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Gerald A Meininger - One of the best experts on this subject based on the ideXlab platform.

  • smooth muscle Cell Stiffness syndrome revisiting the structural basis of arterial Stiffness
    2015
    Co-Authors: Nancy L Sehgel, Stephen F Vatner, Gerald A Meininger
    Abstract:

    In recent decades, the pervasiveness of increased arterial Stiffness in patients with cardiovascular disease has become increasingly apparent. Though, this phenomenon has been well documented in humans and animal models of disease for well over a century, there has been surprisingly limited development in a deeper mechanistic understanding of arterial Stiffness. Much of the historical literature has focused on changes in extraCellular matrix proteins-collagen and elastin. However, extraCellular matrix changes alone appear insufficient to consistently account for observed changes in vascular Stiffness, which we observed in our studies of aortic Stiffness in aging monkeys. This led us to examine novel mechanisms operating at the level of the vascular smooth muscle Cell (VSMC)-that include increased Cell Stiffness and adhesion to extraCellular matrix-which that may be interrelated with other mechanisms contributing to arterial Stiffness. We introduce these observations as a new concept-the Smooth Muscle Cell Stiffness Syndrome (SMCSS)-within the field of arterial Stiffness and posit that stiffening of vascular Cells impairs vascular function and may contribute stiffening to the vasculature with aging and cardiovascular disease. Importantly, this review article revisits the structural basis of arterial Stiffness in light of these novel findings. Such classification of SMCSS and its contextualization into our current understanding of vascular mechanics may be useful in the development of strategic therapeutics to directly target arterial Stiffness.

  • augmented vascular smooth muscle Cell Stiffness and adhesion when hypertension is superimposed on aging
    2015
    Co-Authors: Nancy L Sehgel, Zhongkui Hong, William C Hunter, Michael A Hill, Dorothy E Vatner, Stephen F Vatner, Gerald A Meininger
    Abstract:

    Hypertension and aging are both recognized to increase aortic Stiffness, but their interactions are not completely understood. Most previous studies have attributed increased aortic Stiffness to changes in extraCellular matrix proteins that alter the mechanical properties of the vascular wall. Alternatively, we hypothesized that a significant component of increased vascular Stiffness in hypertension is due to changes in the mechanical and adhesive properties of vascular smooth muscle Cells, and that aging would augment the contribution from vascular smooth muscle Cells when compared with the extraCellular matrix. Accordingly, we studied aortic Stiffness in young (16-week-old) and old (64-week-old) spontaneously hypertensive rats and Wistar–Kyoto wild-type controls. Systolic and pulse pressures were significantly increased in young spontaneously hypertensive rats when compared with young Wistar–Kyoto rats, and these continued to rise in old spontaneously hypertensive rats when compared with age-matched controls. Excised aortic ring segments exhibited significantly greater elastic moduli in both young and old spontaneously hypertensive rats versus Wistar–Kyoto rats. were isolated from the thoracic aorta, and Stiffness and adhesion to fibronectin were measured by atomic force microscopy. Hypertension increased both vascular smooth muscle Cell Stiffness and vascular smooth muscle Cell adhesion, and these increases were both augmented with aging. By contrast, hypertension did not affect histological measures of aortic collagen and elastin, which were predominantly changed by aging. These findings support the concept that Stiffness and adhesive properties of vascular smooth muscle Cells are novel mechanisms contributing to the increased aortic Stiffness occurring with hypertension superimposed on aging.

  • augmented vascular smooth muscle Cell Stiffness and adhesion when hypertension is superimposed on aging
    2015
    Co-Authors: Nancy L Sehgel, Zhongkui Hong, William C Hunter, Michael A Hill, Dorothy E Vatner, Stephen F Vatner, Zhe Sun, Gerald A Meininger
    Abstract:

