 100901990
Informations de publication
Date de publication:
01 03 2020
01 03 2020
Historique:
pubmed:
10
12
2019
medline:
17
7
2020
entrez:
10
12
2019
Statut:
ppublish
Résumé
Failure to mature and venous neointimal hyperplasia formation are the two major causes of hemodialysis arteriovenous fistula (AVF) vascular access failure. Percutaneous transluminal angioplasty (PTA) is the firstline treatment for both of these conditions, but, clinically, women have decreased patency rates compared with men. The hypothesis to be tested in the present study was that female mice after PTA of venous areas of higher intimal thickening have increased gene expression of transforming growth factor-β1 (TGF-β1) and TGF-β receptor 1 (TGFβ-R1) accompanied with histological changes of fibrosis compared with male mice. Seventeen male and eighteen female C57BL/6J mice were used in this study. Chronic kidney disease was induced by partial nephrectomy, and, 28 days later, an AVF was created to connect the left carotid artery to the right jugular vein. Two weeks later, the higher intimal thickening area was treated with PTA, and mice were euthanized 3 days later for gene expression analysis or 14 days later for histopathological analysis. Doppler ultrasound was performed weekly after AVF creation. At
Identifiants
pubmed: 31813252
doi: 10.1152/ajprenal.00474.2019
pmc: PMC7099504
doi:
Substances chimiques
Actins
0
Antigens, CD
0
Antigens, Differentiation, Myelomonocytic
0
CD68 protein, mouse
0
Platelet Endothelial Cell Adhesion Molecule-1
0
S100 Calcium-Binding Protein A4
0
S100a4 protein, mouse
0
Transforming Growth Factor beta1
0
alpha-smooth muscle actin, mouse
0
myosin 11, mouse
0
Receptor, Transforming Growth Factor-beta Type I
EC 2.7.11.30
Arg1 protein, mouse
EC 3.5.3.1
Arginase
EC 3.5.3.1
Myosin Heavy Chains
EC 3.6.4.1
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Langues
eng
Sous-ensembles de citation
IM
Pagination
F565-F575Subventions
Organisme : NHLBI NIH HHS
ID : R01 HL098967
Pays : United States
Organisme : NIDDK NIH HHS
ID : R56 DK107870
Pays : United States
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