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PubMed1999

Response of chick lines selected on carcass quality to dietary lysine supply: live performance and muscle development.

Broiler carcass quality can be improved by conventional selection techniques. In this regard, an experimental "quality" line (QL) was selected for high breast meat yield. We analyzed the effects of this selection on the dietary lysine requirement in chicks from 0 to 3 wk. Control (CL) and QL chicks were provided ad libitum access to isoenergetic diets containing 20% crude protein but differing in their lysine content (0.75, 0.88, 1.01, and 1.13%). Two-way ANOVA showed a significant effect (P < 0.01) of genotype on body weight, growth rate, feed intake, and weight of Pectoralis major and Gastrocnemius muscles. Conversely, the Sartorius muscle weight was not modified (P = 0.21) by genotype. Lysine deficiency markedly reduced body weight, growth rate, and feed intake, and increased feed conversion ratio (P < 0.001). Low dietary levels of lysine also depressed the weight of Gastrocnemius, Sartorius, and P. major (P < 0.001). The body or muscle weight response to diet lysine concentration depended on the line, with QL chicks appearing less sensitive to lysine deficiency. Consequently, their dietary requirements could be lower. Finally, when weight gain and P. major muscle protein deposition were plotted against lysine intake, QL chicks appeared to be more efficient than CL chicks. The underlying mechanisms responsible for this await clarification.

Animal Nutritional Physiological Phenomena↗

PubMed1988

Embryonic acetylcholine receptors guarantee spontaneous contractions in rat developing muscle.

Many proteins are expressed in distinct embryonic and adult forms. However, in most cases we do not know why the embryonic form of proteins is required. This question can be readily addressed for the acetylcholine receptor (AChR) because developmentally specified modifications of this ligand-gated ion channel can be directly related to changes in membrane currents. In developing rat soleus muscle, spontaneous transmitter release causes miniature end-plate currents (m.e.p.cs) to flow into the muscle cell. We show here that these m.e.p.cs in neonatal soleus trigger spontaneous contractions. By injecting m.e.p.cs into young fibres, we showed that only embryonic m.e.p.cs can trigger such contractions; adult m.e.p.cs do not last long enough. Developing muscle fibres must be active for synapse and muscle differentiation. Our experiments indicate that the embryonic form of the AChR is essential for spontaneous contractile activity and may therefore be required for normal neuromuscular development.

Action Potentials↗

PubMed1997

Differentiation dependent expression and distinct subcellular localization of the protooncogene product, PEBP2beta/CBFbeta, in muscle development.

The Pebpb2/Cbfb gene encodes the non-DNA binding subunit of the heterodimeric transcription factor, PEBP2/CBF. To examine the expression of the PEBP2beta/CBFbeta protein in vivo, we carried out immunohistochemistry using the tissues from adult mice as well as embryos. Although PEBP2beta/CBFbeta was detected in various tissues to various degrees, interesting features of expression were observed in the skeletal myogenic cells. Here PEBP2beta/CBFbeta was found mainly to occur as cytoplasmic staining and the intensity of this staining increased depending on the differentiation stage of the cells. In the undifferentiated myoblasts PEBP2beta/CBFbeta was undetectable, whereas moderate levels of PEBP2beta/ CBFbeta were detected in the elongated and aligned myocytes. PEBP2beta/CBFbeta appeared to accumulate further when the cells fused to each other to become multinucleated myotubes. Once the muscle fibers were established, PEBP2beta/CBFbeta was relocated onto or around the Z-lines. PEBP2beta/CBFbeta was also detected in the cytoplasm of cardiac myocytes and in the smooth muscle cells of the digestive tract. In all the above, the skeletal myotubes were the only case that showed both nuclear and cytoplasmic staining of PEBP2beta/CBFbeta. Thus, we could show differentiation dependent pattern of PEBP2beta/CBFbeta expression in muscle development and establish PEBP2beta/CBFbeta to be a cytoplasmic as well as nuclear protein in vivo.

Actinin↗

PubMed1985

Endogenous lectins in normal and dystrophic muscle development.

Two endogenous lectin activities, one specific for beta-D-galactose (beta-D-Gal) residues and purified on asialofetuin-Sepharose and the second specific for iduronic acid containing glycosaminoglycans and purified on heparin-Sepharose, have been studied during myogenesis in both normal and dystrophic chickens. The Storrs strain, homozygous for muscular dystrophy, and the dystrophic strain 413 from the University of California at Davis were both used in this study. Strain 412 and local hatchery chickens were used as controls. The lectins derived from all sources appeared to be identical based on physical properties and carbohydrate specificity. Both normal and dystrophic adult chickens possessed similar lectin levels in lung, spleen, kidney, heart, and muscle tissue. No differences were noted in the temporal appearance of the heparin-binding lectin; however, the beta-D-Gal-binding lectin appeared earlier in the Storrs dystrophic strain than it did in the 413, 412, or hatchery embryos.

