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PubMed2004

Differential contribution of skeletal and cardiac II-III loop sequences to the assembly of dihydropyridine-receptor arrays in skeletal muscle.

The plasmalemmal dihydropyridine receptor (DHPR) is the voltage sensor in skeletal muscle excitation-contraction (e-c) coupling. It activates calcium release from the sarcoplasmic reticulum via protein-protein interactions with the ryanodine receptor (RyR). To enable this interaction, DHPRs are arranged in arrays of tetrads opposite RyRs. In the DHPR alpha(1S) subunit, the cytoplasmic loop connecting repeats II and III is a major determinant of skeletal-type e-c coupling. Whether the essential II-III loop sequence (L720-L764) also determines the skeletal-specific arrangement of DHPRs was examined in dysgenic (alpha(1S)-null) myotubes reconstituted with distinct alpha(1) subunit isoforms and II-III loop chimeras. Parallel immunofluorescence and freeze-fracture analysis showed that alpha(1S) and chimeras containing L720-L764, all of which restored skeletal-type e-c coupling, displayed the skeletal arrangement of DHPRs in arrays of tetrads. Conversely, alpha(1C) and those chimeras with a cardiac II-III loop and cardiac e-c coupling properties were targeted into junctional membranes but failed to form tetrads. However, an alpha(1S)-based chimera with the heterologous Musca II-III loop produced tetrads but did not reconstitute skeletal muscle e-c coupling. These findings suggest an inhibitory role in tetrad formation of the cardiac II-III loop and that the organization of DHPRs in tetrads vis-a-vis the RyR is necessary but not sufficient for skeletal-type e-c coupling.

Animals↗
PubMed2005

Fast and slow skeletal troponin I in serum from patients with various skeletal muscle disorders: a pilot study.

BACKGROUND: Detection of skeletal muscle injury is hampered by a lack of commercially available assays for serum markers specific for skeletal muscle; serum concentrations of skeletal troponin I (sTnI) could meet this need. Moreover, because sTnI exists in 2 isoforms, slow (ssTnI) and fast (fsTnI), corresponding to slow- and fast-twitch muscles, respectively, it could provide insight into differential injury/recovery of specific fiber types. The purpose of this study was to investigate whether the 2 isoforms of sTnI and their modified forms are present in the blood of patients with various skeletal muscle disorders. METHODS: Serial serum samples were obtained from 25 patients with various skeletal muscle injuries. Serum proteins were separated by a modified sodium dodecyl sulfate-polyacrylamide gel electrophoresis protocol followed by Western blotting for sTnI with monoclonal antibodies specific to ssTnI and fsTnI. RESULTS: We observed (a) intact and, in some cases, degraded sTnI products; (b) evidence of posttranslational modifications in addition to proteolysis; and (c) differential detectability of both skeletal isoforms in the same patient. CONCLUSIONS: It is possible to monitor both sTnI isoforms; this could lead to the development of new diagnostic assays for skeletal muscle damage.

Antibodies, Monoclonal↗
PubMed1979

The complete amino acid sequence of actins from bovine aorta, bovine heart, bovine fast skeletal muscle, and rabbit slow skeletal muscle. A protein-chemical analysis of muscle actin differentiation.

