PubMed Health⌕ Search

Biomedical subjects

J R Florini

Publications and source records attributed to J R Florini.

At least 73 records · Page 4Linked to original sources
PubMed1977

Effects of multiplication stimulating activity (MSA) on AIB transport into myoblast and myotube cultures.

The effects of a somatomedian analog, Temin's multiplication stimulating activity (MSA), on amino acid transport into muscle cells have been characterized in a series of experiments on myoblasts and myotubes in culture. Addition of MSA to serum-starved L6 myoblasts increased the rate of aminoisobutyrate (AIB) uptake 50-150% within five hours. This early effect on transport was followed by increases in cell number, protein content and 3H-thymidine incorporation. Kinetic analyses indicated that MSA increased the maximal velocity of AIB uptake but had no effect on the KM for AIB. When myoblasts were allowed to fuse (and dividing cells eliminated by addition of 10(-4) M cytosine arabinoside) the AIB transport system(s) remained similarly responsive to MSA. In myoblasts and in myotubes, both the basal and MSA-stimulated rate of AIB uptake were sodium-dependent processes; little stimrulation occurred if sodium was absent from the labeling medium. Further suggesting the involvement of cations in response to hormone, MSA stimulated uptake of the potassium analog, 86Rb+, and increase net intracellular potassium in both myoblasts and myotubes. MSA was active at concentrations equivalent to in vivo levels of somatomedins; neither insulin nor growth hormone had any effect at or near physiological concentrations.

Aminoisobutyric Acids↗
PubMed1977

Effects of peptide anabolic hormones on growth of myoblasts in culture.

The roles of growth hormone and somatomedin in stimulating muscle cell proliferation were investigated in a series of experiments on myoblast growth in culture. At levels 100 times normal circulating concentrations, neither growth hormone nor insulin stimulated growth of rat muscle cells in serum-free medium. In contrast, Temin's Multiplication Stimulating Activity (MSA), a close biological and chemical analog which served as a somatomedin surrogate in this study, was active at concentrations corresponding to the reported circulating levels of the somatomedins; MSA gave consistent stimulation of myoblast proliferation, protein accumulation, and [3H]thymidine incorporation by rat myoblasts and by Yaffe's L6 myogenic cell line. (The unreliability of [3H]thymidine in corporation as a quantitative assay for mitogenic activity is illustrated.) Addition of insulin at physiological concentrations and at the very high levels often used to stimulate cell growth did not enhance the effects of MSA on myoblast proliferation; effects were barely additive. We interpret these results to support earlier indications from studies on diaphragm muscle that the somatomedins are physiologically important mediators of the growth-promoting actions of growth hormone in muscle.

Animals↗
PubMed1976

Variations among individual mice in binding of growth hormone and insulin to membranes from animals of different ages.

Binding of 125I-labeled insulin and growth hormone to membranes from liver and hearts of C57BL/6J mice was measured and the data analyzed by the graphical method of Scatchard. Animals were studied at ages 2, 10, 20, and 31 months; preparations from each animal were analyzed individually. There was no significant and progressive age-related difference in either dissociation constant or binding capacity for insulin in heart and liver, or for growth hormone in liver. Variations among individual animals were large; in some cases, the standard deviation exceeded the mean for a particular age group. We conclude that there are no large age related differences in binding of these anabolic hormones to the target tissues studied, and that any small changes would be masked by the large variations among individual animals.

Aging↗
PubMed1975

"Spontaneously" hypertensive mice: a potential genetic model for the study of the relationship between heart size and blood pressure.

Mice selected genetically for high and low blood pressure (BP) were compared with regard to heart weight and heart/body ratios. Two experiments were performed with mice ranging in age from 1.3 to 9 months and 11 to 23 months respectively. In a third experiment C57BL/6J mice were compared to the high and low BP mice. Heart/body ratios and heart weights, adjusted fo body weight via covariance analysis, were significantly greater for the high BP mice, but no Age x BP Genotype interaction was observed. Results were discussed in terms of a possible relationship between heart weight and BP via genetic linkage or pleiotropy. The possibility was also raised that compensatory mechanisms for high blood pressure, e.g., cardiac hypertrophy, may operate very early in development for animals who are hypertensive by virtue of selective breeding for blood pressure extremes.

Age Factors↗
PubMed1975

A direct effect of testosterone on muscle cells in tissue culture.

A direct effect of physiological levels of testosterone on skeletal muscle cells in tissue culture is reported. The effect is a 25% stimulation of labeling index by radioautographic analysis of cultures following incubation with [3H]thymidine at the end of a 48-h exposure to 10(-8)M testosterone in 2% gelding serum. This stimulation was observed in primary myoblasts, an established myogenic cell line (Yaffe's L6 cells), and muscle fibroblasts. The effect was specific for testosterone: the labeling index did not change significantly from control values when estradiol, 5beta-pregnanediol, androstenedione, or dihydrotestosterone were added, although small increases were noted in the latter two cases. The effect on the labeling index was localized as a decrease in time spent in the G1 phase of the cell cycle, which decreased about 30% in muscle cells exposed to testosterone. This first report of an effect of testosterone on isolated muscle cells, coupled with the recent description of a receptor for anabolic steroids in muscle cytoplasm, indicates that the effects of male sex hormones result from a direct interaction with muscle rather than from a primary interaction with some other tissue.

Cell Line↗