Animals↗

PubMed2000

A 295-kDA intermediate filament-associated protein in radial glia and developing muscle cells in vivo and in vitro.

The RC2 antibody is frequently used to label mouse radial glial cells in all parts of the nervous system where neuronal migration occurs during embryonic and early postnatal life. The antigen recognized by this antibody still needs to be identified. We have characterized further its localization in vivo, its expression and subcellular localization in vitro, as well as its molecular nature. Histologic investigations of whole mouse embryos reveal an equally intense expression of RC2 immunostaining in radial glial cells in brain and spinal cord and in skeletal muscle. In glial cells cultures, the RC2 antibody recognizes an epitope located on the glial cytoskeleton and identified as an intermediate filament associated protein (IFAP) at the ultrastructural level. RC2 immunostaining in those cells is strongly dependent on the presence of a serum-derived activity. Serum-removal causes a decrease of the staining while adding serum back to the cells induces reexpression of RC2 immunoreactivity. By Western blotting, we find that in intermediate filament (IF) preparations obtained from cultured cerebellar glia, the RC2 antibody recognizes a 295-kDa protein whose expression is also dependent on the presence of serum in culture medium. In developing muscle cells, RC2 immunostaining is observed from the myoblast stage and disappears after complete myotube fusion. Both in vivo and in vitro, staining is first seen as a loose capping around myoblasts nuclei and progressively concentrates into Z-disks in association with the muscle IF protein desmin. The RC2 antibody also recognizes a 295-kDa protein band in muscle tissue protein extracts. Thus, the RC2 antibody recognizes a developmentally regulated cytoskeletal protein that is expressed, like other previously identified IFAPs, by cells of the glial and myogenic lineages and whose expression in vitro seems to be controlled by a signaling mechanism known to modulate astroglial morphology.

Animals↗

PubMed1990

Muscular dysgenesis: a model system for studying skeletal muscle development.

Muscular dysgenesis, caused by an autosomal recessive lethal mutation (mdg) in mice, is characterized by an absence of contraction of skeletal muscle. A historical review of the investigation of this disorder is presented. The early studies of the morphological and physiological aspects of the disorder in vivo and in vitro presented evidence for dysfunction in the skeletal muscle excitation-contraction (E-C) system, and thus suggested that skeletal muscle was the primary target of dysfunction in dysgenesis. Subsequent evidence, including the phenomenon of rescue (restoration of contraction) of dysgenic muscle in culture by spinal cord cells, argued for involvement of the nervous system in the disorder. Experiments demonstrating that dysgenic muscle lacks the slow calcium current associated with E-C coupling, and the protein (the dihydropyridine receptor) also associated with such coupling, led to the discovery of the probable site of the mutation: the gene for the alpha 1 subunit of the dihydropyridine receptor. The neuronal involvement hypothesis was further countered by several lines of evidence, including the phenomenon of fusion of nonmyogenic normal cells with dysgenic myotubes in cocultures of normal cells and dysgenic muscle. The use of the mutant as a model for studying the development of normal skeletal muscle is discussed and future avenues of research are explored.

Aging↗

PubMed2003

Effect of selection for growth rate on muscle damage during turkey breast muscle development.

Damage to the turkey pectoralis major muscle was studied in a randombred control line (RBC2), a subline (F) from the RBC2 line selected long-term for increased 16-wk BW only, and a commercial sire line (B) at 25 d of incubation and at 1, 4, 8, 16, and 20 wk posthatch. Pectoralis major muscle samples were obtained from three females and three males from each line in a manner to avoid contraction. After being fixed and sectioned, the muscle samples were stained with hematoxylin and eosin to view muscle fiber and muscle fiber bundle morphology. Beginning at 8 wk posthatch, differences in muscle fiber morphology were observed among the different lines. The RBC2 line throughout the duration of the study maintained well-organized muscle fibers and muscle fiber bundles with large capillary networks. In contrast, the growth-selected F line began to show muscle fiber degeneration at 8 wk posthatch, and limited capillary beds were observed as development proceeded. The B line had intermediate muscle morphology between the RBC2 and F lines, but by 20 wk posthatch significant muscle fiber degeneration was present with limited capillary supply. The degenerative muscle fiber changes were predominant in the growth-selected F-line, suggesting that growth selection for just BW may be associated with posthatch muscle damage.

