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Journal articles on the topic 'Connective tissues Physiology'
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1
Noda, Sawako, Yoshinori Sumita, Seigo Ohba, Hideyuki Yamamoto, and Izumi Asahina. "Soft tissue engineering with micronized-gingival connective tissues." Journal of Cellular Physiology 233, no. 1 (May 3, 2017): 249–58. http://dx.doi.org/10.1002/jcp.25871.
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Reed, RK, K. Woie, and K. Rubin. "Integrins and Control of Interstitial Fluid Pressure." Physiology 12, no. 1 (February 1, 1997): 42–49. http://dx.doi.org/10.1152/physiologyonline.1997.12.1.42.
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The present review summarizes recent information on the physiology of connective tissues, in particular, control of interstitial fluid pressure (Pif) and, thereby, interstitial volume. A combination of classic physiological techniques and techniques from cellular and molecular biology have provided new insights into control of Pif by connective tissue cells and the adhesion receptors anchoring them to structural connective tissue components.
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Bonnevie, Edward D., and Robert L. Mauck. "Physiology and Engineering of the Graded Interfaces of Musculoskeletal Junctions." Annual Review of Biomedical Engineering 20, no. 1 (June 4, 2018): 403–29. http://dx.doi.org/10.1146/annurev-bioeng-062117-121113.
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The connective tissues of the musculoskeletal system can be grouped into fibrous, cartilaginous, and calcified tissues. While each tissue type has a distinct composition and function, the intersections between these tissues result in the formation of complex, composite, and graded junctions. The complexity of these interfaces is a critical aspect of their healthy function, but poses a significant challenge for their repair. In this review, we describe the organization and structure of complex musculoskeletal interfaces, identify emerging technologies for engineering such structures, and outline the requirements for assessing the complex nature of these tissues in the context of recapitulating their function through tissue engineering.
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Suki, Béla, Satoru Ito, Dimitrije Stamenović, Kenneth R. Lutchen, and Edward P. Ingenito. "Biomechanics of the lung parenchyma: critical roles of collagen and mechanical forces." Journal of Applied Physiology 98, no. 5 (May 2005): 1892–99. http://dx.doi.org/10.1152/japplphysiol.01087.2004.
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The biomechanical properties of connective tissues play fundamental roles in how mechanical interactions of the body with its environment produce physical forces at the cellular level. It is now recognized that mechanical interactions between cells and the extracellular matrix (ECM) have major regulatory effects on cellular physiology and cell-cycle kinetics that can lead to the reorganization and remodeling of the ECM. The connective tissues are composed of cells and the ECM, which includes water and a variety of biological macromolecules. The macromolecules that are most important in determining the mechanical properties of these tissues are collagen, elastin, and proteoglycans. Among these macromolecules, the most abundant and perhaps most critical for structural integrity is collagen. In this review, we examine how mechanical forces affect the physiological functioning of the lung parenchyma, with special emphasis on the role of collagen. First, we overview the composition of the connective tissue of the lung and their complex structural organization. We then describe how mechanical properties of the parenchyma arise from its composition as well as from the architectural organization of the connective tissue. We argue that, because collagen is the most important load-bearing component of the parenchymal connective tissue, it is also critical in determining the homeostasis and cellular responses to injury. Finally, we overview the interactions between the parenchymal collagen network and cellular remodeling and speculate how mechanotransduction might contribute to disease propagation and the development of small- and large-scale heterogeneities with implications to impaired lung function in emphysema.
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Nikoloudaki, Georgia, Sarah Brooks, Alexander P. Peidl, Dylan Tinney, and Douglas W. Hamilton. "JNK Signaling as a Key Modulator of Soft Connective Tissue Physiology, Pathology, and Healing." International Journal of Molecular Sciences 21, no. 3 (February 4, 2020): 1015. http://dx.doi.org/10.3390/ijms21031015.
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In healthy individuals, the healing of soft tissues such as skin after pathological insult or post injury follows a relatively predictable and defined series of cell and molecular processes to restore tissue architecture and function(s). Healing progresses through the phases of hemostasis, inflammation, proliferation, remodeling, and concomitant with re-epithelialization restores barrier function. Soft tissue healing is achieved through the spatiotemporal interplay of multiple different cell types including neutrophils, monocytes/macrophages, fibroblasts, endothelial cells/pericytes, and keratinocytes. Expressed in most cell types, c-Jun N-terminal kinases (JNK) are signaling molecules associated with the regulation of several cellular processes involved in soft tissue wound healing and in response to cellular stress. A member of the mitogen-activated protein kinase family (MAPK), JNKs have been implicated in the regulation of inflammatory cell phenotype, as well as fibroblast, stem/progenitor cell, and epithelial cell biology. In this review, we discuss our understanding of JNKs in the regulation of cell behaviors related to tissue injury, pathology, and wound healing of soft tissues. Using models as diverse as Drosophila, mice, rats, as well as human tissues, research is now defining important, but sometimes conflicting roles for JNKs in the regulation of multiple molecular processes in multiple different cell types central to wound healing processes. In this review, we focus specifically on the role of JNKs in the regulation of cell behavior in the healing of skin, cornea, tendon, gingiva, and dental pulp tissues. We conclude that while parallels can be drawn between some JNK activities and the control of cell behavior in healing, the roles of JNK can also be very specific modes of action depending on the tissue and the phase of healing.
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Borgstrom, P., L. Lindbom, K. E. Arfors, and M. Intaglietta. "Beta-adrenergic control of resistance in individual vessels in rabbit tenuissimus muscle." American Journal of Physiology-Heart and Circulatory Physiology 254, no. 4 (April 1, 1988): H631—H635. http://dx.doi.org/10.1152/ajpheart.1988.254.4.h631.
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The microvascular responses to topically applied isoproterenol and to epinephrine in the intact and beta-adrenoceptor-blocked microcirculation were studied in the rabbit tenuissimus muscle by direct intravital microscopy. The main feeding arterioles in this muscle supply two vascular areas, the muscle capillaries and the adjacent connective tissue. beta-Adrenergic stimulation with isoproterenol and epinephrine dilated the transverse arterioles that supply muscle and connective tissues, whereas their first-order side branches (terminal arterioles), which only supply the muscle capillaries, were little affected. Flow measurements were made at two different sites in the transverse arterioles to determine the relative changes in muscle capillary flow and connective tissue flow. These measurements showed that beta-adrenergic stimulation caused a fractional redistribution of microvascular blood flow from the muscle tissue proper to the adjacent connective tissue.
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Ault, H. K., and A. H. Hoffman. "A Composite Micromechanical Model for Connective Tissues: Part I—Theory." Journal of Biomechanical Engineering 114, no. 1 (February 1, 1992): 137–41. http://dx.doi.org/10.1115/1.2895437.
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A micromechanical model has been developed to study and predict the mechanical behavior of fibrous soft tissues. The model uses the theorems of least work and minimum potential energy to predict upper and lower bounds on material behavior based on the structure and properties of tissue components. The basic model consists of a composite of crimped collagen fibers embedded in an elastic glycosaminoglycan matrix. Upper and lower bound aggregation rules predict composite material behavior under the assumptions of uniform strain and uniform stress, respectively. Input parameters consist of the component material properties and the geometric configuration of the fibers. The model may be applied to a variety of connective tissue structures and is valuable in giving insight into material behavior and the nature of interactions between tissue components in various structures. Application of the model to rat tail tendon and cat knee joint capsule is described in a companion paper [2].
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Wren, T. A. L., and D. R. Carter. "A Microstructural Model for the Tensile Constitutive and Failure Behavior of Soft Skeletal Connective Tissues." Journal of Biomechanical Engineering 120, no. 1 (February 1, 1998): 55–61. http://dx.doi.org/10.1115/1.2834307.
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We propose a microstructural model for the uniaxial tensile constitutive and failure behavior of soft skeletal connective tissues. The model characterizes the tissues as two-phase composites consisting of collagen fibers embedded in ground substance. Nonlinear toe region behavior in the stress versus strain curve results from the straightening of crimped fibers and from fiber reorientation. Subsequent linear behavior results from fiber stretching affected by fiber volume fraction, collagen type, crosslink density, and fiber orientation. Finally, the tissue fails when fibers successively rupture at their ultimate tensile strain. We apply the model to tendon, meniscus, and articular cartilage. The model provides a consistent approach to modeling the tensile behavior of a wide range of soft skeletal connective tissues.
