title: Smooth muscle specific deletion of Ndst1 leads to decreased vessel luminal area and no change in blood pressure in conscious mice.
abstract: Heparan sulfate proteoglycans are abundant matrix and membrane molecules. Smooth muscle specific deletion of one heparan sulfate biosynthetic enzyme, N-deacetylase-N-sulfotransferase1 leads to decreased vascular smooth muscle cell proliferation, and vascular wall thickness. We hypothesized that this may lead to changes in blood pressure in conscious mice. Blood pressure was measured via telemetry in SM22αCre(+)Ndst1(-/-)(n = 4) and wild type (n = 8) mice. Aorta and thoracodorsal artery luminal area is significantly smaller in SM22αCre(+)Ndst1(-/-) (n = 4-8, P = 0.02, P = 0.0002) compared to wild type (n = 7) mice. Diurnal differences were observed in both cohorts for systolic, diastolic, mean arterial blood pressure, and heart rate (P < 0.001 from T test). No significant differences were found in the above parameters between the cohorts in either light or dark times using a linear mixed model. In conclusion, deletion of N-deacetylase-N-sulfotransferase1 in smooth muscle did not influence any of the blood pressure parameters measured despite significant decrease in aorta and thoracodorsal artery luminal area.
authors.affiliation: Division of Cardiology, Department of Medicine, Lillehei Heart Institute, University of Minnesota, 6-242 NHH, 312 Church St SE, Minneapolis, MN 55455, USA.
authors.forename: Kim Ramil C
authors.initials: KR
authors.lastname: Montaniel
authors.forename: Marie
authors.initials: M
authors.lastname: Billaud
authors.forename: Cassandra
authors.initials: C
authors.lastname: Graham
authors.forename: Sun K
authors.initials: SK
authors.lastname: Kim
authors.forename: Marjorie
authors.initials: M
authors.lastname: Carlson
authors.forename: William
authors.initials: W
authors.lastname: Zeng
authors.forename: Orien
authors.initials: O
authors.lastname: Zeng
authors.forename: Wei
authors.initials: W
authors.lastname: Pan
authors.forename: Brant E
authors.initials: BE
authors.lastname: Isakson
authors.forename: Jennifer L
authors.initials: JL
authors.lastname: Hall
authors.forename: Neeta
authors.initials: N
authors.lastname: Adhikari
mesh_terms: D000818:Animals; D001011:Aorta / Q000201:enzymology; D001794:Blood Pressure; D018660:Blood Pressure Monitoring, Ambulatory; D002940:Circadian Rhythm; D003243:Consciousness; D017353:Gene Deletion; D005838:Genotype; D006339:Heart Rate; D019426:Integrases / Q000235:genetics; D016014:Linear Models; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D008840:Microfilament Proteins / Q000235:genetics; D009124:Muscle Proteins / Q000235:genetics; D009131:Muscle, Smooth, Vascular / Q000201:enzymology*; D010641:Phenotype; D015238:Sulfotransferases / Q000172:deficiency* / Q000235:genetics; D013686:Telemetry; D013895:Thoracic Arteries / Q000201:enzymology; D013997:Time Factors
chemical_list: D008840:Microfilament Proteins; D009124:Muscle Proteins; C051615:transgelin; C045073:Cre recombinase; D019426:Integrases; D015238:Sulfotransferases; C021350:heparitin sulfotransferase