Complete amino acid sequences for four mammalian muscle actins are reported: bovine skeletal muscle actin, bovine cardiac actin, the major component of bovine aorta actin, and rabbit slow skeletal muscle actin. The number of different actins in a higher mammal for which full amino acid sequences are now available is therefore increased from two to five. Screening of different smooth muscle tissues revealed in addition to the aorta type actin a second smooth muscle actin, which appears very similar if not identical to chicken gizzard actin. Since the sequence of chicken gizzard actin is known, six different actins are presently characterized in a higher mammal. The two smooth muscle actins--bovine aorta actin and chicken gizzard actin--differ by only three amino acid substitutions, all located in the amino-terminal end. In the rest of their sequences both smooth muscle actins share the same four amino acid substitutions, which distinguish them from skeletal muscle actin. Cardiac muscle actin differs from skeletal muscle actin by only four amino acid exchanges. No amino acid substitutions were found when actins from rabbit fast and slow skeletal muscle were compared. In addition we summarize the amino acid substitution patterns of the six different mammalian actins and discuss their tissue specificity. The results show a very close relationship between the four muscle actins in comparison to the nonmuscle actins. The amino substitution patterns indicate that skeletal muscle actin is the highest differentiated actin form, whereas smooth muscle actins show a noticeably cloer relation to nonmuscle actins. By these criteria cardiac muscle actin lies between skeletal muscle actin and smooth muscle actins.

Actins↗
PubMed2005

Effect of nursing management and skeletal size at weaning on puberty, skeletal growth rate, and milk production during first lactation of dairy heifers.

Forty Israeli-Holstein 5-d-old calves were used to determine the effect of increasing calf body weight (BW) and skeletal size during the nursing period on age and skeletal size at puberty and on skeletal size and performance during first lactation. The calves were randomly allotted to 2 experimental groups as follows: milk replacer (MR) [calves were given 0.450 kg/d dry matter of milk replacer for the first 50 d of life] and milk-fed (MF) [calves had free access to milk in two 30-min meals/d]. From weaning to 180 d of age, all calves were fed the same diet. At 180 d of age, the MR and MF calves were each divided into 2 equal subgroups: one subgroup from each treatment was given only growing ration, and the other was given the same ration supplemented with fish meal to supply 2% crude protein (CP) (treatments MR + CP and MF + CP, respectively). Finally, at 270 d of age, all calves were housed together and fed a growing heifer's ration until first calving. During the entire nursing period, the MF calves consumed 9.8% more DM, 39.7% more CP, and 52.4% more metabolizable energy than the MR calves. At 60 d of age, BW and all skeletal parameters were higher in the MF calves than in the MR calves. During the entire rearing period (60 to 550 d), the average BW of the MF calves was greater by 16 kg than the BW of the MR calves. Nursing management did not affect differences in skeletal parameters at calving. Average age at puberty onset was 272 +/- 26.8 d; MF calves reached puberty 23 d earlier than MR calves. Yields of milk (kg/305 d) and fat-corrected milk (FCM, kg/d) were greater for the MF + CP heifers than for the MR heifers. It was concluded that nursing by ad libitum milk, as compared with milk replacer, affected BW but not skeletal size of the adult animal, decreased age of puberty onset, and increased FCM yield at first lactation. Supplementing the diet with 2% CP during the prepubertal period increased BW but not skeletal size of the adult animal and 305-d milk and FCM yields during first lactation.

Animal Feed↗
PubMedDate not supplied

Anterior cruciate ligament injury versus tibial spine fracture in the skeletally immature knee: a comparison of skeletal maturation and notch width index.

Both midsubstance anterior cruciate ligament (ACL) injury and tibial spine avulsion fracture occur in the skeletally immature knee. The purpose of this study was to determine whether there are differences in skeletal maturation or notch parameters between these two groups. A retrospective case-control study of 25 skeletally immature patients with tibial spine fractures compared with 25 age- and sex-matched skeletally immature patients with midsubstance ACL injuries was performed. Bone age and notch width index were determined from preoperative radiographs. There were no significant differences between the tibial spine fracture group and the ACL injury group with respect to skeletal maturation, comparing bone age to chronological age (-0.5 vs. -0.3 years; P = 0.617). The ACL injury group had narrower notch indices than the tibial spine fracture group (0.230 vs. 0.253; P = 0.020). Thus, in a comparison of age- and sex-matched skeletally immature patients, those with midsubstance ACL injuries had a significantly narrower notch index than those with tibial spine fractures. This association may account for some of the variation in injury patterns in the skeletally immature knee.