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Trotter, JA, G. Lyons-Levy, K. Chino, TJ Koob, DR Keene, and MAL Atkinson. "The molecular design of mutable connective tissues in echinoderms." Comparative Biochemistry and Physiology Part A: Molecular & Integrative Physiology 124 (August 1999): S35. http://dx.doi.org/10.1016/s1095-6433(99)90137-x.
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Maas, Huub. "Significance of epimuscular myofascial force transmission under passive muscle conditions." Journal of Applied Physiology 126, no. 5 (May 1, 2019): 1465–73. http://dx.doi.org/10.1152/japplphysiol.00631.2018.
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In the past 20 yr, force transmission via connective tissue linkages at the muscle belly surface, called epimuscular myofascial force transmission, has been studied extensively. In this article, the effects of epimuscular linkages under passive muscle conditions are reviewed. Several animal studies that included direct (invasive) measurements of force transmission have shown that different connective tissue structures serve as an epimuscular pathway and that these tissues have sufficient stiffness, especially at supraphysiological muscle lengths and relative positions, to transmit substantial passive forces (up to 15% of active optimal force). Exact values of lumped tissue stiffness for different connective tissue structures have not yet been estimated. Experiments using various imaging techniques (ultrasound, MRI, shear wave elastography) have yielded some, but weak, evidence of epimuscular myofascial force transmission for passive muscles in humans. At this point, the functional consequences of epimuscular pathways for muscle and joint mechanics in the intact body are still unknown. Potentially, however, these pathways may affect sensory feedback and, thereby, neuromuscular control. In addition, altered epimuscular force transmission in pathological conditions may also contribute to changes in passive range of joint motion.
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Robalino Gonzaga, Ernesto, Irene Riestra Guiance, Richard Henriquez, Gerri Mortimore, and Jan Freeman. "The Role of the Liver in Iron Homeostasis and What Goes Wrong?" Journal of Renal and Hepatic Disorders 5, no. 2 (September 18, 2021): 26–33. http://dx.doi.org/10.15586/jrenhep.v5i2.110.
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Iron is an essential mineral that is vital for growth development, normal cellular function, synthesis of hormones and connective tissue, and most importantly, serves as a component of hemoglobin to carry oxygen to body tissues. The body finely regulates the amount of circulating and stored iron within the body to maintain concentration levels within range for optimal physiologic function. Without iron, the ability for cells to participate in electron transport and energy metabolism decreases. Furthermore, hemoglobin synthesis is altered, which leads to anemia and decreased oxygen delivery to tissue. Problems arise when there is too little or too much iron. This review explores the role of the liver in iron physiology, iron overload and discusses the most common causes of primary and secondary hepatic iron overload.
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Shrive, N. G., T. C. Lam, E. Damson, and C. B. Frank. "A New Method of Measuring the Cross-Sectional Area of Connective Tissue Structures." Journal of Biomechanical Engineering 110, no. 2 (May 1, 1988): 104–9. http://dx.doi.org/10.1115/1.3108413.
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There appears to be no generally accepted method of measuring in-situ the cross-sectional area of connective tissues, particularly small ones, before mechanical testing. An instrument has therefore been devised to measure the cross-sectional area of one such tissue, the rabbit medial collateral ligament, directly and nondestructively. However, the methodology is general and could be applied to other tissues with appropriate changes in detail. The concept employed in the instrument is to measure the thickness of the tissue as a function of position along the width of the tissue. The plot obtained of thickness versus width position is integrated to provide the cross-sectional area. This area is accurate to within 5 percent, depending mainly on alignment of the instrument and pre-load of the ligament. Results on the mid-substance of the rabbit medial collateral ligaments are repeatable and reproducible. Values of maximum width and thickness are less variable than those obtained with a vernier caliper. The measured area is considerably less than that estimated assuming rectangular cross-section and slightly less than that estimated on the assumption of elliptical cross-section.
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Egea, Gustavo, Francesc Jiménez-Altayó, and Victoria Campuzano. "Reactive Oxygen Species and Oxidative Stress in the Pathogenesis and Progression of Genetic Diseases of the Connective Tissue." Antioxidants 9, no. 10 (October 19, 2020): 1013. http://dx.doi.org/10.3390/antiox9101013.
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Connective tissue is known to provide structural and functional “glue” properties to other tissues. It contains cellular and molecular components that are arranged in several dynamic organizations. Connective tissue is the focus of numerous genetic and nongenetic diseases. Genetic diseases of the connective tissue are minority or rare, but no less important than the nongenetic diseases. Here we review the impact of reactive oxygen species (ROS) and oxidative stress on the onset and/or progression of diseases that directly affect connective tissue and have a genetic origin. It is important to consider that ROS and oxidative stress are not synonymous, although they are often closely linked. In a normal range, ROS have a relevant physiological role, whose levels result from a fine balance between ROS producers and ROS scavenge enzymatic systems. However, pathology arises or worsens when such balance is lost, like when ROS production is abnormally and constantly high and/or when ROS scavenge (enzymatic) systems are impaired. These concepts apply to numerous diseases, and connective tissue is no exception. We have organized this review around the two basic structural molecular components of connective tissue: The ground substance and fibers (collagen and elastic fibers).
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Purslow, P. P., T. J. Wess, and D. W. Hukins. "Collagen orientation and molecular spacing during creep and stress-relaxation in soft connective tissues." Journal of Experimental Biology 201, no. 1 (January 1, 1998): 135–42. http://dx.doi.org/10.1242/jeb.201.1.135.
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Collagen fibres form cross-helical, cross-ply or quasi-random feltworks in extensible connective tissues; strain-induced reorientation of these networks gives rise to the non-linear mechanical properties of connective tissue at finite strains. Such tissues are also generally viscoelastic (i.e. display time-dependent properties). The hypothesis that time-dependent reorientation of collagen fibres is responsible for the viscoelasticity of such tissues is examined here using time-resolved X-ray diffraction measurements during stress-relaxation and creep transients applied to rat skin and bovine intramuscular connective tissue. Differences in the intensity and angular orientation of the third and fifth orders of the 67 nm meridional D-spacing of collagen molecules were shown before and after the application of loads or displacements. However, no changes in the D-spacing or angular orientation of collagen occurred during the time course of either stress-relaxation or creep in both tissues. This indicates that collagen fibre reorientation is not a primary source of their viscoelastic properties. The non-linear (strain-dependent) nature of the stress-relaxation response in these tissues suggests that relaxation processes within the collagen fibres or at the fibre-matrix interface may be responsible for their viscoelastic nature.
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Harwood, F. L., and D. Amiel. "Differential metabolic responses of periarticular ligaments and tendon to joint immobilization." Journal of Applied Physiology 72, no. 5 (May 1, 1992): 1687–91. http://dx.doi.org/10.1152/jappl.1992.72.5.1687.
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Parameters of collagen metabolic behavior were analyzed in the periarticular connective tissues, i.e., medial collateral ligament (MCL), anterior cruciate ligament (ACL), and patellar tendon (PT), of control and immobilized rabbit knees. Two periods of immobilization were studied: 9 and 12 wk. Collagen turnover and collagen cross-links were quantitatively assessed in the three tissues. The results showed that after 9 wk both synthesis and degradation were significantly increased in the MCL and ACL, whereas the PT showed lesser effects. After 12 wk all three tissues experienced significant losses of collagen mass, which resulted in tissue atrophy. The concentrations of the reducible collagen cross-links dihydroxylysinonorleucine and hydroxylysinonorleucine in the immobilized MCL and ACL were greater than their respective controls, indicating an increase in collagen synthesis, whereas concentrations of the nonreducible cross-link hydroxypyridinoline were observed to be decreased in these tissues. Of the reducible cross-links in the PT, only hydroxylysinonorleucine was found to be increased over control, whereas hydroxypyridinoline was slightly less concentrated. These results taken together have demonstrated that the ligamentous tissues are more susceptible to the effects of stress deprivation secondary to joint immobilization than the PT, and, in particular, the ACL of the three tissues studied appears to be most vulnerable.
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Aspden, R. M. "Quantitative measurements of structure and composition of connective tissues from images." Bone 13, no. 1 (1992): 103–4. http://dx.doi.org/10.1016/8756-3282(92)90392-a.
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Hurschler, Christof, Paolo P. Provenzano, and Ray Vanderby,. "Application of a Probabilistic Microstructural Model to Determine Reference Length and Toe-to-Linear Region Transition in Fibrous Connective Tissue." Journal of Biomechanical Engineering 125, no. 3 (June 1, 2003): 415–22. http://dx.doi.org/10.1115/1.1579046.