    Hypertension and aging are both recognized to increase aortic Stiffness, but their interactions are not completely understood. Most previous studies have attributed increased aortic Stiffness to changes in extraCellular matrix proteins that alter the mechanical properties of the vascular wall. Alternatively, we hypothesized that a significant component of increased vascular Stiffness in hypertension is due to changes in the mechanical and adhesive properties of vascular smooth muscle Cells, and that aging would augment the contribution from vascular smooth muscle Cells when compared with the extraCellular matrix. Accordingly, we studied aortic Stiffness in young (16-week-old) and old (64-week-old) spontaneously hypertensive rats and Wistar-Kyoto wild-type controls. Systolic and pulse pressures were significantly increased in young spontaneously hypertensive rats when compared with young Wistar-Kyoto rats, and these continued to rise in old spontaneously hypertensive rats when compared with age-matched controls. Excised aortic ring segments exhibited significantly greater elastic moduli in both young and old spontaneously hypertensive rats versus Wistar-Kyoto rats. were isolated from the thoracic aorta, and Stiffness and adhesion to fibronectin were measured by atomic force microscopy. Hypertension increased both vascular smooth muscle Cell Stiffness and vascular smooth muscle Cell adhesion, and these increases were both augmented with aging. By contrast, hypertension did not affect histological measures of aortic collagen and elastin, which were predominantly changed by aging. These findings support the concept that Stiffness and adhesive properties of vascular smooth muscle Cells are novel mechanisms contributing to the increased aortic Stiffness occurring with hypertension superimposed on aging.

  • Increased vascular smooth muscle Cell Stiffness: a novel mechanism for aortic Stiffness in hypertension
    2013
    Co-Authors: Nancy L Sehgel, Zhongkui Hong, William C Hunter, Dorothy E Vatner, Gerald A Meininger, J. Trzeciakowski, Yi Zhu, Zhe Sun, Stephen F Vatner
    Abstract:

    Increased vascular Stiffness is fundamental to hypertension, and its complications, including atherosclerosis, suggest that therapy should also be directed at vascular Stiffness, rather than just the regulation of peripheral vascular resistance. It is currently held that the underlying mechanisms of vascular Stiffness in hypertension only involve the extraCellular matrix and endothelium. We hypothesized that increased large-artery Stiffness in hypertension is partly due to intrinsic mechanical properties of vascular smooth muscle Cells. After confirming increased arterial pressure and aortic Stiffness in spontaneously hypertensive rats, we found increased elastic Stiffness of aortic smooth muscle Cells of spontaneously hypertensive rats compared with Wistar-Kyoto normotensive controls using both an engineered aortic tissue model and atomic force microscopy nanoindentation. Additionally, we observed different temporal oscillations in the Stiffness of vascular smooth muscle Cells derived from hypertensive and control rats, suggesting that a dynamic component to Cellular elastic Stiffness is altered in hypertension. Treatment with inhibitors of vascular smooth muscle Cell cytoskeletal proteins reduced vascular smooth muscle Cell Stiffness from hypertensive and control rats, suggesting their participation in the mechanism. This is the first study demonstrating that Stiffness of individual vascular smooth muscle Cells mediates vascular Stiffness in hypertension, a novel concept, which may elucidate new therapies for hypertension and for vascular Stiffness.

Nancy L Sehgel - One of the best experts on this subject based on the ideXlab platform.

  • smooth muscle Cell Stiffness syndrome revisiting the structural basis of arterial Stiffness
    2015
    Co-Authors: Nancy L Sehgel, Stephen F Vatner, Gerald A Meininger
    Abstract:

    In recent decades, the pervasiveness of increased arterial Stiffness in patients with cardiovascular disease has become increasingly apparent. Though, this phenomenon has been well documented in humans and animal models of disease for well over a century, there has been surprisingly limited development in a deeper mechanistic understanding of arterial Stiffness. Much of the historical literature has focused on changes in extraCellular matrix proteins-collagen and elastin. However, extraCellular matrix changes alone appear insufficient to consistently account for observed changes in vascular Stiffness, which we observed in our studies of aortic Stiffness in aging monkeys. This led us to examine novel mechanisms operating at the level of the vascular smooth muscle Cell (VSMC)-that include increased Cell Stiffness and adhesion to extraCellular matrix-which that may be interrelated with other mechanisms contributing to arterial Stiffness. We introduce these observations as a new concept-the Smooth Muscle Cell Stiffness Syndrome (SMCSS)-within the field of arterial Stiffness and posit that stiffening of vascular Cells impairs vascular function and may contribute stiffening to the vasculature with aging and cardiovascular disease. Importantly, this review article revisits the structural basis of arterial Stiffness in light of these novel findings. Such classification of SMCSS and its contextualization into our current understanding of vascular mechanics may be useful in the development of strategic therapeutics to directly target arterial Stiffness.

