Potentiation of acetylcholine-induced skeletal muscle contractions in vitro by prostaglandin F2α in the lizard, Crotaphytus collaris

1984 ◽  
Vol 62 (11) ◽  
pp. 2188-2191 ◽  
Author(s):  
Louis J. Guillette Jr. ◽  
David A. Dickey
Keyword(s):  
Skeletal Muscle ◽  
Muscle Function ◽  
Striated Muscle ◽  
Prostaglandin F2α ◽  
Sexually Active ◽  
Crotaphytus Collaris ◽  
Male And Female ◽  
Percent Increase ◽  
Prostaglandin F

Acetylcholine-induced in vitro contractions of the puboischiotibialis muscle was potentiated by pretreatment with prostaglandin F2α (1.5 ng/mL). This phenomenon was exhibited by both sexually active male and female Crotaphytus collaris collaris and the degree of response was similar in both sexes. However, females exhibited a greater mean (±SE) percent increase as well as more variation than males (males, 54.6 ± 10.9%; females, 114.7 ± 61.4%). These data suggest that prostaglandin F2α plays a role in the control of striated muscle function in lizards. Moreover, prostaglandin potentiation of muscle contraction may be important during the reptilian reproductive cycle, particularly at the time of oviposition.

Characterization of a 5.4 kb cDNA fragment from the Z-line region of rabbit cardiac titin reveals phosphorylation sites for proline-directed kinases

1995 ◽  
Vol 108 (9) ◽  
pp. 3029-3037 ◽  
Author(s):  
M.G. Sebestyen ◽  
J.A. Wolff ◽  
M.L. Greaser
Keyword(s):  
Skeletal Muscle ◽  
Striated Muscle ◽  
Sequence Data ◽  
Amino Acid Level ◽  
Adult Rabbit ◽  
Cdna Clones ◽  
Protein Fragment ◽  
Cardiac Titin ◽  
Line Region

Titin is an approximately 3 MDa protein that spans from the M- to the Z-line in the sarcomeres of vertebrate striated muscle. The protein is presumably encoded by unusually large mRNAs of 70–80 kb. Although titin has been studied by several laboratories, barely more than half of the cDNA sequence (approximately 45 kb) has been published, most of it obtained from the A-band and M-line region (corresponding to the C-terminal half of the molecule). A special cDNA library was constructed using size selected total RNA from adult rabbit cardiac muscle in order to obtain sequence data from titin's unknown N-terminal region. A monoclonal antibody (T12), which binds to an epitope close to the Z-line, was used to identify initial cDNA clones. Additional overlapping clones were isolated and sequenced yielding a 5.4 kb contig. The encoded polypeptide contains 16 Type-II domains and four unique intervening segments. Polyclonal sera, raised against an expressed protein fragment encoded by the 5′ end of the contig, strongly stained the Z-line of myofibrils of different species. However, the sequence of this fragment is 83% identical at the amino acid level with the previously reported C-terminal (i.e. M-line) end of chicken embryonic skeletal muscle titin. The expressed protein fragment could be phosphorylated in vitro by embryonic skeletal muscle extract and by the purified proline-directed kinase ERK1, presumably at the xSPxR recognition sites located in the first interdomain segment.

Absence of myofibrillar creatine kinase and diaphragm isometric function during repetitive activation

1998 ◽  
Vol 84 (4) ◽  
pp. 1166-1173 ◽  
Author(s):  
John J. Labella ◽  
Monica J. Daood ◽  
A. P. Koretsky ◽  
Brian B. Roman ◽  
Gary C. Sieck ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Creatine Kinase ◽  
Muscle Function ◽  
Isometric Force ◽  
Force Generation ◽  
Fatigue Properties ◽  
Specific Force ◽  
Null Mutant ◽  
Isometric Muscle

Creatine kinase (CK) provides ATP buffering in skeletal muscle and is expressed as 1) cytosolic myofibrillar CK (M-CK) and 2) sarcomeric mitochondrial CK (ScCKmit) isoforms that differ in their subcellular localization. We compared the isometric contractile and fatigue properties of 1) control CK-sufficient (Ctl), 2) M-CK-deficient (M-CK[−/−]), and 3) combined M-CK/ScCKmit-deficient null mutant (CK[−/−]) diaphragm (Dia) to determine the effect of the absence of M-CK activity on Dia performance in vitro. Baseline contractile properties were comparable across groups except for specific force, which was ∼16% lower in CK[−/−] Dia compared with M-CK[−/−] and Ctl Dia. During repetitive activation (40 Hz, [Formula: see text] duty cycle), force declined in all three groups. This decline was significantly greater in CK[−/−] Dia compared with Ctl and M-CK[−/−] Dia. The pattern of force decline did not differ between M-CK[−/−] and Ctl Dia. We conclude that Dia isometric muscle function is not absolutely dependent on the presence of M-CK, whereas the complete absence of CK acutely impairs isometric force generation during repetitive activation.