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This study shows how a probabilistic microstructural model for fibrous connective tissue behavior can be used to objectively describe soft tissue low-load behavior. More specifically, methods to determine tissue reference length and the transition from the strain-stiffening “toe-region” to the more linear region of the stress-strain curve of fibrous connective tissues are presented. According to a microstructural model for uniaxially loaded collagenous tissues, increasingly more fibers are recruited and bear load with increased tissue elongation. Fiber recruitment is represented statistically according to a Weibull probability density function (PDF). The Weibull PDF location parameter in this formulation corresponds to the stretch at which the first fibers begin to bear load and provides a convenient method of determining reference length. The toe-to-linear region transition is defined by utilizing the Weibull cumulative distribution function (CDF) which relates the fraction of loaded fibers to the tissue elongation. These techniques are illustrated using representative tendon and ligament data from the literature, and are shown to be applicable retrospectively to data from specimens that are not heavily preloaded. The reference length resulting from this technique provides an objective datum from which to calculate stretch, strain, and tangent modulus, while the Weibull CDF provides an objective parameter with which to characterize the limits of low-load behavior.
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BYRNE, MARIA. "The Mechanical Properties of the Autotomy Tissues of the Holothurian Eupentacta Quinquesemita and the Effects of Certain Physico-Chemical Agents." Journal of Experimental Biology 117, no. 1 (July 1, 1985): 69–86. http://dx.doi.org/10.1242/jeb.117.1.69.
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Evisceration in the holothurian Eupentacta quinquesemita (Selenka) results from a rapid softening of autotomy structures comprised of connective tissue. The mechanical properties of two autotomy tissues, the introvert and the retractor muscle tendon, were tested to investigate their function in the non-evisceration state and their behaviour during autotomy. The results show that these structures do not have a pre-existing mechanical weakness to account for their rapid failure during evisceration. The autotomy response was mimicked in vitro by increasing K+ concentration. The introvert exhibited viscous behaviour and the absence of Ca2+ and Mg2+ decreased introvert viscosity, whereas excess Ca2+, and low and high pH, increased viscosity. These agents may influence the mechanical properties of the autotomy structures by directly affecting connective tissue ionic interactions and may induce proteoglycan conformational changes. K+ may also exert an indirect effect through responses of cells controlling connective tissue tensility. The most likely mechanism of autotomy is through an alteration of connective tissue ionic interactions.
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Maas, Huub, and Peter A. Huijing. "Synergistic and antagonistic interactions in the rat forelimb: acute effects of coactivation." Journal of Applied Physiology 107, no. 5 (November 2009): 1453–62. http://dx.doi.org/10.1152/japplphysiol.00328.2009.
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The goals of the present study were 1) to assess effects of antagonist coactivation on mechanical interactions between synergistic muscles, and 2) to quantify the extent of epimuscular myofascial force transmission between synergistic and antagonistic muscles in the rat forelimb. Connective tissues enveloping the muscle bellies in the antebrachium were left intact. Forces exerted at the distal tendons of flexor carpi ulnaris (FCU), palmaris longus (PL), and extensor carpi ulnaris (ECU) muscles were measured at various FCU lengths for two different stimulation protocols: 1) simultaneous stimulation of ulnar/median nerve complex (exciting all wrist flexors, including synergistic FCU and PL) and radial nerve (exciting all wrist extensors, including antagonistic ECU); and 2) stimulation of the ulnar/median nerve exclusively. PL and ECU were kept at a constant length. In addition, muscle forces were measured during stimulation of one of the indicated nerves, with later addition of stimulation of the second nerve during the maintained tetanic contraction. Coactivation of antagonistic muscles increased FCU isometric forces (on average, by 10% of optimal force) and PL forces (on average, by 13% of maximal force), but mechanical interaction between FCU and PL was unchanged. Changing the length and relative position of FCU significantly affected PL (by 20%) as well as ECU forces (by 8%). In addition, distal tetanic force of FCU kept at a constant high length was determined by the order of nerve stimulation onset. These results indicate effects of myofascial pathways between synergistic and antagonistic muscles in the rat forelimb. Coactivation may enhance the stiffness of connective tissues between muscles, but the present data suggest that activation of all wrist flexors already preloaded the myofascial pathways to the greatest extent. The stimulation order effects were explained by dynamic features of muscle and connective tissues (i.e., length-history dependence and viscoelasticity).
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Que, Loretta G., Stephen P. Kantrow, Christopher P. Jenkinson, Claude A. Piantadosi, and Yuh-Chin T. Huang. "Induction of arginase isoforms in the lung during hyperoxia." American Journal of Physiology-Lung Cellular and Molecular Physiology 275, no. 1 (July 1, 1998): L96—L102. http://dx.doi.org/10.1152/ajplung.1998.275.1.l96.
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l-Arginine can be metabolized by nitric oxide (NO) synthase (NOS) to produce NO or by arginase to produce urea andl-ornithine. In the liver, arginase (the AI isoform) is a key enzyme in the urea cycle. In extrahepatic organs including the lung, the function of arginase (the AII isoform) is less clear. Because we found that lung AII was upregulated during 100% O2exposure in preliminary experiments, we sought to characterize expression of the arginase isoforms and inducible NOS and to assess the functions of arginase in hyperoxic lung injury. Male Sprague-Dawley rats were exposed to 100% O2 for 60 h. Protein expression of AI and AII and their cellular distribution were determined. The activities of arginase and NOS were also measured. Expression of arginase was correlated with that of ornithine decarboxylase, a biochemical marker for tissue repair, in a separate group of rats allowed to recover in room air for 48 h. We found by Western blot analyses that both AI and AII proteins were upregulated after 60 h of hyperoxic exposure (403 and 88% increases by densitometry, respectively) and, like ornithine decarboxylase, remained elevated during the recovery phase. Arginase activity increased by 37%. Immunostaining showed that increases in AI and AII were mainly in the peribronchial and perivascular connective tissues. NOS activity was unchanged and inducible NOS was not induced, but the level of nitrogen oxides in the lung decreased by 67%. Our study showed in vivo induction of arginase isoforms during hyperoxia. The strong expression of arginase in the connective tissues suggests that the function of pulmonary arginase may be linked to connective tissue elements, e.g., fibroblasts, during lung injury and recovery.
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Spencer, S. C., and J. W. Fabre. "Characterization of the tissue macrophage and the interstitial dendritic cell as distinct leukocytes normally resident in the connective tissue of rat heart." Journal of Experimental Medicine 171, no. 6 (June 1, 1990): 1841–51. http://dx.doi.org/10.1084/jem.171.6.1841.
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Immunohistological studies with a mouse anti-rat macrophage mAb (BMAC-5) demonstrated the presence of numerous positive cells in the interstitial connective tissues of many organs. The pattern resembled that seen with anti-MHC class II antibodies, with the striking exception that BMAC-5+ cells were rare or absent in the portal triad, the islets of Langerhans, and the kidney. Double-labeling fluorescence studies were therefore performed in rat heart using the BMAC-5 mAb in combination with rabbit antisera to pure rat class II MHC antigens and pure rat leukocyte common (CD45) antigens. The tissue macrophages in heart were identified as BMAC-5+, MHC class II-negative, leukocyte common antigen-positive cells. They could be distinguished from the BMAC-5-, MHC class II-positive, leukocyte common antigen-positive interstitial dendritic cells. Moreover, 7 d after lethal irradiation, the class II-positive interstitial dendritic cells had completely disappeared from heart, whereas the BMAC-5+ macrophages were present in undiminished numbers. These studies strongly suggest that the interstitial dendritic cell and the tissue macrophage represent two distinct populations of leukocytes within the connective tissues of antigenically secluded organs such as the heart. They have potentially important implications for the physiology of the immune system, as well as for autoimmunity and transplantation.
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Bove, G. M., and A. R. Light. "Unmyelinated nociceptors of rat paraspinal tissues." Journal of Neurophysiology 73, no. 5 (May 1, 1995): 1752–62. http://dx.doi.org/10.1152/jn.1995.73.5.1752.