Aging↗

PubMed1998

Tetranectin is a novel marker for myogenesis during embryonic development, muscle regeneration, and muscle cell differentiation in vitro.

Tetranectin, a plasminogen-binding protein with a C-type lectin domain, is found in both serum and the extracellular matrix. In the present study we report that tetranectin is closely associated with myogenesis during embryonic development, skeletal muscle regeneration, and muscle cell differentiation in vitro. We find that tetranectin expression coincides with muscle differentiation and maturation in the second half of gestation and further that tetranectin is enriched at the myotendinous and myofascial junctions. The tetranectin immunostaining declines after birth and no immunostaining is observed in normal adult muscle. However, during skeletal muscle regeneration induced by the intramuscular injection of the myotoxic anesthetic Marcaine, myoblasts, myotubes, and the stumps of damaged myofibers exhibit intense tetranectin immunostaining. Tetranectin is also present in regenerating muscle cells in dystrophic mdx mice. Murine C2C12 myogenic cells and pluripotent embryonic stem cells can undergo muscle cell differentiation in vitro. Tetranectin is not expressed in the undifferentiated myogenic cells, but during the progression of muscle differentiation, tetranectin mRNA is induced, and both cytoplasmic and cell surface tetranectin immunostaining become apparent. Finally, we demonstrate that while tetranectin mRNA is translated to a similar degree in developing limbs and lung, the protein does not seem to be tissue associated in the lung as it is in the limbs. This indicates that in some tissues, such as the limbs, tetranectin may function locally, whereas in other tissues, such as the lung, tetranectin production may be destined for body fluids. In summary, these results suggest that tetranectin is a matricellular protein and plays a role in myogenesis.

Animals↗

PubMed1991

Biogenesis of transverse tubules and triads: immunolocalization of the 1,4-dihydropyridine receptor, TS28, and the ryanodine receptor in rabbit skeletal muscle developing in situ.

Our previous immunofluorescence studies support the conclusion that the temporal appearance and subcellular distribution of TS28 (a marker of transverse (T) tubules and caveolae in adult skeletal muscle [Jorgensen, A. O., W. Arnold, A. C.-Y. Shen. S. Yuan, M. Gover, and K. P. Campbell, 1990, J. Cell Biol. 110:1173-1185]), correspond very closely to those of T-tubules forming de novo in developing rabbit skeletal muscle (Yuan, S., W. Arnold, and A. O. Jorgensen, 1990, J. Cell Biol. 110:1187-1198). To extend our morphological studies of the biogenesis of T-tubules and triads, the temporal appearance and subcellular distribution of the alpha 1-subunit of the 1,4-dihydropyridine receptor (a marker of the T-tubules and caveolae) was compared to (a) that of TS28; and (b) that of the ryanodine receptor (a marker of the junctional sarcoplasmic reticulum) in rabbit skeletal muscle cells developing in situ (day 19 of gestation to 10 d newborn) by double immunofluorescence labeling. The results presented show that the temporal appearance and relative subcellular distribution of the alpha 1-subunit of the 1,4-dihydropyridine receptor (alpha 1-DHPR) are distinct from those of TS28 at the onset of the biogenesis of T-tubules. Thus, in a particular developing myotube the alpha 1-DHPR appeared before TS28 (secondary myotubes; day 19-24 of gestation). Furthermore, the alpha 1-DHPR was distributed in discrete foci at the outer zone of the cytosol, while TS28 was confined to foci and rod-like structures at the cell periphery. As development proceeded (primary myotubes; day 24 of gestation) approximately 50% of the foci were positively labeled for both TS28 and the alpha 1-DHPR, while approximately 20 and 30% of the foci were uniquely labeled for TS28 and the alpha 1-DHPR, respectively. The foci labeled for both TS28 and the alpha 1-DHPR and the foci uniquely labeled for TS28 were generally confined to the cell periphery, while the foci uniquely labeled for the alpha 1-DHPR were mostly confined to the outer zone of the cytosol. 1-2 d after birth, TS28 was distributed in a chickenwire-like network throughout the cytosol, while the alpha 1-DHPR was confined to cytosolic foci. In contrast, the temporal appearance and subcellular distribution of the alpha 1-DHPR and the ryanodine receptor were very similar, if not identical, throughout all the stages of the de novo biogenesis of T-tubules and triads examined.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1983

Fetuses of lean and obese swine in late gestation: body composition, plasma hormones and muscle development.