  • augmented vascular smooth muscle Cell Stiffness and adhesion when hypertension is superimposed on aging
    2015
    Co-Authors: Nancy L Sehgel, Zhongkui Hong, William C Hunter, Michael A Hill, Dorothy E Vatner, Stephen F Vatner, Gerald A Meininger
    Abstract:

    Hypertension and aging are both recognized to increase aortic Stiffness, but their interactions are not completely understood. Most previous studies have attributed increased aortic Stiffness to changes in extraCellular matrix proteins that alter the mechanical properties of the vascular wall. Alternatively, we hypothesized that a significant component of increased vascular Stiffness in hypertension is due to changes in the mechanical and adhesive properties of vascular smooth muscle Cells, and that aging would augment the contribution from vascular smooth muscle Cells when compared with the extraCellular matrix. Accordingly, we studied aortic Stiffness in young (16-week-old) and old (64-week-old) spontaneously hypertensive rats and Wistar–Kyoto wild-type controls. Systolic and pulse pressures were significantly increased in young spontaneously hypertensive rats when compared with young Wistar–Kyoto rats, and these continued to rise in old spontaneously hypertensive rats when compared with age-matched controls. Excised aortic ring segments exhibited significantly greater elastic moduli in both young and old spontaneously hypertensive rats versus Wistar–Kyoto rats. were isolated from the thoracic aorta, and Stiffness and adhesion to fibronectin were measured by atomic force microscopy. Hypertension increased both vascular smooth muscle Cell Stiffness and vascular smooth muscle Cell adhesion, and these increases were both augmented with aging. By contrast, hypertension did not affect histological measures of aortic collagen and elastin, which were predominantly changed by aging. These findings support the concept that Stiffness and adhesive properties of vascular smooth muscle Cells are novel mechanisms contributing to the increased aortic Stiffness occurring with hypertension superimposed on aging.

  • augmented vascular smooth muscle Cell Stiffness and adhesion when hypertension is superimposed on aging
    2015
    Co-Authors: Nancy L Sehgel, Zhongkui Hong, William C Hunter, Michael A Hill, Dorothy E Vatner, Stephen F Vatner, Zhe Sun, Gerald A Meininger
    Abstract:

    Hypertension and aging are both recognized to increase aortic Stiffness, but their interactions are not completely understood. Most previous studies have attributed increased aortic Stiffness to changes in extraCellular matrix proteins that alter the mechanical properties of the vascular wall. Alternatively, we hypothesized that a significant component of increased vascular Stiffness in hypertension is due to changes in the mechanical and adhesive properties of vascular smooth muscle Cells, and that aging would augment the contribution from vascular smooth muscle Cells when compared with the extraCellular matrix. Accordingly, we studied aortic Stiffness in young (16-week-old) and old (64-week-old) spontaneously hypertensive rats and Wistar-Kyoto wild-type controls. Systolic and pulse pressures were significantly increased in young spontaneously hypertensive rats when compared with young Wistar-Kyoto rats, and these continued to rise in old spontaneously hypertensive rats when compared with age-matched controls. Excised aortic ring segments exhibited significantly greater elastic moduli in both young and old spontaneously hypertensive rats versus Wistar-Kyoto rats. were isolated from the thoracic aorta, and Stiffness and adhesion to fibronectin were measured by atomic force microscopy. Hypertension increased both vascular smooth muscle Cell Stiffness and vascular smooth muscle Cell adhesion, and these increases were both augmented with aging. By contrast, hypertension did not affect histological measures of aortic collagen and elastin, which were predominantly changed by aging. These findings support the concept that Stiffness and adhesive properties of vascular smooth muscle Cells are novel mechanisms contributing to the increased aortic Stiffness occurring with hypertension superimposed on aging.

