title: Short communication: vascular smooth muscle cell stiffness as a mechanism for increased aortic stiffness with aging.
abstract: BACKGROUND
  Increased aortic stiffness, an important feature of many vascular diseases, eg, aging, hypertension, atherosclerosis, and aortic aneurysms, is assumed because of changes in extracellular matrix (ECM).
  
  
  OBJECTIVE
  We tested the hypothesis that the mechanisms also involve intrinsic stiffening of vascular smooth muscle cells (VSMCs).
  
  
  RESULTS
  Stiffness was measured in vitro both by atomic force microscopy (AFM) and in a reconstituted tissue model, using VSMCs from aorta of young versus old male monkeys (Macaca fascicularis) (n=7/group), where aortic stiffness increases by 200% in vivo. The apparent elastic modulus was increased (P<0.05) in old (41.7+/-0.5 kPa) versus young (12.8+/-0.3 kPa) VSMCs but not after disassembly of the actin cytoskeleton with cytochalasin D. Stiffness of the VSMCs in the reconstituted tissue model was also higher (P<0.05) in old (23.3+/-3.0 kPa) than in young (13.7+/-2.4 kPa).
  
  
  CONCLUSIONS
  These data support the novel concept, not appreciated previously, that increased vascular stiffness with aging is attributable not only to changes in ECM but also to intrinsic changes in VSMCs.
authors.affiliation: Department of Cell Biology, UMDNJ-New Jersey Medical School, 185 South Orange Ave., Newark, NJ 07103, USA.
authors.forename: Hongyu
authors.initials: H
authors.lastname: Qiu
authors.forename: Yi
authors.initials: Y
authors.lastname: Zhu
authors.forename: Zhe
authors.initials: Z
authors.lastname: Sun
authors.forename: Jerome P
authors.initials: JP
authors.lastname: Trzeciakowski
authors.forename: Meredith
authors.initials: M
authors.lastname: Gansner
authors.forename: Christophe
authors.initials: C
authors.lastname: Depre
authors.forename: Ranillo R G
authors.initials: RR
authors.lastname: Resuello
authors.forename: Filipinas F
authors.initials: FF
authors.lastname: Natividad
authors.forename: William C
authors.initials: WC
authors.lastname: Hunter
authors.forename: Guy M
authors.initials: GM
authors.lastname: Genin
authors.forename: Elliot L
authors.initials: EL
authors.lastname: Elson
authors.forename: Dorothy E
authors.initials: DE
authors.lastname: Vatner
authors.forename: Gerald A
authors.initials: GA
authors.lastname: Meininger
authors.forename: Stephen F
authors.initials: SF
authors.lastname: Vatner
mesh_terms: D000199:Actins / Q000378:metabolism; D000367:Age Factors; D000375:Aging / Q000378:metabolism / Q000473:pathology*; D000818:Animals; D001013:Aorta, Thoracic / Q000473:pathology; D001018:Aortic Diseases / Q000209:etiology / Q000473:pathology*; D002478:Cells, Cultured; D015638:Cytochalasin D / Q000494:pharmacology; D003599:Cytoskeleton / Q000187:drug effects / Q000378:metabolism; D055119:Elastic Modulus; D019012:Integrin beta1 / Q000378:metabolism; D008252:Macaca fascicularis; D008297:Male; D018625:Microscopy, Atomic Force; D009131:Muscle, Smooth, Vascular / Q000187:drug effects / Q000378:metabolism / Q000473:pathology*; D014404:Tubulin / Q000378:metabolism; D014746:Vimentin / Q000378:metabolism
chemical_list: D000199:Actins; D019012:Integrin beta1; D014404:Tubulin; D014746:Vimentin; D015638:Cytochalasin D