scholarly journals Macromolecule permeability of in situ and excised rodent skeletal muscle arterioles and venules

2006 ◽  
Vol 290 (1) ◽  
pp. H474-H480 ◽  
Author(s):  
Ingrid H. Sarelius ◽  
Julia M. Kuebel ◽  
Jianjie Wang ◽  
Virginia H. Huxley
Keyword(s):  
Skeletal Muscle ◽  
Acute Inflammation ◽  
Source Surface ◽  
Leukocyte Transmigration ◽  
Solute Permeability ◽  
Physiol Heart Circ ◽  
Tissue Edema ◽  
Quantitative Fluorescence ◽  
Made In

In microvessels, acute inflammation is typified by an increase in leukocyte-endothelial cell interactions, culminating in leukocyte transmigration into the tissue, and increased permeability to water and solutes, resulting in tissue edema. The goal of this study was to establish a method to quantify solute permeability ( Ps) changes in microvessels in intact predominantly blood-perfused networks in which leukocyte transmigratory behavior could be precisely described using established paradigms. We used intravital confocal microscopy to measure solute (BSA) flux across microvessel walls, hence Ps. A quantitative fluorescence approach (Huxley VH, Curry FE, and Adamson RH. Am J Physiol Heart Circ Physiol 252: H188–H197, 1987) was adapted to the imaged confocal tissue slice in which the fluorescent source volume and source surface area of the microvessel were restricted to the region of vessel that was contained within the imaged confocal tissue section. Ps measurements were made in intact cremaster muscle microvasculature of anesthetized mice and compared with measurements of Ps made in isolated rat skeletal muscle microvessels. Mouse arteriolar Ps was 9.9 ± 1.1 × 10−7 cm/s ( n = 16), which was not different from 8.4 ± 1.3 × 10−7 cm/s ( n = 6) in rat arterioles. Values in venules were significantly ( P < 0.05) higher: 44.4 ± 7.9 × 10−7 cm/s ( n = 14) in mice and 25.0 ± 3.7 × 10−7 cm/s in rats. Convective coupling was estimated to contribute <10% to the measured Ps in both microvessel types and both animal models. We conclude that this approach provides an appropriate quantification of Ps in the intact microvasculature and that arteriolar Ps, while lower than in venules, is nevertheless consistent with arterioles being a significant source of interstitial protein.

scholarly journals Leukocyte rolling and adhesion both contribute to regulation of microvascular permeability to albumin via ligation of ICAM-1

2011 ◽  
Vol 301 (4) ◽  
pp. C804-C813 ◽  
Author(s):  
Ronen Sumagin ◽  
Julia M. Kuebel ◽  
Ingrid H. Sarelius
Keyword(s):  
Leukocyte Rolling ◽  
Endothelial Monolayer ◽  
Solute Permeability ◽  
Signaling Mechanisms ◽  
Tissue Edema ◽  
Tnf Α ◽  
Activated Neutrophils ◽  
Secondary Antibodies ◽  
Blocking Antibodies

Activated neutrophils interacting with the vessel wall can alter vascular permeability to macromolecules such as albumin via release of various secretion products that induce changes in the endothelial monolayer. In the current work we used cremaster microvessels of anesthetized mice to show that, in addition to this paracrine mechanism, leukocyte ligation of endothelial ICAM-1 directly activates endothelial cell (EC) signaling, altering EC permeability to albumin [i.e., solute permeability ( Ps)]. We show that antibody cross-linking of surface ICAM-1 in intact microvessels is sufficient to increase Pseven in the absence of interacting leukocytes. Unstimulated arterioles do not support leukocyte-EC interactions, but despite this, antibody ligation of ICAM-1 in these vessels induced a twofold increase in Ps. Similarly, in venules that were depleted of interacting neutrophils, Pswas decreased to below resting levels and was restored by ligation of ICAM-1. Use of function-blocking antibodies to separately block leukocyte rolling or adhesion under unstimulated or TNF-α-activated conditions established that both rolling and adhered leukocytes contribute to Psregulation in situ. Both rolling and adhesion activated EC-dependent signaling mechanisms that increased Ps. ICAM-1 ligation with primary antibody alone or primary followed by secondary antibodies showed that regulation of Psis directly dependent on the degree of ICAM-1 clustering. Under physiological versus inflamed conditions, respectively, this ICAM-1 clustering-dependent regulation of Psswitches from PKC dependent and Src independent to Src dependent and PKC independent. This study thus identifies a new mechanism by which antiadhesion treatment may constitute a potential therapy for tissue edema.