  • Increased vascular smooth muscle Cell Stiffness: a novel mechanism for aortic Stiffness in hypertension
    2013
    Co-Authors: Nancy L Sehgel, Zhongkui Hong, William C Hunter, Dorothy E Vatner, Gerald A Meininger, J. Trzeciakowski, Yi Zhu, Zhe Sun, Stephen F Vatner
    Abstract:

    Increased vascular Stiffness is fundamental to hypertension, and its complications, including atherosclerosis, suggest that therapy should also be directed at vascular Stiffness, rather than just the regulation of peripheral vascular resistance. It is currently held that the underlying mechanisms of vascular Stiffness in hypertension only involve the extraCellular matrix and endothelium. We hypothesized that increased large-artery Stiffness in hypertension is partly due to intrinsic mechanical properties of vascular smooth muscle Cells. After confirming increased arterial pressure and aortic Stiffness in spontaneously hypertensive rats, we found increased elastic Stiffness of aortic smooth muscle Cells of spontaneously hypertensive rats compared with Wistar-Kyoto normotensive controls using both an engineered aortic tissue model and atomic force microscopy nanoindentation. Additionally, we observed different temporal oscillations in the Stiffness of vascular smooth muscle Cells derived from hypertensive and control rats, suggesting that a dynamic component to Cellular elastic Stiffness is altered in hypertension. Treatment with inhibitors of vascular smooth muscle Cell cytoskeletal proteins reduced vascular smooth muscle Cell Stiffness from hypertensive and control rats, suggesting their participation in the mechanism. This is the first study demonstrating that Stiffness of individual vascular smooth muscle Cells mediates vascular Stiffness in hypertension, a novel concept, which may elucidate new therapies for hypertension and for vascular Stiffness.

Stephen F Vatner - One of the best experts on this subject based on the ideXlab platform.

  • smooth muscle Cell Stiffness syndrome revisiting the structural basis of arterial Stiffness
    2015
    Co-Authors: Nancy L Sehgel, Stephen F Vatner, Gerald A Meininger
    Abstract:

    In recent decades, the pervasiveness of increased arterial Stiffness in patients with cardiovascular disease has become increasingly apparent. Though, this phenomenon has been well documented in humans and animal models of disease for well over a century, there has been surprisingly limited development in a deeper mechanistic understanding of arterial Stiffness. Much of the historical literature has focused on changes in extraCellular matrix proteins-collagen and elastin. However, extraCellular matrix changes alone appear insufficient to consistently account for observed changes in vascular Stiffness, which we observed in our studies of aortic Stiffness in aging monkeys. This led us to examine novel mechanisms operating at the level of the vascular smooth muscle Cell (VSMC)-that include increased Cell Stiffness and adhesion to extraCellular matrix-which that may be interrelated with other mechanisms contributing to arterial Stiffness. We introduce these observations as a new concept-the Smooth Muscle Cell Stiffness Syndrome (SMCSS)-within the field of arterial Stiffness and posit that stiffening of vascular Cells impairs vascular function and may contribute stiffening to the vasculature with aging and cardiovascular disease. Importantly, this review article revisits the structural basis of arterial Stiffness in light of these novel findings. Such classification of SMCSS and its contextualization into our current understanding of vascular mechanics may be useful in the development of strategic therapeutics to directly target arterial Stiffness.

  • augmented vascular smooth muscle Cell Stiffness and adhesion when hypertension is superimposed on aging
    2015
    Co-Authors: Nancy L Sehgel, Zhongkui Hong, William C Hunter, Michael A Hill, Dorothy E Vatner, Stephen F Vatner, Gerald A Meininger
    Abstract:

    Hypertension and aging are both recognized to increase aortic Stiffness, but their interactions are not completely understood. Most previous studies have attributed increased aortic Stiffness to changes in extraCellular matrix proteins that alter the mechanical properties of the vascular wall. Alternatively, we hypothesized that a significant component of increased vascular Stiffness in hypertension is due to changes in the mechanical and adhesive properties of vascular smooth muscle Cells, and that aging would augment the contribution from vascular smooth muscle Cells when compared with the extraCellular matrix. Accordingly, we studied aortic Stiffness in young (16-week-old) and old (64-week-old) spontaneously hypertensive rats and Wistar–Kyoto wild-type controls. Systolic and pulse pressures were significantly increased in young spontaneously hypertensive rats when compared with young Wistar–Kyoto rats, and these continued to rise in old spontaneously hypertensive rats when compared with age-matched controls. Excised aortic ring segments exhibited significantly greater elastic moduli in both young and old spontaneously hypertensive rats versus Wistar–Kyoto rats. were isolated from the thoracic aorta, and Stiffness and adhesion to fibronectin were measured by atomic force microscopy. Hypertension increased both vascular smooth muscle Cell Stiffness and vascular smooth muscle Cell adhesion, and these increases were both augmented with aging. By contrast, hypertension did not affect histological measures of aortic collagen and elastin, which were predominantly changed by aging. These findings support the concept that Stiffness and adhesive properties of vascular smooth muscle Cells are novel mechanisms contributing to the increased aortic Stiffness occurring with hypertension superimposed on aging.