Adolescent↗
PubMedDate not supplied

Diagnostic value of skeletal AP and PSA with respect to skeletal scintigram in patients with prostatic disease.

The aim of this study was to compare the diagnostic value of skeletal AP and PSA with the skeletal scintigram in patients with prostatic cancer. PSA and skeletal AP were measured by Tandem-R-Ostase Assay (IRMA) and Tandem-R-PSA-Assay. 64 patients with prostatic cancer, 20 of them in stage D2 were involved. Patients with a prostatic cancer and bone metastases show remarkable increased skeletal AP concentration with a median concentration of 50ng/ml SAP and 95 ng/ml PSA. Patients without bone metastases have a lower median concentration of SAP at 10 ng/ml and PSA concentration of 40 ng/ml which is within the normal range. Six out of 20 patients at stage D2 showed a significant increase of SAP concentration and even of PSA before bone metastases were seen by skeletal scintigraphy. We conclude when skeletal metastases are assumed in patients with prostatic cancer, a combination of skeletal scintigramm and measurement of SAP seem to be of advantage to recognize patients with bone metastases earlier.

Alkaline Phosphatase↗
PubMed2005

Corticotropin releasing factor 2 receptor agonists reduce the denervation-induced loss of rat skeletal muscle mass and force and increase non-atrophying skeletal muscle mass and force.

Of the two corticotropin releasing factor receptors known, corticotrophin releasing factor 2 receptor (CRF2R) is expressed in skeletal muscle. The function of this receptor in skeletal muscle is at present unknown. In order to better understand the role of the CRF2R in skeletal muscle, we treated rats with CRF2R agonists and evaluated the effect of these agents on normal and denervated muscle mass. Rats treated with the non-selective CRFR agonist, sauvagine, did not demonstrate any significant and consistent change in non-denervated and denervated fast twitch [tibialis anterior (TA) or extensor digitorum longus (EDL)] or slow/mixed twitch [medial gastrocnemius (MG) or soleus] fiber muscle mass. In adrenalectomized rats, sauvagine treatment resulted in no significant and consistent change in non-denervated fast or slow/mixed twitch fiber muscles but did cause a significant and consistent increase in denervated fast twitch (TA and EDL) but not slow/mixed twitch muscle mass. Interestingly adrenalectomy had no effect on the degree of muscle atrophy. Rats treated with the CRF2R selective agonist urocortin 2 demonstrated an increase in non-denervated and denervated fast and slow/mix twitch fiber muscle mass. The urocortin 2 induced increase in muscle mass was accompanied by an increase in muscle fiber cross-sectional area and muscle absolute force. These studies demonstrated that activation of the CRF2R decreased the level of skeletal muscle mass, force, and myocyte cross-sectional area loss resulting from sciatic nerve damage and increased the mass, force and myocyte cross-sectional area of normal (non-atrophying) skeletal muscle. In addition, we also observed that removal of the adrenals increased the effectiveness of the non-selective CRFR agonists sauvagine, presumably via the removal of the pro-atrophy influence of adrenal produced corticosteroids. These results demonstrate that pharmacological modulation of the CRF2R may be a viable method to treat skeletal muscle atrophy.

Amphibian Proteins↗
PubMed2003

Urocortin II treatment reduces skeletal muscle mass and function loss during atrophy and increases nonatrophying skeletal muscle mass and function.

Two corticotropin-releasing factor 2 receptor (CRF2R)-selective peptides have been recently described, urocortin II (also known as stresscopin-related peptide) and urocortin III (stresscopin). We have used urocortin II to evaluate the effects of activation of the CRF2R on skeletal muscle-related physiological processes. Administration of urocortin II to mice prevented the loss of skeletal muscle mass resulting from disuse due to casting, corticosteroid treatment, and nerve damage. In addition, urocortin II treatment prevented the loss of skeletal muscle force and myocyte cross-sectional area that accompanied muscle mass losses resulting from disuse due to casting. Finally, we observed increased skeletal muscle mass and force in normal muscles when mice are treated with urocortin II. These results were confirmed using two additional CRF2R agonists, urocortin I and sauvagine. Thus, activation of the CRF2R modulates skeletal muscle mass in both normal and atrophying muscle. Therefore, CRF2R-selective agonists may find utility in the treatment of skeletal muscle wasting diseases including age-related muscle loss or sarcopenia.