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1. We made recordings from rat dorsal root filaments to study unmyelinated afferent units (conduction velocity < or = 1.5 m/s) associated with deep paraspinal tissues of the dorsal sacrum and proximal tail. Data from 57 unmyelinated units were analyzed in 47 experiments. Receptive fields were identified in intact animals and then surgically isolated using microdissection. Units were characterized using mechanical, noxious chemical, and thermal stimuli. 2. These recordings revealed innervation of the nerve sheaths and surrounding connective tissue, muscles, tendons, and tissue apposed to the undersurface of the skin. No units were found with receptive fields directly on joint capsular tissue. The receptive fields of the units were often multiple and located in more than one tissue; 31 of 57 units showed convergence from different tissues. 3. The units with receptive fields on neurovascular bundles shared sensitivities with other deep tissue units described in this and other reports. These units may have clinical importance in pain due to peripheral neuropathies. 4. The units initially responded to strong mechanical stimulation of the intact animal and often to noxious stretch of the tail. Once surgically isolated, an individual unit's threshold to mechanical stimuli appeared lower. 5. Capsaicin (0.001%-0.1%) elicited responses in 81% (17 of 21) of the units tested. Bradykinin (20 micrograms/ml) elicited responses in 45% (10 of 22) of the units tested. Noxious cold (4-10 degrees C) and hot (55 degrees C) stimulation elicited discharges from 33% (5 of 15) and 25% (5 of 20) of the units tested, respectively. 6. The unmyelinated units had similar mechanical, chemical, and thermal sensitivities. These similarities and the observed convergence only allowed separation of units by the tissue in which the ending was found, and did not allow further classification. 7. The prevalence of background discharge suggested that many units were sensitized during the experiments. 8. The sensitivities of these paraspinal units were similar to those reported for other tissues. Because of the anatomic similarity of the paraspinal tissues of the proximal tail and the lumbar spine, the conclusions of the present study can be related to the lumbar spine. These afferent units are thought to participate in nociception from the deep paraspinal tissues.
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Li, Hongyi, Chongqing Yang, Kuiyuan Lu, Liyang Zhang, Jiefu Yang, Fang Wang, Dongge Liu, et al. "A long-distance fluid transport pathway within fibrous connective tissues in patients with ankle edema." Clinical Hemorheology and Microcirculation 63, no. 4 (October 5, 2016): 411–21. http://dx.doi.org/10.3233/ch-162057.
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Eisenberg, S. R., and A. J. Grodzinsky. "The Kinetics of Chemically Induced Nonequilibrium Swelling of Articular Cartilage and Corneal Stroma." Journal of Biomechanical Engineering 109, no. 1 (February 1, 1987): 79–89. http://dx.doi.org/10.1115/1.3138647.
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An electromechanical model for charged, hydrated tissues is developed to predict the kinetics of changes in swelling and isometric compressive stress induced by changes in bath salt concentration. The model focuses on ionic transport as the rate limiting step in chemically modulating electrical interactions between the charged macromolecules of the extracellular matrix. The swelling response to such changes in local interaction forces is determined by the relative rates of chemical diffusion and fluid redistribution in the tissue sample. We have tested the model by comparing the experimentally observed salt-induced stress relaxation response in bovine articular cartilage and corneal stroma to the response predicted by the model using constitutive relations for the concentration dependent material properties of the tissues reported in a related study. The qualitatively good agreement between our experimental measurements and the predictions of the model supports the physical basis of the model and demonstrates the model’s ability to discriminate between the two soft connective tissues that were examined.
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EYLERS, JOHN P., and ALAN R. GREENBERG. "SWELLING BEHAVIOUR OF THE CATCH CONNECTIVE TISSUE IN HOLOTHURIAN BODY WALL." Journal of Experimental Biology 143, no. 1 (May 1, 1989): 71–85. http://dx.doi.org/10.1242/jeb.143.1.71.
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Swelling tests in a series of isotonic and isoionic solutions of varying calcium-tosodium ratios were conducted on isolated dermal connective tissue of the holothurian Thyonella gemmata Verrill. The tissue swelled rapidly and attained a maximum volume increase of approximately 40 % when transferred from distilled water to NaCl solution; however, the volume did not change significantly in isotonic CaCl2 solution. At Ca2+/Na+ ratios ≤0.04 the tissue swelled at its maximum rate. The rate decreased with increasing calcium concentration, until at Ca2+/Na+ ≥0.40 no detectable swelling occurred. Similar results were obtained for Pentacta pygmaea Goldfuss. When tissues previously swollen in NaCl were placed in CaC2, the volume decreased significantly. Uniaxial tensile tests indicated that the elastic modulus of the tissue was much greater in Ca2+ solutions than in Na+ solutions. We hypothesize that dermal stiffness in holothurians is regulated by cation-sensitive crosslinks
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Boriek, Aladin M., Charles C. Miller, and Joseph R. Rodarte. "Muscle fiber architecture of the dog diaphragm." Journal of Applied Physiology 84, no. 1 (January 1, 1998): 318–26. http://dx.doi.org/10.1152/jappl.1998.84.1.318.
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Boriek, Aladin M., Charles C. Miller III, and Joseph R. Rodarte. Muscle fiber architecture of the dog diaphragm. J. Appl. Physiol. 84(1): 318–326, 1998.—Previous measurements of muscle thickness and length ratio of costal diaphragm insertions in the dog (A. M. Boriek and J. R. Rodarte. J. Appl. Physiol. 77: 2065–2070, 1994) suggested, but did not prove, discontinuous muscle fiber architecture. We examined diaphragmatic muscle fiber architecture using morphological and histochemical methods. In 15 mongrel dogs, transverse sections along the length of the muscle fibers were analyzed morphometrically at ×20, by using the BioQuant System IV software. We measured fiber diameters, cross-sectional fiber shapes, and cross-sectional area distributions of fibers. We also determined numbers of muscle fibers per cross-sectional area and ratio of connective tissue to muscle fibers along a course of the muscle from near the chest wall (CW) to near the central tendon (CT) for midcostal left and right hemidiaphragms, as well as ventral, middle, and dorsal regions of the left costal hemidiaphragm. In six other mongrel dogs, the macroscopic distribution of neuromuscular junctions (NMJ) on thoracic and abdominal diaphragm surfaces was determined by staining the intact diaphragmatic muscle for acetylcholinesterase activity. The average major diameter of muscle fibers was significantly smaller, and the number of fibers was significantly larger midspan between CT and CW than near the insertions. The ratio of connective tissues to muscle fibers was largest at CW compared with other regions along the length of the muscle. The diaphragm is transversely crossed by multiple scattered NMJ bands with fairly regular intervals offset in adjacent strips. Muscle fascicles traverse two to five NMJ, consistent with fibers that do not span the entire fascicle from CT to CW. These results suggest that the diaphragm has a discontinuous fiber architecture in which contractile forces may be transmitted among the muscle fibers through the connective tissue adjacent to the fibers.
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Maas, Huub, Guus C. Baan, Peter A. Huijing, Can A. Yucesoy, Bart H. F. J. M. Koopman, and Henk J. Grootenboer. "The Relative Position of EDL Muscle Affects the Length of Sarcomeres Within Muscle Fibers: Experimental Results and Finite-Element Modeling." Journal of Biomechanical Engineering 125, no. 5 (October 1, 2003): 745–53. http://dx.doi.org/10.1115/1.1615619.
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Background : Effects of extramuscular connective tissues on muscle force (experimentally measured) and lengths of sarcomeres (modeled) were investigated in rat. It was hypothesized that changes of muscle-relative position affect the distribution of lengths of sarcomeres within muscle fibers. Method of approach: The position of extensor digitorum longus muscle (EDL) relative to intact extramuscular connective tissues of the anterior crural compartment was manipulated without changing its muscle-tendon complex length. Results: Significant effects of EDL muscle relative position on proximal and distal EDL forces were found, indicating changes of extramuscular myofascial force transmission. EDL isometric force exerted at its proximal and distal tendons differed significantly. Finite-element modeling showed that the distribution of lengths of sarcomeres is altered by changes of muscle-relative position. Conclusions: It is concluded that forces exerted on a muscle via extramuscular myofascial pathways augment distributions of lengths of sarcomeres within that muscle.
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Uchiyama, E., K. Yamakoshi, and T. Sasaki. "Measurement of Mechanical Characteristics of Tibial Periosteum and Evaluation of Local Differences." Journal of Biomechanical Engineering 120, no. 1 (February 1, 1998): 85–91. http://dx.doi.org/10.1115/1.2834311.