  • augmented vascular smooth muscle Cell Stiffness and adhesion when hypertension is superimposed on aging
    2015
    Co-Authors: Nancy L Sehgel, Zhongkui Hong, William C Hunter, Michael A Hill, Dorothy E Vatner, Stephen F Vatner, Zhe Sun, Gerald A Meininger
    Abstract:

    Hypertension and aging are both recognized to increase aortic Stiffness, but their interactions are not completely understood. Most previous studies have attributed increased aortic Stiffness to changes in extraCellular matrix proteins that alter the mechanical properties of the vascular wall. Alternatively, we hypothesized that a significant component of increased vascular Stiffness in hypertension is due to changes in the mechanical and adhesive properties of vascular smooth muscle Cells, and that aging would augment the contribution from vascular smooth muscle Cells when compared with the extraCellular matrix. Accordingly, we studied aortic Stiffness in young (16-week-old) and old (64-week-old) spontaneously hypertensive rats and Wistar-Kyoto wild-type controls. Systolic and pulse pressures were significantly increased in young spontaneously hypertensive rats when compared with young Wistar-Kyoto rats, and these continued to rise in old spontaneously hypertensive rats when compared with age-matched controls. Excised aortic ring segments exhibited significantly greater elastic moduli in both young and old spontaneously hypertensive rats versus Wistar-Kyoto rats. were isolated from the thoracic aorta, and Stiffness and adhesion to fibronectin were measured by atomic force microscopy. Hypertension increased both vascular smooth muscle Cell Stiffness and vascular smooth muscle Cell adhesion, and these increases were both augmented with aging. By contrast, hypertension did not affect histological measures of aortic collagen and elastin, which were predominantly changed by aging. These findings support the concept that Stiffness and adhesive properties of vascular smooth muscle Cells are novel mechanisms contributing to the increased aortic Stiffness occurring with hypertension superimposed on aging.

  • Increased vascular smooth muscle Cell Stiffness: a novel mechanism for aortic Stiffness in hypertension
    2013
    Co-Authors: Nancy L Sehgel, Zhongkui Hong, William C Hunter, Dorothy E Vatner, Gerald A Meininger, J. Trzeciakowski, Yi Zhu, Zhe Sun, Stephen F Vatner
    Abstract:

    Increased vascular Stiffness is fundamental to hypertension, and its complications, including atherosclerosis, suggest that therapy should also be directed at vascular Stiffness, rather than just the regulation of peripheral vascular resistance. It is currently held that the underlying mechanisms of vascular Stiffness in hypertension only involve the extraCellular matrix and endothelium. We hypothesized that increased large-artery Stiffness in hypertension is partly due to intrinsic mechanical properties of vascular smooth muscle Cells. After confirming increased arterial pressure and aortic Stiffness in spontaneously hypertensive rats, we found increased elastic Stiffness of aortic smooth muscle Cells of spontaneously hypertensive rats compared with Wistar-Kyoto normotensive controls using both an engineered aortic tissue model and atomic force microscopy nanoindentation. Additionally, we observed different temporal oscillations in the Stiffness of vascular smooth muscle Cells derived from hypertensive and control rats, suggesting that a dynamic component to Cellular elastic Stiffness is altered in hypertension. Treatment with inhibitors of vascular smooth muscle Cell cytoskeletal proteins reduced vascular smooth muscle Cell Stiffness from hypertensive and control rats, suggesting their participation in the mechanism. This is the first study demonstrating that Stiffness of individual vascular smooth muscle Cells mediates vascular Stiffness in hypertension, a novel concept, which may elucidate new therapies for hypertension and for vascular Stiffness.

William C Hunter - One of the best experts on this subject based on the ideXlab platform.

