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Publications (4)8.13 Total impact

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    ABSTRACT: A three dimensional (3D) computational simulation of dynamic process of trabecular bone remodeling was developed with all the parameters derived from physiological and clinical data. Contributions of the microstructural bone formation deficits: trabecular plate perforations, trabecular rod breakages, and isolated bone fragments, to the rapid bone loss and disruption of trabecular microarchitecture during menopause were studied. Eighteen human trabecular bone samples from femoral neck (FN) and spine were scanned using a micro computed tomography (microCT) system. Bone resorption and formation were simulated as a computational cycle corresponding to 40-day resorption/160-day formation. Resorption cavities were randomly created over the bone surface according to the activation frequency, which was strictly based on clinical data. Every resorption cavity was refilled during formation unless it caused trabecular plate perforation, trabecular rod breakage or isolated fragments. A 20-year-period starting 5 years before and ending 15 years after menopause was simulated for each specimen. Elastic moduli, standard and individual trabeculae segmentation (ITS)-based morphological parameters were evaluated for each simulated 3D image. For both spine and FN groups, the time courses of predicted bone loss pattern by microstructural bone formation deficits were fairly consistent with the clinical measurements. The percentage of bone loss due to trabecular plate perforation, trabecular rod breakage, and isolated bone fragments were 73.2%, 18.9% and 7.9% at the simulated 15 years after menopause. The ITS-based plate fraction (pBV/BV), mean plate surface area (pTb.S), plate number density (pTb.N), and mean rod thickness (rTb.Th) decreased while rod fraction (rBV/BV) and rod number density (rTb.N) increased after the simulated menopause. The dynamic bone remodeling simulation based on microstructural bone formation deficits predicted the time course of menopausal bone loss pattern of spine and FN. Microstructural plate perforation could be the primary cause of menopausal trabecular bone loss. The combined effect of trabeculae perforation, breakage, and isolated fragments resulted in fewer and smaller trabecular plates and more but thinner trabecular rods.
    Bone 09/2008; 43(2):292-301. · 4.46 Impact Factor
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    ABSTRACT: Cells require optimal substrate stiffness for normal function and differentiation. The mechanisms for sensing matrix rigidity and durotaxis, however, are not clear. Here we showed that control, Shp2-/-, integrin beta1-/-, and talin1-/- cell lines all spread to a threefold greater area on fibronectin (FN)-coated rigid polyacrylamide surfaces than soft. In contrast, RPTPalpha-/- cells spread to the same area irrespective of rigidity on FN surfaces but spread 3x greater on rigid collagen IV-coated surfaces than soft. RPTPalpha and alphavbeta3 integrins were shown previously to be colocalized at leading edges and antibodies to alphavbeta3 blocked FN rigidity sensing. When FN beads were held with a rigid laser trap at the leading edge, stronger bonds to the cytoskeleton formed than when held with a soft trap; whereas back from the leading edge and in RPTPalpha-/- cells, weaker bonds were formed with both rigid and soft laser traps. From the rigidity of the trap, we calculate that a force of 10 pN generated in 1 s is sufficient to activate the rigidity response. We suggest that RPTPalpha and alphavbeta3 at the leading edge are critical elements for sensing FN matrix rigidity possibly through SFK activation at the edge and downstream signaling.
    Biophysical Journal 04/2006; 90(5):1804-9. · 3.67 Impact Factor
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    X. S. Liu, A. H. Huang, P. Sajda, X. E. Guo
    Journal of Biomechanics - J BIOMECH; 01/2006
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    ABSTRACT: Cells require optimal substrate stiffness for normal function and differentiation. The mechanisms for sensing matrix rigidity and durotaxis, however, are not clear. Here we showed that control, Shp2 ÿ/ÿ , integrin b1 ÿ/ÿ , and talin1 ÿ/ÿ cell lines all spread to a threefold greater area on fibronectin (FN)-coated rigid polyacrylamide surfaces than soft. In contrast, RPTPa ÿ/ÿ cells spread to the same area irrespective of rigidity on FN surfaces but spread 3 3 greater on rigid collagen IV-coated surfaces than soft. RPTPa and a v b 3 integrins were shown previously to be colocalized at leading edges and antibodies to a v b 3 blocked FN rigidity sensing. When FN beads were held with a rigid laser trap at the leading edge, stronger bonds to the cytoskeleton formed than when held with a soft trap; whereas back from the leading edge and in RPTPa ÿ/ÿ cells, weaker bonds were formed with both rigid and soft laser traps. From the rigidity of the trap, we calculate that a force of 10 pN generated in 1 s is sufficient to activate the rigidity response. We suggest that RPTPa and a v b 3 at the leading edge are critical elements for sensing FN matrix rigidity possibly through SFK activation at the edge and downstream signaling.