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Stress–strain relationships of bovine tibial periosteum, harvested from anterior, medial, lateral, and posterior aspects of tibia, were successfully measured using a newly developed experimental system. Results showed a curvilinear stress–strain pattern having three regions, i.e., toe, almost linear, and rupture regions, which resembled those of biological soft tissues like ligaments, skin, etc. Tensile moduli in the toe region (Ee) and in the linear region (Ec) were obtained by linear regressional analyses. These values and the tensile strength (σt) showed clear local differences. The values of Ee, Ec, and σt, in the longitudinal direction in the metaphyseal regions where ligaments or connective tissues attach were approximately two times larger than those in the diaphysis, where muscles or connective tissues attach. However, these properties in the metaphyseal and diaphyseal regions with muscle attachments were almost the same. In the transverse direction, these properties in the anterior proximal metaphysis were approximately two times larger than those in the diaphysis and in the distal metaphysis. In the other regions, these properties appeared not to be significantly different. These results clearly demonstrate that the mechanical properties of periosteum are strongly influenced by the ligament and muscle attachments.
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Ae, Takako, Takashi Ohno, Youichiro Hattori, Tatsunori Suzuki, Kanako Hosono, Tsutomu Minamino, Takehito Sato, et al. "Role of microsomal prostaglandin E synthase-1 in the facilitation of angiogenesis and the healing of gastric ulcers." American Journal of Physiology-Gastrointestinal and Liver Physiology 299, no. 5 (November 2010): G1139—G1146. http://dx.doi.org/10.1152/ajpgi.00013.2010.
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The importance of prostaglandin E2 in various pathophysiological events emphasizes the necessity of understanding the role of PGE synthases (PGESs) in vivo. However, there has been no report on the functional relevance of microsomal PGES-1 (mPGES-1) to the physiological healing processes of gastric ulcers, or to angiogenesis, which is indispensable to the healing processes. In this report, we tested whether mPGES-1 plays a role in the healing of gastric ulcers and in the enhancement of angiogenesis using mPGES-1 knockout mice (mPGES-1 KO mice) and their wild-type (WT) counterparts. Gastric ulcers were induced by the serosal application of 100% acetic acid, and the areas of the ulcers were measured thereafter. mPGES-1 together with cyclooxygenase-2 were induced in the granulation tissues compared with normal stomach tissues. The healing of acetic acid-induced ulcers was significantly delayed in mPGES-1 KO mice compared with WT. This was accompanied with reduced angiogenesis in ulcer granulation tissues, as estimated by CD31 mRNA levels determined by real-time PCR and the microvessel density in granulation tissues. The mRNA levels of proangiogenic growth factors, such as transforming growth factor-β, basic fibroblast growth factor, and connective tissue growth factor in ulcer granulation tissues determined were reduced in mPGES-1 KO mice compared with WT. The present results suggest that mPGES-1 enhances the ulcer-healing processes and the angiogenesis indispensable to ulcer healing, and that a selective mPGES-1 inhibitor should be used with care in patients with gastric ulcers.
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Ookawara, Tomomi, Nobuo Imazeki, Osamu Matsubara, Takako Kizaki, Shuji Oh-Ishi, Chitose Nakao, Yuzo Sato, and Hideki Ohno. "Tissue distribution of immunoreactive mouse extracellular superoxide dismutase." American Journal of Physiology-Cell Physiology 275, no. 3 (September 1, 1998): C840—C847. http://dx.doi.org/10.1152/ajpcell.1998.275.3.c840.
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Protein content and mRNA expression of extracellular superoxide dismutase (EC-SOD) were investigated in 16 mouse tissues. We developed a double-antibody sandwich ELISA using the affinity-purified IgG against native mouse EC-SOD. EC-SOD could be detected in all of the tissues examined (lung, kidney, testis, brown fat, liver, adrenal gland, pancreas, colon, white fat, thymus, stomach, spleen, heart, skeletal muscle, ileum, and brain, in decreasing order of content measured as μg/g wet tissue). Lung showed a markedly higher value of EC-SOD than other tissues. Interestingly, white fat had a high content of EC-SOD in terms of micrograms per milligram protein, which corresponded to that of lung. Kidney showed the strongest expression of EC-SOD mRNA. Relatively strong expression of the mRNA was observed in lung, white fat, adrenal gland, brown fat, and testis. Heart and brain showed only weak signals, and no such expression could be detected in either digestive organs or skeletal muscle. Immunohistochemically, EC-SOD was localized mainly to connective tissues and vascular walls in the tissues examined. Deep staining in the cytosol was observed in the cortical tubular cells of kidney. These results suggest that EC-SOD is distributed systemically in mice and that the physiological importance of this enzyme may be a compensatory adaptation to oxidative stress, particularly in lung and kidney.
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Lodhi, K. M., H. Sakaguchi, S. Hirose, S. Shibabe, and H. Hagiwara. "Perichondrial localization of ETA receptor in rat tracheal and xiphoid cartilage and in fetal rat epiphysis." American Journal of Physiology-Cell Physiology 268, no. 2 (February 1, 1995): C496—C502. http://dx.doi.org/10.1152/ajpcell.1995.268.2.c496.
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Autoradiographic studies using 125I-labeled endothelin-1 (ET-1) on sections of rat cartilage tissues, including the trachea, xiphisternum, and fetal rat epiphysis, revealed dense localization of endothelin receptors in the perichondrium. In contrast, the binding of ET-1 was not detected in the chondrocytes, cartilage matrix, and other connective tissues of the cartilage tissues tested. The perichondrial binding of 125I-ET-1 was completely abolished with BQ-123 [an endothelin receptor subtype A (ETA) antagonist] but not with BQ-3020 (an ETB agonist), and we demonstrated the perichondrial localization of ETA receptors. [3H]thymidine incorporation in vitro was significantly increased in rat xiphoid cartilage tissues exposed to ET-1. These findings suggest that the ET-1/ETA receptor system plays an important role in regulating cartilage metabolism and endochondral bone formation.
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Sivakumar, Pitchumani, Lonchin Suguna, and Gowri Chandrakasan. "Molecular species of collagen in the intramuscular connective tissues of the marine crab, Scylla serrata." Comparative Biochemistry and Physiology Part B: Biochemistry and Molecular Biology 125, no. 4 (April 2000): 555–62. http://dx.doi.org/10.1016/s0305-0491(00)00167-x.
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Lekic, P. C., N. Pender, and C. A. G. McCulloch. "Is Fibroblast Heterogeneity Relevant To the Health, Diseases, and Treatments of Periodontal Tissues?" Critical Reviews in Oral Biology & Medicine 8, no. 3 (July 1997): 253–68. http://dx.doi.org/10.1177/10454411970080030201.
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There are wide variations of gene expression and strikingly different responses to extracellular signals among different fibroblast populations. This has prompted a large number of in vitro studies which suggest that fibroblasts are not homogeneous but instead comprise multiple subpopulations with extensive site-to-site and intra-site variations. Conceivably, either fibroblasts are not all created equal, or, alternatively, discrete subpopulations may emerge in development, inflammatory lesions, or wound healing. While the heterogeneous nature of cultured fibroblasts has been known for some time, are these variations relevant to our understanding of the biology of oral tissues, their involvement in disease, and their response to therapy? Since fibroblasts are the predominant cell type in soft connective tissue matrices, the regulation of their proliferative, synthetic, and degradative behavior is likely to be important in tissue physiology and pathology. In this review, we use the current literature to assess whether fibroblast subpopulations really make a difference in the health and disease of periodontal tissues. We address the following questions: ( 1 ) Is fibroblast heterogeneity a real in vivo phenomenon? (2) How can we advance our knowledge of phenotypic variations and the regulation of fibroblast differentiation? (3) Could a knowledge of fibroblast heterogeneity have an impact on the development of new approaches to pathogenesis and the treatment of periodontal tissues?
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Humphrey, J. D. "Remodeling of a Collagenous Tissue at Fixed Lengths." Journal of Biomechanical Engineering 121, no. 6 (December 1, 1999): 591–97. http://dx.doi.org/10.1115/1.2800858.
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Mature tissues can often adapt to changes in their chemical, mechanical, or thermal environment. For example, in response to sustained increases or decreases in mechanical loads, some tissues grow and remodel so as to restore the stress or strain to its homeostatic state. Whereas most previous work addresses gross descriptors of tissue growth, this paper introduces a possible cell-mediated mechanism by which remodeling may occur in a soft connective tissue—that the kinetics of collagen deposition and degradation is similar regardless of the configuration of the body at which it occurs. The proposed theoretical framework applies to three-dimensional settings, but it is illustrated by focusing on the remodeling of a uniaxial collagenous tissue that is maintained at a fixed length for an extended period. It is shown that qualitative features expected of such remodeling (e.g., an increased compliance and increased stress-free length when remodeling occurs at an extended length) are easily realized. Growth and remodeling are complex phenomena, however, and are likely accomplished via multiple complementary mechanisms. There is a need, therefore, to identify other candidate mechanisms and, of course, to collect experimental data suitable for testing and refining the possible theories.