The development of obesity in porcine fetuses was investigated using a lean and obese strain of pigs at 80, 90, 100 and 110 d of gestation. In absolute terms, fetuses of obese gilts (FO) generally had lower carcass weight and contained less total protein, dry matter and ash than fetuses of lean gilts (FL). In relative terms (percentage of wet carcass weight) FO, compared with FL, generally had decreased percentages of water and increased percentages of protein and lipid. Comparisons based on absolute terms revealed body composition of the strains to be different at 90 d, indicating that factors responsible for obese-type growth were active before that time. Both body composition and hormone concentration differences were most pronounced at later gestation ages. Depressed growth hormone, elevated cortisol, and a tendency toward elevated insulin concentrations in fetal plasma were apparent in late gestation for FO compared with FL. These hormonal patterns are consistent with onset of obesity in FO in late gestation. Greater weights of semitendinosus and longissimus muscles were observed in FL vs FO at 90, 100 and 110 d of gestation (P less than .05). These greater muscle weights were generally accompanied by greater contents of RNA, DNA and protein in FL muscles at these same ages. However, at 80 d, FL had greater absolute DNA content in semitendinosus muscle whereas muscle weight was similar between the strains. This suggests that greater muscle weights for FL than FO were caused by more nuclei in muscle of FL. In general, indices of hypertrophy (protein/DNA) and protein synthetic capacity (RNA/DNA) of muscle were usually similar for both strains at all gestation ages. It is concluded that decreased muscle growth in late gestation of FO compared with FL is more related to fewer total nuclei and perhaps fewer myofibers than to an impaired cellular capacity for protein synthesis.

Animals↗

PubMed1986

The origins and insertions of the extraocular muscles: development, histologic features, and clinical significance.

The tendinous origins and insertions of the extraocular muscles were studied embryologically by macroscopic and microscopic methods. It is concluded from this investigation that these tendons of origin and insertion arise from mesenchymal tissue similar to that of their respective muscles. These tendon-muscle groups have developed from superior and inferior mesenchymal complexes. The origins of the extraocular muscles are attached to the periorbita by an interlocking of the tendinous and muscular fibers, which allows for mobility of the extraocular muscles in all extreme directions of gaze and also results in a strong mechanical mooring for these muscles. Avulsion at the origins of the extraocular muscles following severe traction or trauma is rare. The additional origin of the superior and medial rectus muscles to the dura of the optic nerve explains the pain that may occur on movement of the eye in optic neuritis. Optic nerve compression and thyroid myopathy is explained by mucopolysaccharide and inflammatory cell infiltration of the muscular interdigitations that extend up to the site of origin of the rectus muscles. Findings of this investigation suggest that the association of ptosis and superior rectus muscle underaction may be due to a persistence of fibrous tissue that has endured from embryologic development between the superior rectus and levator palpebrae superioris muscles. Superior oblique tendon sheath syndrome is explained by embryologic strands remaining between the tendon of the superior oblique muscle and the trochlea. The insertions of the rectus muscles extend from the equator of the eye to the limbus early on in development. By processes of differential degeneration between the sclera and the rectus tendon, posterior recession of the tendon from the limbus, and contemporaneous growth of the anterior segment of the eye, these tendons reach their adult location only between the ages of 18 months and 2 years. In strabismus surgery, measurements for muscle adjustments should be assessed from the limbus rather than from the sites of insertion of these tendons. In the series of patients with esotropia, no mechanical abnormalities were noted in relationship to the insertions of the medial or lateral recti muscles. Furthermore, no correlation was found between the site of insertion of the medial rectus muscle and the degree of esotropia.

Child, Preschool↗

PubMed1989

Effects of perinatal high dose dexamethasone on skeletal muscle development in rats.

