Capillary growth in relation to blood flow and performance in overloaded rat skeletal muscle

Egginton, Stuart; Hudlická, O; Brown, Margaret D.; Walter, Mboto Helen; Weiss, Jacqueline B.; Bate, A.

doi:10.1152/jappl.1998.85.6.2025

Cited by 97 publications

(117 citation statements)

References 37 publications

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“…In skeletal muscle cells and osteoblast-like cells, mechanical stretch increased FGF-2 expression (7,35), but other models that generate mechanical stretch did not find an effect on FGF-2 expression in the heart, in skeletal muscle, or in mesangial cells (14,30,55). Our results are the first to demonstrate that mechanical stretch increases the expression of FGF-2 mRNA in vascular smooth muscle cells.…”

Section: Discussioncontrasting

confidence: 38%

Cyclic mechanical stretch induces VEGF and FGF-2 expression in pulmonary vascular smooth muscle cells

Quinn

Schlueter

Soifer

et al. 2002

American Journal of Physiology-Lung Cellular and Molecular Phys

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Vascular endothelial growth factor (VEGF) and basic (b) fibroblast growth factor (FGF-2/bFGF) are involved in vascular development and angiogenesis. Pulmonary artery smooth muscle cells express VEGF and FGF-2 and are subjected to mechanical forces during pulsatile blood flow. The effect of stretch on growth factor expression in these cells is not well characterized. We investigated the effect of cyclic stretch on the expression of VEGF and FGF-2 in ovine pulmonary artery smooth muscle cells. Primary confluent cells from 6-wk-old lambs were cultured on flexible silicon membranes and subjected to cyclic biaxial stretch (1 Hz; 5–25% stretch; 4–48 h). Nonstretched cells served as controls. Expression of VEGF and FGF-2 was determined by Northern blot analysis. Cyclic stretch induced expression of both VEGF and FGF-2 mRNA in a time- and amplitude-dependent manner. Maximum expression was found at 24 h and 15% stretch (VEGF: 1.8-fold; FGF-2: 1.9-fold). These results demonstrate that mechanical stretch regulates VEGF and FGF-2 gene expression, which could play a role in pulmonary vascular development or in postnatal pulmonary artery function or disease.

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Section: Discussioncontrasting

confidence: 38%

Cyclic mechanical stretch induces VEGF and FGF-2 expression in pulmonary vascular smooth muscle cells

Quinn

Schlueter

Soifer

et al. 2002

American Journal of Physiology-Lung Cellular and Molecular Phys

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“…It has long been held that shear stress on endothelial cells induced by increased blood flow as well as by active and passive stretch of muscle tissue is key to the angiogenic response (Egginton et al, 1998;Hellsten and Hoier, 2014). A pivotal role in angiogenesis is played by VEGF.…”

Section: Stressors Involved In Angiogenesismentioning

confidence: 99%

Molecular networks in skeletal muscle plasticity

Hoppeler

2016

Journal of Experimental Biology

168

117

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The skeletal muscle phenotype is subject to considerable malleability depending on use as well as internal and external cues. In humans, low-load endurance-type exercise leads to qualitative changes of muscle tissue characterized by an increase in structures supporting oxygen delivery and consumption, such as capillaries and mitochondria. High-load strength-type exercise leads to growth of muscle fibers dominated by an increase in contractile proteins. In endurance exercise, stress-induced signaling leads to transcriptional upregulation of genes, with Ca 2+ signaling and the energy status of the muscle cells sensed through AMPK being major input determinants. Several interrelated signaling pathways converge on the transcriptional co-activator PGC-1α, perceived to be the coordinator of much of the transcriptional and post-transcriptional processes. Strength training is dominated by a translational upregulation controlled by mTORC1. mTORC1 is mainly regulated by an insulin-and/or growth-factor-dependent signaling cascade as well as mechanical and nutritional cues. Muscle growth is further supported by DNA recruitment through activation and incorporation of satellite cells. In addition, there are several negative regulators of muscle mass. We currently have a good descriptive understanding of the molecular mechanisms controlling the muscle phenotype. The topology of signaling networks seems highly conserved among species, with the signaling outcome being dependent on the particular way individual species make use of the options offered by the multi-nodal networks. As a consequence, muscle structural and functional modifications can be achieved by an almost unlimited combination of inputs and downstream signaling events.

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“…At T b Ϸ37 and 25°C some animals received radiolabelled microspheres ( 113 Sn,46 Sc; DuPont NEN, Mechelen, Belgium) delivered into the left ventricle via a right carotid arterial cannula. Reference flow was obtained by sampling from one brachial artery using a precision withdrawal pump (Braun, Melsungen, Germany), and MABP was measured using a catheter in the other brachial artery (for details, see Egginton et al, 1998).…”

Section: In Vivo Cardiac Performancementioning

confidence: 99%

Cold-impaired cardiac performance in rats is only partially overcome by cold acclimation

Hui‐Kang

May

Sabharwal

et al. 2011

Journal of Experimental Biology

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SUMMARYThe consequences of acute hypothermia include impaired cardiovascular performance, ultimately leading to circulatory collapse. We examined the extent to which this results from intrinsic limitations to cardiac performance or physiological dysregulation/autonomic imbalance, and whether chronic cold exposure could ameliorate the impaired function. Wistar rats were held at a 12h:12h light:dark (L:D) photoperiod and room temperature (21°C; euthermic controls), or exposed to a simulated onset of winter in an environmental chamber by progressive acclimation to 1h:23h L:D and 4°C over 4 weeks. In vivo, acute cold exposure (core temperature, T b 25°C) resulted in hypotension (approximately -20%) due to low cardiac output (approximately -30%) accompanying a bradycardia (approximately -50%). Cold acclimation (CA) induced only partial compensation for this challenge, including increased coronary flow at T b 37°C (but not at T b 25°C), maintenance of ventricular capillarity and altered sympathovagal balance (increased low:high frequency in power spectral analysis, PSA), suggesting physiological responses alone were insufficient to maintain cardiovascular performance. However, PSA showed maintenance of cardiorespiratory coupling on acute cold exposure in both groups. Ex vivo cardiac performance revealed no change in intrinsic heart rate, but a mechanical impairment of cardiac function at low temperatures following CA. While CA involved an increased capacity for -oxidation, there was a paradoxical reduction in developed pressure as a result of adrenergic down-regulation. These data suggest that integrated plasticity is the key to cardiovascular accommodation of chronic exposure to a cold environment, but with the potential for improvement by intervention, for example with agents such as non-catecholamine inotropes. Supplementary material available online at

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Capillary growth in relation to blood flow and performance in overloaded rat skeletal muscle

Cited by 97 publications

References 37 publications

Cyclic mechanical stretch induces VEGF and FGF-2 expression in pulmonary vascular smooth muscle cells

Cyclic mechanical stretch induces VEGF and FGF-2 expression in pulmonary vascular smooth muscle cells

Molecular networks in skeletal muscle plasticity

Cold-impaired cardiac performance in rats is only partially overcome by cold acclimation

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