Adrenal Cortex Hormones↗
PubMed2000

Identification of skeletal muscle satellite cells by transfecting EGFP driven by skeletal alpha-actin promoter.

In isolating skeletal muscle satellite cells, sometimes a problem is encountered in removing contaminating nonmyogenic cells. In the present study, we constructed a novel vector, pSKA-EGFP, which achieves the expression of enhanced green fluorescent protein (EGFP) exclusively in myogenic cells under the control of skeletal alpha-actin promoter when transfected to primary cultured cells from skeletal muscle. Cells from rat skeletal muscle positive for EGFP after transfecting with pSKA-EGFP were all positive for desmin and none of the nonmyogenic cells expressed EGFP, indicating that the expression of EGFP is specific to myogenic cells. Among the cells positive for EGFP were proliferating cells, presumably satellite cells. In addition, EGFP positive cells derived from horse skeletal muscle after transfecting pSKA-EGFP in vitro formed multinuclear myotubes, indicating that myogenic expression of EGFP driven by skeletal alpha-actin was achieved also in the equine cells. These results indicated that pSKA-EGFP vector will be useful in identifying and following up the satellite cells in real time, and also permit us to isolate satellite cells in combination with fluorescence-activated cell sorting (FACS).

Actins↗
PubMed2001

[Leptin: factor in the central nervous system regulation of bone mass. Development of a new understanding of bone remodeling, skeletal reconstruction, skeletal preservation and skeletal repair].

Bone remodeling is the physiologic process used by vertebrates to maintain a constant bone mass between the end of puberty and gonadal failure. Besides the well-characterized and critical local regulation of bone remodeling, recent genetic studies have shown that there is a central control of bone formation, one aspect of bone remodeling. This central regulation involves leptin, an adipocyte-secreted hormone that controls body weight, reproduction, and bone remodeling following binding to its receptor located on the hypothalamic nuclei. This genetic result in rodents is in line with clinical observations in humans and offers a whole new direction for research in bone physiology.

Adolescent↗
PubMed1982

Quantitative genetics of skeletal nonmetric traits in the rhesus macaques of Cayo Santiago. III. Relative heritability of skeletal nonmetric and metric traits.

This study addresses the long-standing controversy in skeletal biology concerning the relative utility of skeletal metric and nonmetric traits for studies of biological relationship. This controversy centers on the relative heritability of these two trait sets. This paper presents heritabilities for a series of skeletal metric and nonmetric traits measured with the same sample of mother-offspring pairs from the Cayo Santiago skeletal collection of rhesus macaques. Skeletal nonmetric traits display significantly greater heritability estimates than metric traits. This difference is due primarily to the high heritability estimates of hyperostotic nonmetric traits. Foraminal traits are not significantly more heritable than skeletal metric traits. The generality of this pattern of heritability values, in which hyperostotic nonmetric traits are more highly heritable than foraminal nonmetric and metric traits, depends on future empirical study of the correlation of heritability values in populations and theoretical work.

Animals↗
PubMed2007

Environmental effects on skeletal versus dental development: Using a documented subadult skeletal sample to test a basic assumption in human osteological research.