Five litters of suckling rats were given either dexamethasone (DEX), 1 mg/kg, subcutaneously, three times daily (n = 4/litter) or vehicle control (n = 4/litter) from day 3 through day 7 after birth. Rats were weighed weekly and were weaned on day 30. On day 60, rats were killed and the soleus (SOL) and extensor digitorum longus (EDL) were removed for the following analyses: 1) wet weight, 2) light microscopic examination of hematoxylin and eosin stained transverse sections, 3) quantitative morphometric analysis of myosin ATPase stained transverse sections (fiber numbers, fiber type percentages and mean fiber diameters), and 4) DNA (total and mg/g wet weight). The following parameters were significantly reduced in treated rats: 1) body weight, 2) wet weight of SOL and EDL, and 3) mean diameter of SOL type I fibers. There was a trend for total DNA of SOL and EDL to be decreased in treated rats but this was not statistically significant. In a second experiment, pregnant rats (n = 4) were given DEX, 1 mg/kg, subcutaneously, twice daily, on days 17 and 18 of gestation. Two rats served as vehicle controls. The prenatally DEX-exposed rats weighed significantly less on weeks 3, 4, 6, 7 and 8. There were significant reductions in the following parameters for treated rats: 1) SOL wet weight, and 2) total number of SOL type I fibers. There was a trend for SOL DNA to be reduced but this was not statistically significant.

Animals↗

PubMed2026

Comprehensive Analysis of miRNAs and Predicted Protein Interaction Networks in Skeletal Muscle Development of Myostatin-Deficient Rabbits.

Myostatin (MSTN), encoded by the MSTN gene, is a critical negative regulator of skeletal muscle mass. This study aims to identify and characterize the miRNAs involved in the development of the double-muscling phenotype in MSTN-deficient rabbits. We performed high-throughput sequencing to analyze the miRNA expression profiles in gluteus maximus tissue from wild type (MSTN+/+) and MSTN-KO (MSTN+/- and MSTN-/- inclusive) rabbits. Differentially expressed miRNAs (DEmiRNAs) were identified, and their potential target genes were predicted. Functional enrichment analysis of these target mRNAs was conducted using Gene Ontology (GO) and the Kyoto Encyclopedia of Genes and Genomes (KEGG) database to elucidate the involved biological pathways and regulatory networks. A total of 25 DEmiRNAs (13 downregulated and 12 upregulated, |log2FC| ≥ 1.0, adjusted p < 0.05) and 1178 differentially expressed mRNAs (408 upregulated and 770 downregulated, |log2FC| ≥ 2.0, adjusted p < 0.05) were identified in MSTN-KO compared to MSTN+/+ rabbits. Bioinformatics analysis revealed that the target genes of these DEmiRNAs were significantly enriched in key pathways governing muscle growth and metabolism, including the PI3K-Akt signaling pathway, MAPK signaling pathway, and pathways related to ECM-receptor interaction and insulin signaling. Notably, many predicted target mRNAs are expressed by genes that encode key inhibitors of myogenesis (e.g., HDAC4) and major extracellular matrix components (e.g., COL4A3, POSTN). Our results demonstrate that MSTN deficiency induces a distinct and widespread change in the miRNA expression landscape of skeletal muscle.

Animals↗

PubMed1989

Fast myosin heavy chain expression during the early and late embryonic stages of chicken skeletal muscle development.

The development of embryonic skeletal muscles in the chick can be divided into two periods of fiber specialization--an early one during which the different muscles of the limb are formed and an initial round of fiber specialization occurs and a late or fetal period during which there is extensive growth of this previously established fiber pattern. This latter period of growth is dependent on the establishment and maintenance of functional neuromuscular contacts. As has been described for other developmental stages, we show here that there are different embryonic fast skeletal muscle myosin heavy chain (MHC) isoforms expressed during the different embryonic periods of muscle growth. The identification of these isoforms was based on differences in their reactivity with various fast MHC monoclonal antibodies and on their different peptide banding patterns. The in ovo accumulation of the late embryonic MHC isoform pattern was similar to the time course of the previously described changes in alpha-actin and troponin T isotype switching during embryogenesis. The appearances of the late embryonic isoforms were blocked by chronic treatment with the neuromuscular blocking agent, d-tubocurarine, and cell cultures of embryonic chicken skeletal muscle which differentiated in the absence of motorneurons expressed little of the late embryonic isoform, indicating that the expression of the late embryonic isoform was dependent on functional nerve-muscle interactions. These different embryonic fast MHC isoforms provide important markers for monitoring the progression of muscle through its embryonic stages and its interaction with motorneurons.

Animals↗

PubMed1998

Muscle development: a transcriptional pathway in myogenesis.

Recent studies have substantially advanced our understanding of the transcriptional program regulating development of the different muscle types in Drosophila. For body wall muscle, a pathway can now be drawn that links the transcription factor Dorsal, inherited from the egg, with the differentiated-muscle protein tropomyosin.

Animals↗

PubMed1998

Mesenchymal-epithelial interactions in bladder smooth muscle development: epithelial specificity.

