The Experts below are selected from a list of 309 Experts worldwide ranked by ideXlab platform

Michael Wiederholt - One of the best experts on this subject based on the ideXlab platform.

  • the regulation of trabecular meshwork and ciliary Muscle Contractility
    Progress in Retinal and Eye Research, 2000
    Co-Authors: Michael Wiederholt, Hagen Thieme, Friederike Stumpff
    Abstract:

    Abstract Current models of aqueous humor outflow no longer treat trabecular meshwork (TM) as an inert tissue passively distended by the ciliary Muscle (CM). Instead, ample evidence supports the theory that trabecular meshwork possesses smooth Muscle-like properties and is actively involved in the regulation of aqueous humor outflow and intraocular pressure. In this model, trabecular meshwork and ciliary Muscle appear as functional antagonists, with ciliary Muscle contraction leading to a distension of trabecular meshwork with subsequent reduction in outflow, and with trabecular meshwork contraction leading to the opposite effect. Smooth-Muscle relaxing substances would therefore appear to be ideal candidates for glaucoma therapy with the dual goal of reducing intraocular pressure via the trabecular meshwork and of improving vascular perfusion of the optic nerve head. However, for such substances to effectively lower intraocular pressure, the effect on the ciliary Muscle would have to be minimal. For this reason, more information is needed on the signalling processes involved in regulating trabecular meshwork and ciliary Muscle Contractility. This review attempts to outline current knowledge of signal transduction pathways leading to relaxation and contraction of ciliary Muscle and trabecular meshwork. Pathways can be classified as involving or not involving changes of membrane voltage and of requiring or not requiring external calcium; possibly, other pathways exist. These different pathways involve different ion channels and isoforms of PKC and are expressed to a differing degree in ciliary Muscle and trabecular meshwork, leading to differential responses when exposed to relaxing or contracting pharmacological agents. Some of these agents, like tyrosine kinase inhibitors and inhibitors of PKC, have been shown to relax trabecular meshwork while leaving ciliary Muscle comparatively unaffected. This profile makes these substances appear as ideal drugs for simultaneously improving ocular outflow and retinal circulation, parameters that determine the time course of visual deterioration in glaucoma.

  • Relaxation of trabecular meshwork and ciliary Muscle by release of nitric oxide.
    Investigative Ophthalmology & Visual Science, 1994
    Co-Authors: Michael Wiederholt, A. Sturm, Albrecht Lepple-wienhues
    Abstract:

    Purpose. Recent evidence suggests that nitric oxide (NO) is a major messenger molecule regulating smooth Muscle Contractility. A role for NO in aqueous humor dynamics, and thus regulation of intraocular pressure, has been postulated. Recently, we described contractile properties of isolated bovine trabecular meshwork and ciliary Muscle strips. To assess whether vasodilators contribute to the regulation of trabecular meshwork and ciliary Muscle Contractility, we measured the effect of various substances known to induce vasodilation by increasing intracellular cGMP production. Methods. Measurements of isometric tension were performed on isolated bovine ciliary Muscle and trabecular meshwork strips using a custom-built electromagnetic force-length transducer

Patrick W. Alford - One of the best experts on this subject based on the ideXlab platform.

  • Amyloid Beta Influences Vascular Smooth Muscle Contractility and Mechanoadaptation
    Journal of biomechanical engineering, 2016
    Co-Authors: Eric S. Hald, Connor D. Timm, Patrick W. Alford
    Abstract:

    Amyloid beta accumulation in neuronal and cerebrovascular tissue is a key precursor to development of Alzheimer's disease and can result in neurodegeneration. While its persistence in Alzheimer's cases is well-studied, amyloid beta's direct effect on vascular function is unclear. Here, we measured the effect of amyloid beta treatment on vascular smooth Muscle cell functional Contractility and modeled the mechanoadaptive growth and remodeling response to these functional perturbations. We found that the amyloid beta 1-42 isoform induced a reduction in vascular smooth Muscle cell mechanical output and reduced response to vasocontractile cues. These data were used to develop a thin-walled constrained mixture arterial model that suggests vessel growth, and remodeling in response to amyloid betamediated alteration of smooth Muscle function leads to decreased ability of cerebrovascular vessels to vasodilate. These findings provide a possible explanation for the vascular injury and malfunction often associated with the development of neurodegeneration in Alzheimer's disease.