scholarly journals Role of TRPC1 channel in skeletal muscle function

2010 ◽  
Vol 298 (1) ◽  
pp. C149-C162 ◽  
Author(s):  
Nadège Zanou ◽  
Georges Shapovalov ◽  
Magali Louis ◽  
Nicolas Tajeddine ◽  
Chiara Gallo ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Muscle Function ◽  
Transient Receptor Potential ◽  
Force Production ◽  
Receptor Potential ◽  
Cross Sectional Area ◽  
Sectional Area ◽  
Skeletal Muscle Function ◽  
Cross Sectional

Skeletal muscle contraction is reputed not to depend on extracellular Ca2+. Indeed, stricto sensu , excitation-contraction coupling does not necessitate entry of Ca2+. However, we previously observed that, during sustained activity (repeated contractions), entry of Ca2+is needed to maintain force production. In the present study, we evaluated the possible involvement of the canonical transient receptor potential (TRPC)1 ion channel in this entry of Ca2+and investigated its possible role in muscle function. Patch-clamp experiments reveal the presence of a small-conductance channel (13 pS) that is completely lost in adult fibers from TRPC1−/−mice. The influx of Ca2+through TRPC1 channels represents a minor part of the entry of Ca2+into muscle fibers at rest, and the activity of the channel is not store dependent. The lack of TRPC1 does not affect intracellular Ca2+concentration ([Ca2+]i) transients reached during a single isometric contraction. However, the involvement of TRPC1-related Ca2+entry is clearly emphasized in muscle fatigue. Indeed, muscles from TRPC1−/−mice stimulated repeatedly progressively display lower [Ca2+]itransients than those observed in TRPC1+/+fibers, and they also present an accentuated progressive loss of force. Interestingly, muscles from TRPC1−/−mice display a smaller fiber cross-sectional area, generate less force per cross-sectional area, and contain less myofibrillar proteins than their controls. They do not present other signs of myopathy. In agreement with in vitro experiments, TRPC1−/−mice present an important decrease of endurance of physical activity. We conclude that TRPC1 ion channels modulate the entry of Ca2+during repeated contractions and help muscles to maintain their force during sustained repeated contractions.

Ovarian production of progesterone and 20α-dihydroprogesterone in vitro following prostaglandin F2α induced luteolysis in the superluteinized rat

1984 ◽  
Vol 105 (2) ◽  
pp. 258-265 ◽  
Author(s):  
P. A. Torjesen ◽  
A. Aakvaag
Keyword(s):  
Adenylyl Cyclase ◽  
Prostaglandin F2α ◽  
Mitochondrial Fraction ◽  
Supernatant Fraction ◽  
Production Rates ◽  
Cyclic Monophosphate ◽  
Progesterone Production ◽  
Progesterone Secretion ◽  
Prostaglandin F

Abstract. Superluteinized rats were injected with the prostaglandin F2α (PGF2α) analogue cloprostenol to induce luteolysis. The treatment decreased progesterone production of ovarian homogenates from 8.9 ± 0.5 to 4.0 ± 0.7 nmol/ovary/10 min (mean ± sem) within 40 min. tochondrial fractions isolated from control and cloprostenol treated animals produced 4.7 ± 0.4 and 2.8 ± 0.3 nmol progesterone/ovary/10 min, respectively. Thus, the PGF2α analogue treatment significantly reduced mitochondrial progesterone production. Addition of the 15 000 × g supernatant fraction did not influence the progesterone production rates of the mitochondrial fraction. The basal progesterone secretion from quartered ovaries decreased from 1.50 ± 0.15 to 0.38 ± 0.05 nmol/ovary during the initial 15 min of incubation following cloprostenol administration. hCG and N6,O2'-dibutyryladenosine 3':5'-cyclic monophosphate (DBC) stimulated the progesterone secretion from quartered ovaries, but the response was delayed in ovaries obtained from cloprostenol treated animals. Although the response was delayed, the progesterone secretion following cloprostenol treatment was re-activated with cAMP either directly or via hCG. The increment in progesterone secretion above unstimulated controls in response to DBC was not influenced by the cloprostenol treatment while the increment caused by hCG was decreased. Our data suggest that: 1) PGF2α deactivates mitochondrial progesterone production, 2) this deactivation may be overcome by cAMP, and 3) PGF2α decreases gonadotrophin responsive adenylyl cyclase.