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Doehring, Todd C., Alan D. Freed, Evelyn O. Carew, and Ivan Vesely. "Fractional Order Viscoelasticity of the Aortic Valve Cusp: An Alternative to Quasilinear Viscoelasticity." Journal of Biomechanical Engineering 127, no. 4 (January 21, 2005): 700–708. http://dx.doi.org/10.1115/1.1933900.
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Background: Quasilinear viscoelasticity (QLV) theory has been widely and successfully used to describe the time-dependent response of connective tissues. Difficulties remain, however, particularly in material parameter estimation and sensitivities. In this study, we introduce a new alternative: the fractional order viscoelasticity (FOV) theory, which uses a fractional order integral to describe the relaxation response. FOV implies a fractal-like tissue structure, reflecting the hierarchical arrangement of collagenous tissues. Method of Approach: A one-dimensional (1-D) FOV reduced relaxation function was developed, replacing the QLV “box-spectrum” function with a fractional relaxation function. A direct-fit, global optimization method was used to estimate material parameters from stress relaxation tests on aortic valve tissue. Results: We found that for the aortic heart valve, FOV had similar accuracy and better parameter sensitivity than QLV, particularly for the long time constant (τ2). The mean (n=5) fractional order was 0.29, indicating that the viscoelastic response of the tissue was strongly fractal-like. Results summary: mean QLV parameters were C=0.079, τ1=0.004, τ2=76, and mean FOV parameters were β=0.29, τ=0.076, and ρ=1.84. Conclusions: FOV can provide valuable new insights into tissue viscoelastic behavior. Determining the fractional order can provide a new and sensitive quantitative measure for tissue comparison.
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Niklason, Laura E., and Jeffrey H. Lawson. "Bioengineered human blood vessels." Science 370, no. 6513 (October 8, 2020): eaaw8682. http://dx.doi.org/10.1126/science.aaw8682.
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Since the advent of the vascular anastomosis by Alexis Carrel in the early 20th century, the repair and replacement of blood vessels have been key to treating acute injuries, as well as chronic atherosclerotic disease. Arteries serve diverse mechanical and biological functions, such as conducting blood to tissues, interacting with the coagulation system, and modulating resistance to blood flow. Early approaches for arterial replacement used artificial materials, which were supplanted by polymer fabrics in recent decades. With recent advances in the engineering of connective tissues, including arteries, we are on the cusp of seeing engineered human arteries become mainstays of surgical therapy for vascular disease. Progress in our understanding of physiology, cell biology, and biomanufacturing over the past several decades has made these advances possible.
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Ault, H. K., and A. H. Hoffman. "A Composite Micromechanical Model for Connective Tissues: Part II—Application to Rat Tail Tendon and Joint Capsule." Journal of Biomechanical Engineering 114, no. 1 (February 1, 1992): 142–46. http://dx.doi.org/10.1115/1.2895438.
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A micromechanical model of fibrous soft tissue has been developed which predicts upper and lower bounds on mechanical properties based on the structure and properties of tissue components by Ault and Hoffman [3, 4]. In this paper, two types of biological tissue are modeled and the results compared to experimental test data. The highly organized structure of rat tail tendon is modeled using the upper bound aggregation rule which predicts uniform strain behavior in the composite material. This model fits the experimental data and results in a correlation coefficient of 0.98. Applied to cat knee joint capsule, the lower bound aggregation rule of the model correlates with the data and predicts uniform stress within this more loosely organized tissue structure. These studies show that the nature of the interactions between the components in tissue differs depending upon its structure and that the biomechanical model is capable of analyzing such differences in structure.
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Chen, Ling, Jun Tang, Yixiao Feng, Shuman Li, Qin Xiang, Xiaoqian He, Guosheng Ren, Weiyan Peng, and Tingxiu Xiang. "ADAMTS9 is Silenced by Epigenetic Disruption in Colorectal Cancer and Inhibits Cell Growth and Metastasis by Regulating Akt/p53 Signaling." Cellular Physiology and Biochemistry 44, no. 4 (2017): 1370–80. http://dx.doi.org/10.1159/000485534.
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Background/Aims: ADAMTS (disintegrin-like and metalloproteinase with thrombospondin motifs) proteins are extracellular zinc metalloproteinases that play an important role in extracellular matrix assembly and degradation, connective tissue structuring, angiogenesis, and cell migration. Multiple studies suggest that ADAMTS proteins (e.g. ADAMTS9) can act as tumor suppressors. In gastric, esophageal, and nasopharyngeal carcinomas ADAMTS9 is frequently down-regulated by promoter methylation. Whether ADAMTS9 can function as a tumor suppressor gene (TSG) in colorectal cancer is still unclear. Methods: We performed immunohistochemistry, RT-PCR, and qRT-PCR, to examine the expression of ADAMTS9 in colorectal cancer cell lines and primary colorectal cancer tissues. Methylation-specific PCR was also carried out to investigate the promoter methylation status of ADAMTS9. We also explored the functions of ADAMTS9 in colorectal cancer cell lines through in vitro experiments. Results: ADAMTS9 expression was down-requlated or silenced in 83.3% (5/6) of colorectal cancer cell lines, and frequently repressed in 65.6% (21/32) of colorectal cancer tissues. Down-regulation of ADAMTS9 was partially due to promoter methylation. Exogenous expression of ADAMTS9 in colorectal cancer cell lines inhibited cell proliferation and migration through the regulation of cell cycle and apoptosis. In addition, ADAMTS9 prevented the activation of Akt, and its downstream targets in colorectal cancer cell lines. Conclusion: Our findings suggest ADAMTS9 is a TSG in colorectal cancer.
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Chen, Liyang, Chaoyin Jiang, Shashi Ranjan Tiwari, Amrit Shrestha, Pengcheng Xu, Wenqing Liang, Yeqing Sun, Shisheng He, and Biao Cheng. "TGIF1 Gene Silencing in Tendon-Derived Stem Cells Improves the Tendon-to-Bone Insertion Site Regeneration." Cellular Physiology and Biochemistry 37, no. 6 (2015): 2101–14. http://dx.doi.org/10.1159/000438568.
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Background/Aims: The slow healing process of tendon-to-bone junctions can be accelerated via implanted tendon-derived stem cells (TDSCs) with silenced transforming growth interacting factor 1 (TGIF1) gene. Tendon-to-bone insertion site is the special form of connective tissues derivatives of common connective progenitors, where TGF-β plays bidirectional effects (chondrogenic or fibrogenic) through different signaling pathways at different stages. A recent study revealed that TGF-β directly induces the chondrogenic gene Sox9. However, TGIF1 represses the expression of the cartilage master Sox9 gene and changes its expression rate against the fibrogenesis gene Scleraxis (Scx). Methods: TGIF1 siRNA was transduced or TGIF1 was over-expressed in tendon-derived stem cells. Following suprapinatus tendon repair, rats were either treated with transduced TDSCs or nontransduced TDSCs. Histologic examination and Western blot were performed in both groups. Results: In this study, the silencing of TGIF1 significantly upregulated the chondrogenic genes and markers. Similarly, TGIF1 inhibited TDSC differentiation into cartilage via interactions with TGF-β-activated Smad2 and suppressed the phosphorylation of Smad2. The area of fibrocartilage at the tendon-bone interface was significantly increased in the TGIF1 (-) group compared with the control and TGIF1-overexpressing groups in the early stages of the animal model. The interface between the tendon and bone showed a increase of new bone and fibrocartilage in the TGIF1 (-) group at 4 weeks. Fibrovascular scar tissue was observed in the TGIF1-overexpressing group and the fibrin glue only group. Low levels of fibrocartilage and fibrovascular scar tissue were found in the TDSCs group. Conclusion: Collectively, this study shows that the tendon-derived stem cell modified with TGIF1 gene silencing has promising effects on tendon-to-bone healing which can be further explored as a therapeutic tool in regenerative medicine.