Electron Probe Analysis of Muscle

1982 ◽  
Vol 40 ◽  
pp. 398-401
Author(s):  
A. V. Somlyo ◽  
H. Shuman ◽  
A. P. Somlyo
Keyword(s):  
Skeletal Muscle ◽  
Smooth Muscle ◽  
Sarcoplasmic Reticulum ◽  
Resting State ◽  
Binding Sites ◽  
Electron Probe ◽  
Frog Skeletal Muscle ◽  
Electron Probe Analysis ◽  
Probe Analysis

Electron probe analysis of frozen dried cryosections of frog skeletal muscle, rabbit vascular smooth muscle and of isolated, hyperpermeab1 e rabbit cardiac myocytes has been used to determine the composition of the cytoplasm and organelles in the resting state as well as during contraction. The concentration of elements within the organelles reflects the permeabilities of the organelle membranes to the cytoplasmic ions as well as binding sites. The measurements of [Ca] in the sarcoplasmic reticulum (SR) and mitochondria at rest and during contraction, have direct bearing on their role as release and/or storage sites for Ca in situ.

Interphase Quantitative Fluorescence in Situ Hybridization (IQ-FISH)

2019 ◽  
Vol 3 (1) ◽  
Author(s):  
Ivan Y. Iourov ◽  
◽  
Ilia V. Soloviev ◽  
Yuri B. Yurov ◽  
Svetlana G. Vorsanova ◽  
...  
Keyword(s):  
In Situ Hybridization ◽  
Fluorescence In Situ Hybridization ◽  
Quantitative Fluorescence

Engaging with the science and politics of biodiversity futures: a literature review

2021 ◽  
pp. 1-8
Author(s):  
Carina Wyborn ◽  
Elena Louder ◽  
Mike Harfoot ◽  
Samantha Hill
Keyword(s):  
Human Life ◽  
Global Environmental Change ◽  
Life Forms ◽  
Trade Offs ◽  
Global Environmental ◽  
Science And Politics ◽  
Science Community ◽  
Impact On Biodiversity ◽  
Made In

Summary Future global environmental change will have a significant impact on biodiversity through the intersecting forces of climate change, urbanization, human population growth, overexploitation, and pollution. This presents a fundamental challenge to conservation approaches, which seek to conserve past or current assemblages of species or ecosystems in situ. This review canvases diverse approaches to biodiversity futures, including social science scholarship on the Anthropocene and futures thinking alongside models and scenarios from the biophysical science community. It argues that charting biodiversity futures requires processes that must include broad sections of academia and the conservation community to ask what desirable futures look like, and for whom. These efforts confront political and philosophical questions about levels of acceptable loss, and how trade-offs can be made in ways that address the injustices in the distribution of costs and benefits across and within human and non-human life forms. As such, this review proposes that charting biodiversity futures is inherently normative and political. Drawing on diverse scholarship united under a banner of ‘futures thinking’ this review presents an array of methods, approaches and concepts that provide a foundation from which to consider research and decision-making that enables action in the context of contested and uncertain biodiversity futures.

scholarly journals Skeletal muscle PGC-1β signaling is sufficient to drive an endurance exercise phenotype and to counteract components of detraining in mice

2017 ◽  
Vol 312 (5) ◽  
pp. E394-E406 ◽  
Author(s):  
Samuel Lee ◽  
Teresa C. Leone ◽  
Lisa Rogosa ◽  
John Rumsey ◽  
Julio Ayala ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Exercise Training ◽  
Early Stage ◽  
Peroxisome Proliferator ◽  
Disuse Atrophy ◽  
Proof Of Concept ◽  
Peroxisome Proliferator Activated Receptor ◽  
Muscle Disuse ◽  
Training Response

Peroxisome proliferator-activated receptor-γ coactivator (PGC)-1α and -1β serve as master transcriptional regulators of muscle mitochondrial functional capacity and are capable of enhancing muscle endurance when overexpressed in mice. We sought to determine whether muscle-specific transgenic overexpression of PGC-1β affects the detraining response following endurance training. First, we established and validated a mouse exercise-training-detraining protocol. Second, using multiple physiological and gene expression end points, we found that PGC-1β overexpression in skeletal muscle of sedentary mice fully recapitulated the training response. Lastly, PGC-1β overexpression during the detraining period resulted in partial prevention of the detraining response. Specifically, an increase in the plateau at which O2 uptake (V̇o2) did not change from baseline with increasing treadmill speed [peak V̇o2 (ΔV̇o2max)] was maintained in trained mice with PGC-1β overexpression in muscle 6 wk after cessation of training. However, other detraining responses, including changes in running performance and in situ half relaxation time (a measure of contractility), were not affected by PGC-1β overexpression. We conclude that while activation of muscle PGC-1β is sufficient to drive the complete endurance phenotype in sedentary mice, it only partially prevents the detraining response following exercise training, suggesting that the process of endurance detraining involves mechanisms beyond the reversal of muscle autonomous mechanisms involved in endurance fitness. In addition, the protocol described here should be useful for assessing early-stage proof-of-concept interventions in preclinical models of muscle disuse atrophy.