  • augmented vascular smooth muscle Cell Stiffness and adhesion when hypertension is superimposed on aging
    2015
    Co-Authors: Nancy L Sehgel, Zhongkui Hong, William C Hunter, Michael A Hill, Dorothy E Vatner, Stephen F Vatner, Gerald A Meininger
    Abstract:

    Hypertension and aging are both recognized to increase aortic Stiffness, but their interactions are not completely understood. Most previous studies have attributed increased aortic Stiffness to changes in extraCellular matrix proteins that alter the mechanical properties of the vascular wall. Alternatively, we hypothesized that a significant component of increased vascular Stiffness in hypertension is due to changes in the mechanical and adhesive properties of vascular smooth muscle Cells, and that aging would augment the contribution from vascular smooth muscle Cells when compared with the extraCellular matrix. Accordingly, we studied aortic Stiffness in young (16-week-old) and old (64-week-old) spontaneously hypertensive rats and Wistar–Kyoto wild-type controls. Systolic and pulse pressures were significantly increased in young spontaneously hypertensive rats when compared with young Wistar–Kyoto rats, and these continued to rise in old spontaneously hypertensive rats when compared with age-matched controls. Excised aortic ring segments exhibited significantly greater elastic moduli in both young and old spontaneously hypertensive rats versus Wistar–Kyoto rats. were isolated from the thoracic aorta, and Stiffness and adhesion to fibronectin were measured by atomic force microscopy. Hypertension increased both vascular smooth muscle Cell Stiffness and vascular smooth muscle Cell adhesion, and these increases were both augmented with aging. By contrast, hypertension did not affect histological measures of aortic collagen and elastin, which were predominantly changed by aging. These findings support the concept that Stiffness and adhesive properties of vascular smooth muscle Cells are novel mechanisms contributing to the increased aortic Stiffness occurring with hypertension superimposed on aging.

  • augmented vascular smooth muscle Cell Stiffness and adhesion when hypertension is superimposed on aging
    2015
    Co-Authors: Nancy L Sehgel, Zhongkui Hong, William C Hunter, Michael A Hill, Dorothy E Vatner, Stephen F Vatner, Zhe Sun, Gerald A Meininger
    Abstract:

    Hypertension and aging are both recognized to increase aortic Stiffness, but their interactions are not completely understood. Most previous studies have attributed increased aortic Stiffness to changes in extraCellular matrix proteins that alter the mechanical properties of the vascular wall. Alternatively, we hypothesized that a significant component of increased vascular Stiffness in hypertension is due to changes in the mechanical and adhesive properties of vascular smooth muscle Cells, and that aging would augment the contribution from vascular smooth muscle Cells when compared with the extraCellular matrix. Accordingly, we studied aortic Stiffness in young (16-week-old) and old (64-week-old) spontaneously hypertensive rats and Wistar-Kyoto wild-type controls. Systolic and pulse pressures were significantly increased in young spontaneously hypertensive rats when compared with young Wistar-Kyoto rats, and these continued to rise in old spontaneously hypertensive rats when compared with age-matched controls. Excised aortic ring segments exhibited significantly greater elastic moduli in both young and old spontaneously hypertensive rats versus Wistar-Kyoto rats. were isolated from the thoracic aorta, and Stiffness and adhesion to fibronectin were measured by atomic force microscopy. Hypertension increased both vascular smooth muscle Cell Stiffness and vascular smooth muscle Cell adhesion, and these increases were both augmented with aging. By contrast, hypertension did not affect histological measures of aortic collagen and elastin, which were predominantly changed by aging. These findings support the concept that Stiffness and adhesive properties of vascular smooth muscle Cells are novel mechanisms contributing to the increased aortic Stiffness occurring with hypertension superimposed on aging.

  • Increased vascular smooth muscle Cell Stiffness: a novel mechanism for aortic Stiffness in hypertension
    2013
    Co-Authors: Nancy L Sehgel, Zhongkui Hong, William C Hunter, Dorothy E Vatner, Gerald A Meininger, J. Trzeciakowski, Yi Zhu, Zhe Sun, Stephen F Vatner
    Abstract:

    Increased vascular Stiffness is fundamental to hypertension, and its complications, including atherosclerosis, suggest that therapy should also be directed at vascular Stiffness, rather than just the regulation of peripheral vascular resistance. It is currently held that the underlying mechanisms of vascular Stiffness in hypertension only involve the extraCellular matrix and endothelium. We hypothesized that increased large-artery Stiffness in hypertension is partly due to intrinsic mechanical properties of vascular smooth muscle Cells. After confirming increased arterial pressure and aortic Stiffness in spontaneously hypertensive rats, we found increased elastic Stiffness of aortic smooth muscle Cells of spontaneously hypertensive rats compared with Wistar-Kyoto normotensive controls using both an engineered aortic tissue model and atomic force microscopy nanoindentation. Additionally, we observed different temporal oscillations in the Stiffness of vascular smooth muscle Cells derived from hypertensive and control rats, suggesting that a dynamic component to Cellular elastic Stiffness is altered in hypertension. Treatment with inhibitors of vascular smooth muscle Cell cytoskeletal proteins reduced vascular smooth muscle Cell Stiffness from hypertensive and control rats, suggesting their participation in the mechanism. This is the first study demonstrating that Stiffness of individual vascular smooth muscle Cells mediates vascular Stiffness in hypertension, a novel concept, which may elucidate new therapies for hypertension and for vascular Stiffness.

  • short communication vascular smooth muscle Cell Stiffness as a mechanism for increased aortic Stiffness with aging
    2010
    Co-Authors: Hongyu Qiu, William C Hunter, J. Trzeciakowski, Yi Zhu, Zhe Sun, Meredith Gansner, Christophe Depre, Ranillo R G Resuello, Filipinas F Natividad, Guy M Genin
    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 vas...

Bianxiao Cui - One of the best experts on this subject based on the ideXlab platform.

  • nanoscale surface topography reduces focal adhesions and Cell Stiffness by enhancing integrin endocytosis
    2021
    Co-Authors: Lasse Hyldgaard Klausen, Wei Zhang, Zeinab Jahed, Chingting Tsai, Bianxiao Cui
    Abstract:

    Both substrate Stiffness and surface topography regulate Cell behavior through mechanotransduction signaling pathways. Such intertwined effects suggest that engineered surface topographies might substitute or cancel the effects of substrate Stiffness in biomedical applications. However, the mechanisms by which Cells recognize topographical features are not fully understood. Here we demonstrate that the presence of nanotopography drastically alters Cell behavior such that neurons and stem Cells cultured on rigid glass substrates behave as if they were on soft hydrogels. With atomic force microscopy, we show that rigid nanotopography resembles the effects of soft hydrogels in reducing Cell Stiffness and membrane tension. Further, we reveal that nanotopography reduces focal adhesions and Cell Stiffness by enhancing the endocytosis and the subsequent removal of integrin receptors. This mechanistic understanding will support the rational design of nanotopography that directs Cells on rigid materials to behave as if they were on soft ones.

  • nanoscale surface topography reduces focal adhesions and Cell Stiffness by enhancing integrin endocytosis
    2021
    Co-Authors: Lasse Hyldgaard Klausen, Wei Zhang, Zeinab Jahed, Chingting Tsai, Bianxiao Cui
    Abstract:

    Both substrate Stiffness and surface topography regulate Cell behavior through mechanotransduction signaling pathways. Such intertwined effects suggest that engineered surface topographies might substitute or cancel the effects of substrate Stiffness in biomedical applications. However, the mechanisms by which Cells recognize topographical features are not fully understood. Here we demonstrate that the presence of nanotopography drastically alters Cell behavior such that neurons and stem Cells cultured on rigid glass substrates behave as if they were on soft hydrogels. We further show that rigid nanotopography resembles the effect of soft hydrogels in reducing Cell Stiffness and membrane tension as measured by atomic force microscopy. Finally, we demonstrate that nanotopography reduces focal adhesions and Cell Stiffness by enhancing the endocytosis and the subsequent removal of integrin receptors. This mechanistic understanding will support the rational design of nanotopography that directs Cells on rigid materials to behave as if they were on soft ones. TOC graphic O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=104 SRC="FIGDIR/small/448920v1_ufig1.gif" ALT="Figure 1"> View larger version (41K): org.highwire.dtl.DTLVardef@17ef10org.highwire.dtl.DTLVardef@15038d3org.highwire.dtl.DTLVardef@1c2e3e4org.highwire.dtl.DTLVardef@1ffb6a5_HPS_FORMAT_FIGEXP M_FIG C_FIG