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Zhu, Yin, Sultan Almuntashiri, Yohan Han, Xiaoyun Wang, Payaningal Somanath, and Duo Zhang. "The Roles of CCN1/CYR61 in Pulmonary Diseases." International Journal of Molecular Sciences 21, no. 21 (October 22, 2020): 7810. http://dx.doi.org/10.3390/ijms21217810.
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CCN1 (cysteine-rich 61, connective tissue growth factor, and nephroblastoma-1), previously named CYR61 (cysteine-rich angiogenic inducer 61) belongs to the CCN family of matricellular proteins. CCN1 plays critical roles in the regulation of proliferation, differentiation, apoptosis, angiogenesis, and fibrosis. Recent studies have extensively characterized the important physiological and pathological roles of CCN1 in various tissues and organs. In this review, we summarize both basic and clinical aspects of CCN1 in pulmonary diseases, including acute lung injury (ALI), chronic obstructive pulmonary disease (COPD), lung fibrosis, pulmonary arterial hypertension (PAH), lung infection, and lung cancer. We also emphasize the important challenges for future investigations to better understand the CCN1 and its role in physiology and pathology, as well as the questions that need to be addressed for the therapeutic development of CCN1 antagonists in various lung diseases.
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Rebolledo, Daniela L., María José Acuña, and Enrique Brandan. "Role of Matricellular CCN Proteins in Skeletal Muscle: Focus on CCN2/CTGF and Its Regulation by Vasoactive Peptides." International Journal of Molecular Sciences 22, no. 10 (May 15, 2021): 5234. http://dx.doi.org/10.3390/ijms22105234.
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The Cellular Communication Network (CCN) family of matricellular proteins comprises six proteins that share conserved structural features and play numerous biological roles. These proteins can interact with several receptors or soluble proteins, regulating cell signaling pathways in various tissues under physiological and pathological conditions. In the skeletal muscle of mammals, most of the six CCN family members are expressed during embryonic development or in adulthood. Their roles during the adult stage are related to the regulation of muscle mass and regeneration, maintaining vascularization, and the modulation of skeletal muscle fibrosis. This work reviews the CCNs proteins’ role in skeletal muscle physiology and disease, focusing on skeletal muscle fibrosis and its regulation by Connective Tissue Growth factor (CCN2/CTGF). Furthermore, we review evidence on the modulation of fibrosis and CCN2/CTGF by the renin-angiotensin system and the kallikrein-kinin system of vasoactive peptides.
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BYRNE, MARIA. "Induction of Evisceration in the Holothurian Eupentacta Quinquesemita and Evidence for the Existence of an Endogenous Evisceration Factor." Journal of Experimental Biology 120, no. 1 (January 1, 1986): 25–39. http://dx.doi.org/10.1242/jeb.120.1.25.
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The stimuli provoking evisceration of Eupentacta quinquesemita (Selenka) and autotomy of isolated pharyngeal retractor muscle (PRM) tendons were investigated. Tendon autotomy is a two-part response involving PRM contraction and breakdown of tendon connective tissue. An evisceration factor (EF) was detected in coelomic fluid expelled during evisceration. EF was isolated in tissue extracts and the haemal system and peritoneum were sources of EF activity. Autotomy and evisceration were induced by electrical stimulation, K+ and EF, and the effect of these agents was inhibited by anaesthetics. The acetylcholine antagonist tubocurarine chloride elicited evisceration, suggesting that evisceration may involve inhibition of cholinergic transmission. Evisceration and autotomy appear to be neurally controlled and the presence of an endogenous EF suggests neurosecretory or hormonal activity. Cells involved in evisceration may be located at a distance from the autotomy tissues and effect connective tissue breakdown through the medium of the coelomic fluid. Hypothetical sequences of events and possible roles for EF are presented.
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Aukland, K., and R. K. Reed. "Interstitial-lymphatic mechanisms in the control of extracellular fluid volume." Physiological Reviews 73, no. 1 (January 1, 1993): 1–78. http://dx.doi.org/10.1152/physrev.1993.73.1.1.
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While the study of the physiochemical composition and structure of the interstitium on a molecular level is a large and important field in itself, the present review centered mainly on the functional consequences for the control of extracellular fluid volume. As pointed out in section I, a biological monitoring system for the total extracellular volume seems very unlikely because a major part of that volume is made up of multiple, separate, and functionally heterogeneous interstitial compartments. Even less likely is a selective volume control of each of these compartments by the nervous system. Instead, as shown by many studies cited in this review, a local autoregulation of interstitial volume is provided by automatic adjustment of the transcapillary Starling forces and lymph flow. Local vascular control of capillary pressure and surface area, of special importance in orthostasis, has been discussed in several recent reviews and was mentioned only briefly in this article. The gel-like consistency of the interstitium is attributed to glycosaminoglycans, in soft connective tissues mainly hyaluronan. However, the concept of a gel phase and a free fluid phase now seems to be replaced by the quantitatively more well-defined distribution spaces for glycosaminoglycans and plasma protein, apparently in osmotic equilibrium with each other. The protein-excluded space, determined mainly by the content of glycosaminoglycans and collagen, has been measured in vivo in many tissues, and the effect of exclusion on the oncotic buffering has been clarified. The effect of protein charge on its excluded volume and on interstitial hydraulic conductivity has been studied only in lungs and is only partly clarified. Of unknown functional importance is also the recent finding of a free interstitial hyaluronan pool with relatively rapid removal by lymph. The postulated preferential channels from capillaries to lymphatics have received little direct support. Thus the variation of plasma-to-lymph passage times for proteins may probably be ascribed to heterogeneity with respect to path length, linear velocity, and distribution volumes. Techniques for measuring interstitial fluid pressure have been refined and reevaluated, approaching some concensus on slightly negative control pressures in soft connective tissues (0 to -4 mmHg), zero, or slightly positive pressure in other tissues. Interstitial pressure-volume curves have been recorded in several tissues, and progress has been made in clarifying the dependency of interstitial compliance on glycosaminoglycan-osmotic pressure, collagen, and microfibrils.(ABSTRACT TRUNCATED AT 400 WORDS)
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Fredberg, J. J., and D. Stamenovic. "On the imperfect elasticity of lung tissue." Journal of Applied Physiology 67, no. 6 (December 1, 1989): 2408–19. http://dx.doi.org/10.1152/jappl.1989.67.6.2408.
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This paper deals with a unifying hypothesis addressed at lung tissue resistance and its responses to neurohumoral and biophysical stimuli. The hypothesis holds that dissipative and elastic processes within lung tissue are coupled at the level of the stress-bearing element. Such a description leads naturally to consideration of a readily measured attribute of organ-level dissipative behavior called lung tissue hysteresivity, eta. On preliminary analysis this attribute is found to be nearly frequency independent and numerically conserved across species. To the degree that the numerical value of eta might be conserved during an intervention in which tissue dynamic elastance changes, such behavior would be consistent with the notion that elastic energy storage and dissipative energy loss reside within the very same stress-bearing element and, moreover, that those processes within the stress-bearing element bear an approximately fixed relationship. Tissue hysteresivity is closely related to the parameter K used by Bachofen and Hildebrandt (J. Appl. Physiol. 30: 493-497, 1971) to describe energy dissipation per cycle, and both lend themselves directly to interpretation based on processes ongoing at the levels of microstructure and molecule. Intraparenchymal connective tissues, surface film, and contractile elements appear to submit individually to this description and, in doing so, yield respective hysteresivities that are relatively well matched; this suggests that such hysteretic matching may be a necessary condition for synchronous expansion of the alveolar duct. The overriding simplicity with which this description organizes diverse observations implies that it may capture some unifying attribute of underlying mechanism.
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Kwan, M. K., S. A. Hacker, S. L. Y. Woo, and J. S. Wayne. "The Effect of Storage on the Biomechanical Behavior of Articular Cartilage—A Large Strain Study." Journal of Biomechanical Engineering 114, no. 1 (February 1, 1992): 149–53. http://dx.doi.org/10.1115/1.2895440.
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The transplantation of stored shell osteochondral allografts is a potentially useful alternative to total joint replacements for the treatment of joint ailments. The maintenance of normal cartilage properties of the osteochondral allografts during storage is important for the allograft to function properly and survive in the host joint. Since articular cartilage is normally under large physiological stresses, this study was conducted to investigate the biomechanical behavior under large strain conditions of cartilage tissue stored for various time periods (i.e., 3, 7, 28, and 60 days) in tissue culture media. A biphasic large strain theory developed for soft hydrated connective tissues was used to describe and determine the biomechanical properties of the stored cartilage. It was found that articular cartilage stored for up to 60 days maintained the ability to sustain large compressive strains of up to 40 percent or more, like normal articular cartilage. Moreover, the equilibrium stress-strain behavior and compressive modulus of the stored articular cartilage were unchanged after up to 60 days of storage.