This study examines the relationship between measures of skeletal and dental development and socioeconomic factors in a 20th century documented skeletal sample of children from Portugal. The skeletons are of known sex and chronological age, and include other biographic data, such as cause of death. Growth in the length of the long bone is used as a measure of skeletal growth, and schedules of tooth formation are used as a measure of dental development. These two measures of physiological age were compared to chronological age, to assess growth and developmental status. Socioeconomic indicators were obtained from the supporting documentation, and include the occupation of the father and the place of residence, which were used to build a socioeconomic classification based on two groups, one of low and the other of high socioeconomic status. Growth and development status was then compared in these two groups. Results show that socioeconomic differences are much more pronounced in skeletal growth than in dental development. This largely supports the assertion that dental development is buffered against environmental factors relative to skeletal development. However, in this study, skeletal maturation could not be assessed, and findings indicate that dental development can show significant delays at the lower end of the socioeconomic gradient.

Adolescent↗
PubMed1995

Phosphate regulates the stability of skeletal alkaline phosphatase activity in human osteosarcoma (SaOS-2) cells without equivalent effects on the level of skeletal alkaline phosphatase immunoreactive protein.

Inorganic phosphate (P(i)) can regulate the level of skeletal alkaline phosphatase (ALP) activity in human osteoblast-like cells, but not by means of changes in transcription or release from the cell surface. The current studies were intended to determine whether (1) P(i) affected the inactivation of ALP activity in human osteosarcoma (SaOS-2) cells; and (2) P(i)-dependent changes in ALP-specific activity were associated with equal, concomitant changes in the level of ALP immunoreactive protein. The results of these studies revealed that P(i) increased the stability of skeletal ALP activity without equivalent effects on the level of ALP immunoreactive protein. An increase in P(i) (from 0 to 1.8 mmol/liter) caused a time-dependent increase in the amount of skeletal ALP activity in the SaOS-2 cells, without a parallel increase in the amount of skeletal ALP immunoreactive protein, and a decrease in P(i) (from 1.8 to 0 mmol/liter) caused a time-dependent decrease in the amount of ALP activity, without a significant decrease in the total cellular content of ALP immunoreactive protein. Together, these observations suggest that P(i) may alter the level of skeletal ALP activity in SaOS-2 cells by inhibiting a process of irreversible inactivation that does not effect equal, concomitant changes in the level of skeletal ALP immunoreactive protein.

Alkaline Phosphatase↗
PubMed1988

Differential expression of slow and fast skeletal muscle troponin C. Slow skeletal muscle troponin C is expressed in human fibroblasts.

We have isolated and sequenced the cDNAs for human slow and fast skeletal muscle troponin C (TnC). Each cDNA is encoded by one of the two TnC genes in the human genome. The fast skeletal muscle TnC gene appears to be expressed exclusively in skeletal muscle. Only the slow TnC gene is expressed in human cardiac ventricle. The slow skeletal TnC gene is also expressed in skeletal muscle and, surprisingly, in several human fibroblast cell lines. Thus, at least one of the three proteins of the troponin complex appears to be expressed in non-muscle cells of higher vertebrates. The relative steady-state amounts of the slow and fast skeletal TnC mRNAs in various adult and embryonic striated muscles are similar to the expected amounts of the corresponding protein, suggesting that the expression of TnC genes is controlled predominantly by the production or accumulation of mRNA rather than by translational or post-translational mechanisms.

Amino Acid Sequence↗
PubMed1997

Skeletal morphogenesis in the sea urchin embryo: regulation of primary mesenchyme gene expression and skeletal rod growth by ectoderm-derived cues.

The skeleton of the sea urchin embryo is synthesized by the primary mesenchyme cells (PMCs). Previous studies have shown that local interactions between PMCs and the neighboring ectoderm regulate several aspects of skeletal morphogenesis, including PMC distribution in the blastocoel, the size of the skeleton and its branching pattern. In the present study, we have further examined the regulation of skeletogenesis by the ectoderm. We generated a 'rate map' of skeletal growth, which revealed stereotypical changes in the rates at which specific skeletal elements elongate during development. We showed that three transcripts encoding PMC-specific gene products known to be involved in the synthesis of the skeleton exhibited dynamic, spatially regulated patterns of expression within the PMC syncytium. All three gene products showed high levels of expression at sites of skeletal rod growth, although the specific patterns varied among the genes. We present direct evidence, based upon cell transplantation experiments, that the expression of one of these genes, SM30, is responsive to local, ectoderm-derived cues. Based upon our studies, we suggest that short-range signals from different ectodermal territories may regulate the expression of PMC-specific gene products that are rate-limiting in skeletal biosynthesis, thereby locally influencing skeletal rod growth.