PURPOSE: We previously showed that mesenchymal-epithelial interactions are necessary for the development of bladder smooth muscle. Specifically without bladder epithelium embryonic bladder mesenchyme does not differentiate into smooth muscle. We determine whether this process is specific to bladder epithelium or whether epithelial cells from other organ systems induce bladder mesenchyme to differentiate into smooth muscle, as well as whether epithelial age is an important variable. MATERIALS AND METHODS: We recombined 14-day bladder mesenchyme before smooth muscle differentiation with rat epithelium from 14-day, 19-day, newborn and adult bladder, ureter, colon, ileum, stomach, cornea and epidermis. In addition, bladder epithelium was recombined with 14-day embryonic small intestinal, 14-day embryonic gastric and newborn seminal vesicle mesenchyme. All tissue recombinants were grafted under the renal capsule of an adult rat syngeneic host for 3 weeks. RESULTS: Immunohistochemical analysis with antibodies directed against smooth muscle alpha-actin revealed that all epithelial types studied induced bladder mesenchyme to differentiate into smooth muscle, although to different degrees. Induction of smooth muscle was independent of urothelial age. In addition, bladder epithelium induced intestinal, gastric and seminal vesicle mesenchyme to differentiate into smooth muscle and express an overall morphological pattern indicative of the bladder fibromuscular wall. CONCLUSIONS: The mechanism whereby urothelium induces bladder mesenchyme to differentiate into smooth muscle is not specific to embryonic urothelium. Older urothelium and heterotypic epithelium also induce smooth muscle differentiation. With the common use of bowel, stomach and ureteral segments for bladder augmentation it is important to understand the interaction of different types of epithelium with the native bladder.

Animals↗

PubMed2001

Mesenchymal-epithelial interactions in bladder smooth muscle development: effects of the local tissue environment.

PURPOSE: We have previously shown that mesenchymal-epithelial interactions are necessary for the development of bladder smooth muscle. Specifically without fetal or adult urothelium embryonic rat bladder mesenchyma does not differentiate into smooth muscle. The mechanism responsible for this interaction is not known, although it is postulated that diffusable growth factors have a role. Our hypothesis is that diffusable factors within adult rat bladders influence smooth muscle differentiation. MATERIALS AND METHODS: Chimeric bladders were created by surgically implanting 14-day embryonic rat bladder mesenchyma before smooth muscle differentiation into the detrusor space of adult syngeneic hosts to test whether the host urothelium would induce smooth muscle differentiation without being in direct contact with fetal bladder mesenchymal tissue. Sub-detrusor pockets were created between the serosa and smooth muscle layer, between the smooth muscle layer and lamina propria, and between the lamina propria and urothelium in direct contact with urothelium. Controls consisted of intact 14-day embryonic rat bladders with the urothelium not removed, and 14-day embryonic bladder mesenchyma recombined with urothelium (direct contact) placed within the sub-detrusor space of the bladder and under the renal capsule. RESULTS: Immunohistochemical staining with antibodies directed against smooth muscle alpha-actin and urothelium (cytokeratin 7) revealed smooth muscle differentiation in intact embryonic bladders and bladder mesenchyma plus urothelium recombinants in contrast to bladder mesenchyma alone, which had no alpha-actin staining (morphometric smooth muscle analysis p = 0). There was no alpha-actin staining in chimeric bladders even when bladder mesenchymal grafts were placed directly in contact with host urothelium. In addition, bladder mesenchyma plus urothelial recombinants within the host bladder had less alpha-actin staining than their counterparts placed under the renal capsule (p = 0.001). CONCLUSIONS: A diffusable factor most likely exists within adult rat bladders that inhibits smooth muscle differentiation.

Animals↗

PubMed1985

Membrane crystals of Ca2+-ATPase in sarcoplasmic reticulum of developing muscle.

The vanadate-induced crystallization of Ca2+-ATPase was analyzed on sarcoplasmic reticulum vesicles isolated between 10 and 28 days of development from pectoralis muscles of chicken. After exposure to Na3VO4 in a Ca2+-free medium, Ca2+-ATPase crystals begin to appear on portions of the surface of a few vesicles, isolated at 18 days of development. Thereafter, the number of vesicles containing Ca2+-ATPase crystals rapidly increases and after 1 week of postnatal development (28 days), it reaches the adult level of about 30% of the vesicle population. These observations are discussed with reference to the mechanism of Ca2+-ATPase crystallization and the regulation of sarcoplasmic reticulum biosynthesis.

Animals↗