scholarly journals The Influence of Supplemental Dietary Linoleic Acid on Skeletal Muscle Contractile Function in a Rodent Model of Barth Syndrome

2021 ◽  
Vol 12 ◽  
Author(s):  
Mario Elkes ◽  
Martin Andonovski ◽  
Daislyn Vidal ◽  
Madison Farago ◽  
Ryan Modafferi ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Linoleic Acid ◽  
Muscle Function ◽  
Barth Syndrome ◽  
Dietary Linoleic Acid ◽  
Skeletal Muscle Function ◽  
Contractile Phenotype ◽  
Muscle Contractile

Barth syndrome is a rare and incurable X-linked (male-specific) genetic disease that affects the protein tafazzin (Taz). Taz is an important enzyme responsible for synthesizing biologically relevant cardiolipin (for heart and skeletal muscle, cardiolipin rich in linoleic acid), a critical phospholipid of mitochondrial form and function. Mutations to Taz cause dysfunctional mitochondria, resulting in exercise intolerance due to skeletal muscle weakness. To date, there has been limited research on improving skeletal muscle function, with interventions focused on endurance and resistance exercise. Previous cell culture research has shown therapeutic potential for the addition of exogenous linoleic acid in improving Taz-deficient mitochondrial function but has not been examined in vivo. The purpose of this study was to examine the influence of supplemental dietary linoleic acid on skeletal muscle function in a rodent model of Barth syndrome, the inducible Taz knockdown (TazKD) mouse. One of the main findings was that TazKD soleus demonstrated an impaired contractile phenotype (slower force development and rates of relaxation) in vitro compared to their WT littermates. Interestingly, this impaired contractile phenotype seen in vitro did not translate to altered muscle function in vivo at the whole-body level. Also, supplemental linoleic acid attenuated, to some degree, in vitro impaired contractile phenotype in TazKD soleus, and these findings appear to be partially mediated by improvements in cardiolipin content and resulting mitochondrial supercomplex formation. Future research will further examine alternative mechanisms of dietary supplemental LA on improving skeletal muscle contractile dysfunction in TazKD mice.

scholarly journals Global and local tension measurements in biomimetic skeletal muscle tissues reveals early mechanical homeostasis

eLife ◽  
2021 ◽  
Vol 10 ◽  
Author(s):  
Arne D Hofemeier ◽  
Tamara Limon ◽  
Till Moritz Muenker ◽  
Bernhard Wallmeyer ◽  
Alejandro Jurado ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
High Resolution ◽  
Muscle Tissue ◽  
Muscle Function ◽  
Force Measurements ◽  
Skeletal Muscle Function ◽  
Hydrogel Beads ◽  
Investigation Methods ◽  
Global Force

Tension and mechanical properties of muscle tissue are tightly related to proper skeletal muscle function, which makes experimental access to the biomechanics of muscle tissue formation a key requirement to advance our understanding of muscle function and development. Recently developed elastic in vitro culture chambers allow for raising 3D muscle tissue under controlled conditions and to measure global tissue force generation. However, these chambers are inherently incompatible with high-resolution microscopy limiting their usability to global force measurements, and preventing the exploitation of modern fluorescence based investigation methods for live and dynamic measurements. Here, we present a new chamber design pairing global force measurements, quantified from post-deflection, with local tension measurements obtained from elastic hydrogel beads embedded in muscle tissue. High-resolution 3D video microscopy of engineered muscle formation, enabled by the new chamber, shows an early mechanical tissue homeostasis that remains stable in spite of continued myotube maturation.

scholarly journals Tissue-Engineered Skeletal Muscle Models to Study Muscle Function, Plasticity, and Disease

2021 ◽  
Vol 12 ◽  
Author(s):  
Alastair Khodabukus
Keyword(s):  
Skeletal Muscle ◽  
Animal Models ◽  
Muscle Fiber ◽  
Muscle Function ◽  
Fiber Type ◽  
Small Animal ◽  
Muscle Fiber Type ◽  
Small Animal Models ◽  
Muscle Models

Skeletal muscle possesses remarkable plasticity that permits functional adaptations to a wide range of signals such as motor input, exercise, and disease. Small animal models have been pivotal in elucidating the molecular mechanisms regulating skeletal muscle adaptation and plasticity. However, these small animal models fail to accurately model human muscle disease resulting in poor clinical success of therapies. Here, we review the potential of in vitro three-dimensional tissue-engineered skeletal muscle models to study muscle function, plasticity, and disease. First, we discuss the generation and function of in vitro skeletal muscle models. We then discuss the genetic, neural, and hormonal factors regulating skeletal muscle fiber-type in vivo and the ability of current in vitro models to study muscle fiber-type regulation. We also evaluate the potential of these systems to be utilized in a patient-specific manner to accurately model and gain novel insights into diseases such as Duchenne muscular dystrophy (DMD) and volumetric muscle loss. We conclude with a discussion on future developments required for tissue-engineered skeletal muscle models to become more mature, biomimetic, and widely utilized for studying muscle physiology, disease, and clinical use.