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Ishida, K., P. D. Pare, J. Hards, and R. R. Schellenberg. "Mechanical properties of human bronchial smooth muscle in vitro." Journal of Applied Physiology 73, no. 4 (October 1, 1992): 1481–85. http://dx.doi.org/10.1152/jappl.1992.73.4.1481.
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The in vitro mechanical properties of smooth muscle strips from 10 human main stem bronchi obtained immediately after pneumonectomy were evaluated. Maximal active isometric and isotonic responses were obtained at varying lengths by use of electrical field stimulation (EFS). At the length (Lmax) producing maximal force (Pmax), resting tension was very high (60.0 +/- 8.8% Pmax). Maximal fractional muscle shortening was 25.0 +/- 9.0% at a length of 75% Lmax, whereas less shortening occurred at Lmax (12.2 +/- 2.7%). The addition of increasing elastic loads produced an exponential decrease in the shortening and velocity of shortening but increased tension generation of muscle strips stimulated by EFS. Morphometric analysis revealed that muscle accounted for 8.7 +/- 1.5% of the total cross-sectional tissue area. Evaluation of two human tracheal smooth muscle preparations revealed mechanics similar to the bronchial preparations. Passive tension at Lmax was 10-fold greater and maximal active shortening was threefold less than that previously demonstrated for porcine trachealis by us of the same apparatus. We attribute the limited shortening of human bronchial and tracheal smooth muscle to the larger load presumably provided by a connective tissue parallel elastic component within the evaluated tissues, which must be overcome for shortening to occur. We suggest that a decrease in airway wall elastance could increase smooth muscle shortening, leading to excessive responses to contractile agonists, as seen in airway hyperresponsiveness.
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Lutsenko, Svetlana, Natalie L. Barnes, Mee Y. Bartee, and Oleg Y. Dmitriev. "Function and Regulation of Human Copper-Transporting ATPases." Physiological Reviews 87, no. 3 (July 2007): 1011–46. http://dx.doi.org/10.1152/physrev.00004.2006.
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Copper-transporting ATPases (Cu-ATPases) ATP7A and ATP7B are evolutionarily conserved polytopic membrane proteins with essential roles in human physiology. The Cu-ATPases are expressed in most tissues, and their transport activity is crucial for central nervous system development, liver function, connective tissue formation, and many other physiological processes. The loss of ATP7A or ATP7B function is associated with severe metabolic disorders, Menkes disease, and Wilson disease. In cells, the Cu-ATPases maintain intracellular copper concentration by transporting copper from the cytosol across cellular membranes. They also contribute to protein biosynthesis by delivering copper into the lumen of the secretory pathway where metal ion is incorporated into copper-dependent enzymes. The biosynthetic and homeostatic functions of Cu-ATPases are performed in different cell compartments; targeting to these compartments and the functional activity of Cu-ATPase are both regulated by copper. In recent years, significant progress has been made in understanding the structure, function, and regulation of these essential transporters. These studies raised many new questions related to specific physiological roles of Cu-ATPases in various tissues and complex mechanisms that control the Cu-ATPase function. This review summarizes current data on the structural organization and functional properties of ATP7A and ATP7B as well as their localization and functions in various tissues, and discusses the current models of regulated trafficking of human Cu-ATPases.
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Sharkey, John. "Fascia and living tensegrity considerations in: lower extremity and pelvic entrapment neuropathies." International Journal of Anatomy and Research 9, no. 1.2 (February 20, 2021): 7881–85. http://dx.doi.org/10.16965/ijar.2020.254.
Full textAbstract:
Peripheral neuropathies can have a plethora of origins including physical insults resulting from connective tissue compression and entrapment. Observational investigations, using biotensegrity focused dissections, have identified site-specific fascial structures that are hypothesised to afford integrity to neurovascular structures by providing appropriate tension and compression. These myofascial structures act as site-specific fascia tuning pegs. While these ‘tuning pegs’ are capable of having a whole body impact, this paper will look specifically at the local influences on pelvis and lower limb. The analogy of a fascia ‘tuning peg’, similar to the tuning peg of a string instrument, is adopted to help explain this unfamiliar concept. An ‘out of tune’ fascial system would lead to hypertonic and inhibited tissues, dissonant notes, one could say. Hypertonic tissues increase tensional forces acting within local and global networks leading to inappropriate densification of fascial structures, fibrosis and neurovascular fascial adhesions. Inhibited tissues, unable to generate sufficient force to ensure appropriate fascial integrity, lead to excessive compression on neurovascular structures like a dissonant note striking a wrong cord. Site-specific fascia tuning pegs provide appropriate frequency and note specific tension and compression ensuring combined forces operate in an omnidirectional manner resulting in pain free physiology, neurology and motion. The role of muscles in metabolism, physiology, heat production and motion is well described within the scientific literature. Less understood is the local role of myofascial structures providing mechanotransductive forces resulting in fascial expansive responses ensuring appropriate gliding and decompression of neurovascular structures. It is proposed that failure of site-specific fascia tuning pegs results in excessive compression, friction, inflammation, pathology, pain and changes in sensations. KEY WORDS: Biotensegrity, Fascia, Site specific fascia tuning pegs, Tensegrity, Neuropathy, Dynamic ischemia.
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Oldmixon, E. H., J. P. Butler, and F. G. Hoppin. "Dihedral angles between alveolar septa." Journal of Applied Physiology 64, no. 1 (January 1, 1988): 299–307. http://dx.doi.org/10.1152/jappl.1988.64.1.299.
Full textAbstract:
To determine the dihedral angle, alpha, at the characteristic three-way septal junctions of lung parenchyma, we examined photomicrographs of sections. The three angles, A, formed where three septal traces meet on section, were measured and found to range between approximately 50 and 170 degrees. Theoretical considerations predicted that the dispersion of alpha is much narrower than that of A. The mean of A and alpha is identically 120 degrees. The standard deviation of alpha was inferred from the cumulative distribution function of A. In lungs inflated to 30 cmH2O (VL30), the standard deviation of alpha was very small (approximately 2 degrees) and increased to approximately 6 degrees in lungs inflated to 0.4 VL30. These findings imply that at VL30 tensions exerted by septa are locally homogeneous (2% variation) and at lower lung volumes become less so (6% variation). At high distending pressures, tissue forces are thought to dominate interfacial forces, and therefore the local uniformity of tensions suggests a stress-responsive mechanism for forming or remodeling the connective tissues. The source of the local nonuniformity at lower volumes is unclear but could relate to differences in mechanical properties of alveolar duct and alveoli. Finally, local uniformity does not imply global uniformity.
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Hirose, Tatsuro, Koichi Nakazato, Hongsun Song, and Naokata Ishii. "TGF-β1 and TNF-α are involved in the transcription of type I collagen α2 gene in soleus muscle atrophied by mechanical unloading." Journal of Applied Physiology 104, no. 1 (January 2008): 170–77. http://dx.doi.org/10.1152/japplphysiol.00463.2006.
Full textAbstract:
The aim of this study was to examine the effect of hindlimb suspension (HS) on the expressions of COL1A2 (type I collagen α2 chain) mRNA and its regulatory factors, transforming growth factors (TGF)-β1, -β2, and -β3, phosphorylated Smad3, and tumor necrosis factor-α (TNF-α) in rat hindlimb muscles. Forty-eight male Wistar rats (age, 5 wk) were randomly assigned to HS for 1, 3, 7, and 14 days and control ( n = 6 for each). During the exposure to HS, COL1A2 mRNA expression decreased in the soleus muscle at day 3 and recovered to control level at day 7. The content of TNF-α, one of the negative regulatory factors for COL1A2, increased from day 3 until day 14. On the other hand, the contents of TGF-β1, TGF-β3, and Smad3, positive regulatory factors for COL1A2, increased at day 7. The in situ hybridization for COL1A2 and the immunohistochemistry of TGF-β1 and TNF-α revealed their expressions around nerve-related tissues, including muscle spindles and connective tissue sheath. The results indicate that the transcriptional activity of COL1A2 in the soleus muscle initially decreases in response to unloading through an increase in TNF-α production; thereafter, it returns toward normal level through the activated TGF-β/Smad pathway.