Animals↗
PubMed1976

A comparison of skeletal, cardiac, and smooth muscle actions of dantrolene sodium--a skeletal muscle relaxant.

Dantroline sodium, a skeletal muscle relaxant, has been proposed to inhibit the relase of Ca++ from the sarcoplasmic reticulum. Such a mechanism suggests that other muscle contractile systems operating with the same Ca++ denominator should also be affected by the drug. In the present studies dantrolene sodium effects on smooth, cardiac and skeletal muscle have been evaluated with in situ and in vitro techniques. In anesthetized dogs in situ skeletal muscle contractions were inhibitied in a dose-dependent manner, but cardiac muscle contractions were not. Effects on intestinal smooth muscle responses were highly variable and of short duration. In vitro, ED50 values were developed with dantrolene sodium (0.15-120 mg/l) in DMSO for each tissue. Skeletal muscle was the most sensitive (ED50 = 4.1 mg/l), cardiac muscle contractions were not inhibited by the drug and intestinal smooth muscle (ED50 = 59.0 mg/l) was approximately 1/14 as sensitive as skeletal muscle. It is concluded that skeletal muscle is uniquely sensitive to dantrolene sodium. A hypothesis for this specific action is offered.

Animals↗
PubMed1975

[New formation of the skeletal muscles and skeletal muscle and myocardial-like structures in rabbits in experiments with diffusion chambers].

The rabbit skeletal and cardiac muscles treated by 1% water solution of Trypan Blue for 48 hrs are necrotized and, having been transplanted under the skin in the diffusion chambers impermeable for cells, do not develop. When transplanting such necrotized muscles under the skin or in the abdominal cavity in the diffusion chambers permeable for cells (with pores of 1.5 mu in diameter), cells penetrate through the chamber wall and develop, under the influence of the products of decomposition of phagocytized transplant, into myoblasts, muscular tubes and differentiated cross-striated muscle fibers; undifferentiated muscle fibers of the skeletal type arise outside the chamber. The necrotized cardiac muscle did not induce the formation of muscle fibers after the transplantation under the skin or in the omentum. If they were transplanted together with the diffusion chambers containing the necrotized skeletal muscles, myocardium-like structures arose outside the chamber. The formation de novo of skeletal muscles and skeletal muscle- and myocardium-like structures under the influence of decomposition products released from the necrotized skeletal and cardiac muscles proceeds by means of induction; some pluripotent cells of the recipient, possibly polyblasts, are the source of de novo formation.

Animals↗
PubMed2002

Expression of midkine in regenerating skeletal muscle fibers and cultured myoblasts of human skeletal muscle.

Midkine is a member of a family of developmentally regulated neurotrophic and heparin-binding growth factors. The expression of midkine was examined immunohistochemically in biopsied muscle specimens from patients with various myopathies. The intense immunoreactivity of midkine was observed in the sarcoplasm at an early stage regenerating fibers of small diameter. Midkine immunoreactivity was also detected in cultured human skeletal muscle myoblasts from the proliferation stage to the differentiation stage. These results suggest that midkine may be an important skeletal muscle growth-promoting factor that participates in the growth process during skeletal muscle development, proliferation, and differentiation, and in the skeletal muscle regeneration in various neuromuscular disorders. This is the first report demonstrating the presence of midkine in skeletal muscle cells.

Biopsy↗