scholarly journals Taurine supplementation increases skeletal muscle force production and protects muscle function during and after high-frequency in vitro stimulation

2009 ◽  
Vol 107 (1) ◽  
pp. 144-154 ◽  
Author(s):  
Craig A. Goodman ◽  
Deanna Horvath ◽  
Christos Stathis ◽  
Trevor Mori ◽  
Kevin Croft ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
High Frequency ◽  
Muscle Function ◽  
Muscle Force ◽  
High Frequency Stimulation ◽  
Specific Force ◽  
Tetanic Force ◽  
Control Muscle ◽  
Frequency Stimulation

Recent studies report that depletion and repletion of muscle taurine (Tau) to endogenous levels affects skeletal muscle contractility in vitro. In this study, muscle Tau content was raised above endogenous levels by supplementing male Sprague-Dawley rats with 2.5% (wt/vol) Tau in drinking water for 2 wk, after which extensor digitorum longus (EDL) muscles were examined for in vitro contractile properties, fatigue resistance, and recovery from fatigue after two different high-frequency stimulation bouts. Tau supplementation increased muscle Tau content by ∼40% and isometric twitch force by 19%, shifted the force-frequency relationship upward and to the left, increased specific force by 4.2%, and increased muscle calsequestrin protein content by 49%. Force at the end of a 10-s (100 Hz) continuous tetanic stimulation was 6% greater than controls, while force at the end of the 3-min intermittent high-frequency stimulation bout was significantly higher than controls, with a 12% greater area under the force curve. For 1 h after the 10-s continuous stimulation, tetanic force in Tau-supplemented muscles remained relatively stable while control muscle force gradually deteriorated. After the 3-min intermittent bout, tetanic force continued to slowly recover over the next 1 h, while control muscle force again began to decline. Tau supplementation attenuated F2-isoprostane production (a sensitive indicator of reactive oxygen species-induced lipid peroxidation) during the 3-min intermittent stimulation bout. Finally, Tau transporter protein expression was not altered by the Tau supplementation. Our results demonstrate that raising Tau content above endogenous levels increases twitch and subtetanic and specific force in rat fast-twitch skeletal muscle. Also, we demonstrate that raising Tau protects muscle function during high-frequency in vitro stimulation and the ensuing recovery period and helps reduce oxidative stress during prolonged stimulation.

Autocrine production of prostaglandin F2α enhances phenotypic transformation of normal rat kidney fibroblasts

2005 ◽  
Vol 289 (1) ◽  
pp. C130-C137 ◽  
Author(s):  
E. G. A. Harks ◽  
P. H. J. Peters ◽  
J. L. J. van Dongen ◽  
E. J. J. van Zoelen ◽  
A. P. R. Theuvenet
Keyword(s):  
Transforming Growth Factor ◽  
Cell Transformation ◽  
Rat Kidney ◽  
Prostaglandin F2α ◽  
Transforming Growth Factor Β ◽  
Ionization Mass ◽  
Prostaglandin F ◽  
Normal Rat ◽  
Phenotypic Transformation

We have used normal rat kidney (NRK) fibroblasts as an in vitro model system to study cell transformation. These cells obtain a transformed phenotype upon stimulation with growth-modulating factors such as retinoic acid (RA) or transforming growth factor-β (TGF-β). Patch-clamp experiments showed that transformation is paralleled by a profound membrane depolarization from around −70 to −20 mV. This depolarization is caused by a compound in the medium conditioned by transformed NRK cells, which enhances intracellular Ca2+ levels and thereby activates Ca2+-dependent Cl− channels. This compound was identified as prostaglandin F2α (PGF2α) using electrospray ionization mass spectrometry. The active concentration in the medium conditioned by transformed NRK cells as determined using an enzyme immunoassay was 19.7 ± 2.5 nM ( n = 6), compared with 1.5 ± 0.1 nM ( n = 3) conditioned by nontransformed NRK cells. Externally added PGF2α was able to trigger NRK cells that had grown to density arrest to restart their proliferation. This proliferation was inhibited when the FP receptor (i.e., natural receptor for PGF2α) was blocked by AL-8810. RA-induced phenotypic transformation of NRK cells was partially (∼25%) suppressed by AL-8810. Our results demonstrate that PGF2α acts as an autocrine enhancer and paracrine inducer of cell transformation and suggest that it may play a crucial role in carcinogenesis in general.

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