  • vascular smooth Muscle Contractility depends on cell shape
    Integrative Biology, 2011
    Co-Authors: Patrick W. Alford, Alexander P Nesmith, Johannes N Seywerd, Anna Grosberg, Kevin Kit Parker
    Abstract:

    The physiologic role of smooth Muscle structure in defining arterial function is poorly understood. We aimed to elucidate the relationship between vascular smooth Muscle architecture and functional contractile output. Using microcontact printing and muscular thin film technology, we engineered in vitro vascular tissues with strictly defined geometries and tested their contractile function. In all tissues, vascular smooth Muscle cells (VSMCs) were highly aligned with in vivo-like spindle architecture, and contracted physiologically in response to stimulation with endothelin-1. However, tissues wherein the VSMCs were forced into exaggerated spindle elongation exerted significantly greater contraction force per unit cross-sectional area than those with smaller aspect ratios. Moreover, this increased contraction did not occur in conjunction with an increase in traditionally measured contractile phenotype markers. These results suggest that cellular architecture within vascular tissues plays a significant role in conferring tissue function and that, in some systems, traditional phenotype characterization is not sufficient to define a functionally contractile population of VSMCs.

Dawn A. Lowe - One of the best experts on this subject based on the ideXlab platform.

  • deletion of estrogen receptor α in skeletal Muscle results in impaired Contractility in female mice
    Journal of Applied Physiology, 2018
    Co-Authors: Brittany C Collins, Tara L Mader, Christine A Cabelka, Melissa R Inigo, Espen E Spangenburg, Dawn A. Lowe
    Abstract:

    We comprehensively measured in vitro and in vivo skeletal Muscle Contractility in female estrogen receptor α (ERα) skeletal Muscle-specific knockout mice and report that force generation is impaire...

  • Influence of Ovarian Hormones on Skeletal Muscle Contractility
    Integrative Biology of Women’s Health, 2013
    Co-Authors: Dawn A. Lowe, Sarah M. Greising
    Abstract:

    There is a loss of skeletal Muscle strength around the time of menopause in women, probably due to the decline of ovarian hormone production. The maintenance of Muscle strength and Contractility with age and with loss of ovarian hormones are critical issues because the risk for disability and dependent living increases with Muscle weakness. There is substantial evidence that estradiol is beneficial to Muscle strength. Thus, better understanding of the mechanisms by which estradiol affects Contractility and how the loss of this hormone is detrimental to skeletal Muscle function is critical. This chapter focuses on ovarian hormones, specifically how the lack of estradiol affects skeletal Muscle Contractility in both postmenopausal women and rodent models.

  • Effects of prednisolone on skeletal Muscle Contractility in mdx mice.
    Muscle & nerve, 2009
    Co-Authors: Kristen A. Baltgalvis, Jarrod A. Call, Jason B. Nikas, Dawn A. Lowe
    Abstract:

    Current treatment for Duchenne Muscular Dystrophy (DMD) is chronic administration of the glucocorticoid prednisolone. Prednisolone improves Muscle strength in boys with DMD, but the mechanism is unknown. The purpose of this study was to determine how prednisolone improves Muscle strength by examining Muscle Contractility in dystrophic mice over time and in conjunction with eccentric injury. Mdx mice began receiving prednisolone (n=23) or placebo (n=16) at 5-wks of age. Eight wks of prednisolone increased specific force of the EDL Muscle 26%, but other parameters of Contractility were not affected. Prednisolone also improved the histological appearance of Muscle by decreasing the number of centrally-nucleated fibers. Prednisolone treatment did not affect force loss during eccentric contractions or recovery of force following injury. These data are of clinical relevance, because the increase in Muscle strength in boys with DMD taking prednisolone does not appear to occur via the same mechanism in dystrophic mice.

