Short communication

Vascular smooth muscle cell stiffness as a mechanism for increased aortic stiffness with aging

Hongyu Qiu, Yi Zhu, Zhe Sun, Jerome P. Trzeciakowski, Meredith Gansner, Christophe Depre, Ranillo R.G. Resuello, Filipinas F. Natividad, William C. Hunter, Guy M. Genin, Elliot L. Elson, Dorothy Vatner, Gerald A. Meininger, Stephen Vatner

Research output: Contribution to journalArticle

157 Citations (Scopus)

Abstract

Rationale: 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). Methods and 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.

Original languageEnglish (US)
Pages (from-to)615-619
Number of pages5
JournalCirculation research
Volume107
Issue number5
DOIs
StatePublished - Sep 3 2010

Fingerprint

Vascular Stiffness
Vascular Smooth Muscle
Smooth Muscle Myocytes
Communication
Extracellular Matrix
Cytochalasin D
Macaca fascicularis
Aortic Aneurysm
Atomic Force Microscopy
Elastic Modulus
Actin Cytoskeleton
Vascular Diseases
Haplorhini
Aorta
Atherosclerosis
Hypertension

All Science Journal Classification (ASJC) codes

  • Physiology
  • Cardiology and Cardiovascular Medicine

Keywords

  • AFM
  • aging
  • stiffness
  • vascular smooth muscle cell

Cite this

Qiu, Hongyu ; Zhu, Yi ; Sun, Zhe ; Trzeciakowski, Jerome P. ; Gansner, Meredith ; Depre, Christophe ; Resuello, Ranillo R.G. ; Natividad, Filipinas F. ; Hunter, William C. ; Genin, Guy M. ; Elson, Elliot L. ; Vatner, Dorothy ; Meininger, Gerald A. ; Vatner, Stephen. / Short communication : Vascular smooth muscle cell stiffness as a mechanism for increased aortic stiffness with aging. In: Circulation research. 2010 ; Vol. 107, No. 5. pp. 615-619.
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abstract = "Rationale: 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). Methods and 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.",
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author = "Hongyu Qiu and Yi Zhu and Zhe Sun and Trzeciakowski, {Jerome P.} and Meredith Gansner and Christophe Depre and Resuello, {Ranillo R.G.} and Natividad, {Filipinas F.} and Hunter, {William C.} and Genin, {Guy M.} and Elson, {Elliot L.} and Dorothy Vatner and Meininger, {Gerald A.} and Stephen Vatner",
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Qiu, H, Zhu, Y, Sun, Z, Trzeciakowski, JP, Gansner, M, Depre, C, Resuello, RRG, Natividad, FF, Hunter, WC, Genin, GM, Elson, EL, Vatner, D, Meininger, GA & Vatner, S 2010, 'Short communication: Vascular smooth muscle cell stiffness as a mechanism for increased aortic stiffness with aging', Circulation research, vol. 107, no. 5, pp. 615-619. https://doi.org/10.1161/CIRCRESAHA.110.221846

Short communication : Vascular smooth muscle cell stiffness as a mechanism for increased aortic stiffness with aging. / Qiu, Hongyu; Zhu, Yi; Sun, Zhe; Trzeciakowski, Jerome P.; Gansner, Meredith; Depre, Christophe; Resuello, Ranillo R.G.; Natividad, Filipinas F.; Hunter, William C.; Genin, Guy M.; Elson, Elliot L.; Vatner, Dorothy; Meininger, Gerald A.; Vatner, Stephen.

In: Circulation research, Vol. 107, No. 5, 03.09.2010, p. 615-619.

Research output: Contribution to journalArticle

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T1 - Short communication

T2 - Vascular smooth muscle cell stiffness as a mechanism for increased aortic stiffness with aging

AU - Qiu, Hongyu

AU - Zhu, Yi

AU - Sun, Zhe

AU - Trzeciakowski, Jerome P.

AU - Gansner, Meredith

AU - Depre, Christophe

AU - Resuello, Ranillo R.G.

AU - Natividad, Filipinas F.

AU - Hunter, William C.

AU - Genin, Guy M.

AU - Elson, Elliot L.

AU - Vatner, Dorothy

AU - Meininger, Gerald A.

AU - Vatner, Stephen

PY - 2010/9/3

Y1 - 2010/9/3

N2 - Rationale: 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). Methods and 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.

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KW - AFM

KW - aging

KW - stiffness

KW - vascular smooth muscle cell

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