The cell adhesion molecule M-cadherin is specifically expressed in developing and regenerating, but not denervated skeletal muscle

Development ◽  
1993 ◽  
Vol 117 (4) ◽  
pp. 1409-1420 ◽  
Author(s):  
R. Moore ◽  
F.S. Walsh
Keyword(s):  
Skeletal Muscle ◽  
Tissue Distribution ◽  
Cell Adhesion Molecule ◽  
Muscle Denervation ◽  
Regulatory Factor ◽  
Myogenic Regulatory Factor ◽  
Adult Skeletal Muscle ◽  
Specific Tissue ◽  
Alpha Actin

The spatiotemporal distribution of M-cadherin mRNA has been determined by in situ hybridization in the mouse embryo and in adult skeletal muscle following experimental regeneration and denervation. M-cadherin mRNA is highly tissue specific and is found only in developing skeletal muscle. In contrast, N-cadherin mRNA has a broader tissue distribution in the embryo, being found on both neural elements and skeletal and cardiac muscle. M-cadherin is expressed in the myotomes shortly after they form, along with the myogenic regulatory factor myogenin. M-cadherin is expressed in muscles derived from the myotomes and is detected in forelimb bud precursor cells at embryonic day 11.5. In the latter case M-cadherin expression appears co-ordinately with that of myogenin and cardiac alpha-actin. Shortly before birth, M-cadherin expression is down regulated. M-cadherin can, however, be re-expressed following experimental regeneration of skeletal muscle. Here M-cadherin is transiently expressed on regenerating myoblasts but not myotubes. Following muscle denervation no evidence was found for re-expression of M-cadherin under conditions where there was strong expression of the nicotinic acetylcholine receptor on myofibres. The highly specific tissue distribution and unique developmental profile distinguishes M-cadherin from other cadherins and suggests a role in cell surface events during early myogenesis.

Assignment of the human slow skeletal muscle troponin gene (TNNI1) to 1q32 by fluorescence in situ hybridisation

1993 ◽  
Vol 62 (2-3) ◽  
pp. 181-182 ◽  
Author(s):  
H.J. Eyre ◽  
P.A. Akkari ◽  
C. Meredith ◽  
S.D. Wilton ◽  
D.C. Callen ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
In Situ Hybridisation ◽  
Fluorescence In Situ Hybridisation ◽  
Slow Skeletal Muscle

An integrative, in situ approach to examining K+ flux in resting skeletal muscle

2001 ◽  
Vol 79 (12) ◽  
pp. 996-1006 ◽  
Author(s):  
Michael I Lindinger ◽  
Thomas J Hawke ◽  
Lisa Vickery ◽  
Laurie Bradford ◽  
Shonda L Lipskie
Keyword(s):  
Skeletal Muscle ◽  
Drug Effects ◽  
Potassium Transport ◽  
Mammalian Skeletal Muscle ◽  
Minimal Effect ◽  
Bovine Erythrocyte ◽  
Perfusion Medium ◽  
Sodium Potassium ◽  
Unidirectional Flux

The contributions of Na+/K+-ATPase, K+ channels, and the NaK2Cl cotransporter (NKCC) to total and unidirectional K+ flux were determined in mammalian skeletal muscle at rest. Rat hindlimbs were perfused in situ via the femoral artery with a bovine erythrocyte perfusion medium that contained either 86Rb or 42K, or both simultaneously, to determine differences in ability to trace unidirectional K+ flux in the absence and presence of K+-flux inhibitors. In most experiments, the unidirectional flux of K+ into skeletal muscle (JinK) measured using 86Rb was 8–10% lower than JinK measured using 42K. Ouabain (5 mM) was used to inhibit Na+/K+-ATPase activity, 0.06 mM bumetanide to inhibit NKCC activity, 1 mM tetracaine or 0.5 mM barium to block K+ channels, and 0.05 mM glybenclamide (GLY) to block ATP-sensitive K+ (KATP) channels. In controls, JinK remained unchanged at 0.31 ± 0.03 µmol·g–1·min–1 during 55 min of perfusion. The ouabain-sensitive Na+/K+-ATPase contributed to 50 ± 2% of basal JinK, K+ channels to 47 ± 2%, and the NKCC to 12 ± 1%. GLY had minimal effect on JinK, and both GLY and barium inhibited unidirectional efflux of K+ (JoutK) from the cell through K+ channels. Combined ouabain and tetracaine reduced JinK by 55 ± 2%, while the combination of ouabain, tetracaine, and bumetanide reduced JinK by 67 ± 2%, suggesting that other K+-flux pathways may be recruited because the combined drug effects on inhibiting JinK were not additive. The main conclusions are that the NKCC accounted for about 12% of JinK, and that KATP channels accounted for nearly all of the JoutK, in resting skeletal muscle in situ.Key words: sodium potassium chloride cotransporter, NKCC, Na+/K+-ATPase, potassium channels, potassium transport, in situ rat hindlimb.

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