  • Estradiol replacement reverses ovariectomy-induced Muscle contractile and myosin dysfunction in mature female mice
    Journal of applied physiology (Bethesda Md. : 1985), 2007
    Co-Authors: Amy L. Moran, Steven A. Nelson, Rachel M. Landisch, Gordon L. Warren, Dawn A. Lowe
    Abstract:

    Skeletal Muscle Contractility and myosin function decline following ovariectomy in mature female mice. In the present study we tested the hypothesis that estradiol replacement can reverse those dec...

Friederike Stumpff - One of the best experts on this subject based on the ideXlab platform.

  • the regulation of trabecular meshwork and ciliary Muscle Contractility
    Progress in Retinal and Eye Research, 2000
    Co-Authors: Michael Wiederholt, Hagen Thieme, Friederike Stumpff
    Abstract:

    Abstract Current models of aqueous humor outflow no longer treat trabecular meshwork (TM) as an inert tissue passively distended by the ciliary Muscle (CM). Instead, ample evidence supports the theory that trabecular meshwork possesses smooth Muscle-like properties and is actively involved in the regulation of aqueous humor outflow and intraocular pressure. In this model, trabecular meshwork and ciliary Muscle appear as functional antagonists, with ciliary Muscle contraction leading to a distension of trabecular meshwork with subsequent reduction in outflow, and with trabecular meshwork contraction leading to the opposite effect. Smooth-Muscle relaxing substances would therefore appear to be ideal candidates for glaucoma therapy with the dual goal of reducing intraocular pressure via the trabecular meshwork and of improving vascular perfusion of the optic nerve head. However, for such substances to effectively lower intraocular pressure, the effect on the ciliary Muscle would have to be minimal. For this reason, more information is needed on the signalling processes involved in regulating trabecular meshwork and ciliary Muscle Contractility. This review attempts to outline current knowledge of signal transduction pathways leading to relaxation and contraction of ciliary Muscle and trabecular meshwork. Pathways can be classified as involving or not involving changes of membrane voltage and of requiring or not requiring external calcium; possibly, other pathways exist. These different pathways involve different ion channels and isoforms of PKC and are expressed to a differing degree in ciliary Muscle and trabecular meshwork, leading to differential responses when exposed to relaxing or contracting pharmacological agents. Some of these agents, like tyrosine kinase inhibitors and inhibitors of PKC, have been shown to relax trabecular meshwork while leaving ciliary Muscle comparatively unaffected. This profile makes these substances appear as ideal drugs for simultaneously improving ocular outflow and retinal circulation, parameters that determine the time course of visual deterioration in glaucoma.

Albrecht Lepple-wienhues - One of the best experts on this subject based on the ideXlab platform.

  • Relaxation of trabecular meshwork and ciliary Muscle by release of nitric oxide.
    Investigative Ophthalmology & Visual Science, 1994
    Co-Authors: Michael Wiederholt, A. Sturm, Albrecht Lepple-wienhues
    Abstract:

    Purpose. Recent evidence suggests that nitric oxide (NO) is a major messenger molecule regulating smooth Muscle Contractility. A role for NO in aqueous humor dynamics, and thus regulation of intraocular pressure, has been postulated. Recently, we described contractile properties of isolated bovine trabecular meshwork and ciliary Muscle strips. To assess whether vasodilators contribute to the regulation of trabecular meshwork and ciliary Muscle Contractility, we measured the effect of various substances known to induce vasodilation by increasing intracellular cGMP production. Methods. Measurements of isometric tension were performed on isolated bovine ciliary Muscle and trabecular meshwork strips using a custom-built electromagnetic force-length transducer