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Biomedical subjects

M Pines

Publications and source records attributed to M Pines.

At least 19 recordsLinked to original sources
PubMed1992

Differential post-receptor responses of adenylate cyclase in white and brown adipose tissue membranes of rats fed high-energy diets.

1. Adenylate cyclase activity was determined in membranes of white and brown adipose tissue (WAT and BAT, respectively) from rats fed a high-energy diet (EXP group) vs those fed a nutritionally balanced one (CON group). 2. The isoproterenol- and guanine nucleotide-induced adenylate cyclase activity in WAT membranes of EXP rats was lower than that in CON rats. 3. Relative adenylate cyclase activity in like treated BAT membranes was higher in EXP than in CON rats. 4. It is concluded that feeding high-energy diets to rats induces similar post-receptor modifications of adenylate cyclase as found in genetic obese rodents.

Adenylyl Cyclases↗
PubMed1992

Group-analytic psychotherapy.

Group analysis is a flexible and effective method of providing group psychotherapy, thereby promoting maturation and symptom relief. Its metapsychology remains incompletely worked out but provides potentially exciting interfaces with biological and physical sciences, through Foulkes's (1973) seminal concept of the group matrix.

Humans↗
PubMed1992

Tibia development in turkeys and chickens as affected by early-age feed restriction.

Tibia development was studied by histomorphometry in male chickens and turkeys fed ad libitum throughout the growing period, or subjected to an early-age (1-week) severe feed restriction for 6 and 14 days, respectively. In turkeys, the rates of longitudinal bone growth and epiphyseal width growth, both dependent on the activity of chondrocytes, proceeded rapidly and reached maxima at early ages of 24 and 11 days, respectively. Moreover, longitudinal bone growth and the growth of epiphyseal width were reduced during early-age feed restriction, in both chickens and turkeys. On the other hand, the rate of growth of metaphyseal width, determined by activity of bone cells such as osteoclasts and osteoblasts, reached in turkeys a maximum at the relatively late age of 70 days, and was not influenced by feed restriction. Rhythmic variation characterized the temporal behavior of the height of the hypertrophic and non-hypertrophic zones of the growth plate, the trabecular width, and the osteoclasts number at the subchondral region. Rhythmicity appeared similar in both ad libitum-fed and early-age feed-restricted birds of both species. The height of the non-hypertrophic epiphyseal cartilage appeared not to change, whereas the hypertrophic zone decreased with age and early-age feed restriction, demonstrating the importance of cartilage cell hypertrophy as a main determinant of longitudinal bone growth. Sexual maturation was accompanied by the disappearance of both hypertrophic and non-hypertrophic zones of the epiphyseal growth plate and the end of bone elongation. Trabecular width at the end of bone elongation. Trabecular width at the subchondral region increased while osteoclast number decreased with age, reflecting the net increase in bone mass, but were not affected significantly by early age feed restriction. Compensatory growth of the early-age feed-restricted birds, resulted in the complete recovery of affected bone variables within a few weeks of resumed ad libitum feed intake.

Aging↗
PubMed1991

Natriuretic peptide receptors regulate endothelin synthesis and release from parathyroid cells.

Cloned rat parathyroid cells (PTr cell line) that produce parathyroid hormone-related peptide plus endothelin 1 and primary cultures of human parathyroid cells were tested for growth and differentiation responses to atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP). High- and low-affinity binding sites for ANP were found on PTr cells; BNP appeared to bind to the same receptors with similar affinities. Either ANP or BNP stimulated production of cGMP and caused a 30% decrease in Na(+)-K(+)-Cl- cotransport. Each peptide increased synthesis and secretion of endothelin 1 by PTr cells in a dose-dependent fashion, but cell growth was not affected. Human parathyroid cells (normal and pathological) also responded to ANP or BNP with an increase in cGMP production. The finding of receptors for natriuretic hormones on parathyroid cells with consequent effects on release of endothelin 1 might be of relevance in understanding the clinical association between hyperparathyroidism and hypertension.

Animals↗
PubMed1991

Growth hormone and insulin-like growth factor I regulate collagen gene expression and extracellular collagen in cultures of avian skin fibroblasts.

Avian skin fibroblasts were isolated, cultured and incubated with [3H]proline for 24 h. The cells exported radiolabeled collagenase-digestible (CDP) and non-collagenase-digestible (NCDP) proteins into the medium. Human, bovine and avian growth hormone (GH) as well as insulin-like growth factor I (IGF-I) attenuated the appearance of [3H]CDP in the medium without affecting [3H]NCDP. The appearance of [3H]CDP was not affected by prolactin. The effects of GH and IGF-I were enhanced by increasing concentrations of fetal calf serum (FCS). A synergism was observed between GH and IGF-I in their effect on CDP. Each peptide, at an ineffective concentration, increased the sensitivity of the cells to the other peptide. Collagenase activity in the medium was enhanced by IGF-I, but not modified by GH, FCS, or by their interaction with IGF-I. GH and IGF-I inhibition of type I procollagen gene expression was demonstrated with the aid of probes containing sequences corresponding to the mRNAs for avian alpha I and alpha II chains. The results suggest that GH and IGF-I cooperate in regulating collagen synthesis, but collagen degradation is affected by IGF-I and not by GH.

Animals↗
PubMed1991

Epidermal growth factor receptor gene expression in avian epiphyseal growth-plate cartilage cells: effect of serum, parathyroid hormone and atrial natriuretic peptide.

Avian chondrocytes and fibroblasts, derived from epiphyseal growth-plate and skin, respectively, were cultured in vitro. In chondrocytes, epidermal growth factor (EGF) caused a dose-dependent stimulation of proliferation. EGF receptor mRNA was not detected with the v-erb B probe in chondrocytes cultured in the presence of 5% fetal calf serum (FCS). In the absence of FCS in the medium, a time-dependent increase in the level of EGF receptor mRNA was observed. Parallel changes were also observed in the level of EGF receptor, as demonstrated by immunofluorescence using antibodies directed against avian EGF receptor. In avian fibroblasts, EGF receptor mRNA and EGF receptor levels were not affected by FCS. Furthermore, FCS did not affect the level of thyroid hormone receptor mRNA (using v-erb A as a probe) in either chondrocytes or fibroblasts. Parathyroid hormone (PTH), which acts as a mitogen in avian chondrocytes attenuated--whereas atrial natriuretic peptide (ANP), a suppressor of chondrocyte proliferation, enhanced--EGF receptor mRNA. The present results show that avian growth-plate chondrocytes respond to EGF and bear EGF receptors. The levels of EGF mRNA and EGF receptor are inversely related to cell proliferation. The results also support previous suggestions that PTH and ANP play important roles in chondrocyte proliferation, possibly through their effect on the synthesis of the EGF receptor.

Animals↗
PubMed1991

Increased skin tearing in broilers and reduced collagen synthesis in skin in vivo and in vitro in response to the coccidiostat halofuginone.

In vivo and in vitro experiments were conducted in an effort to elucidate the mechanism of suppression by halofuginone of skin strength in broilers. In the in vivo study, halofuginone was included at concentrations of 0, 1.5, 3, and 6 mg/kg of diet, corresponding to 0, 50, 100, and 200%, respectively, of the amount recommended for use as a coccidiostat. Each dietary treatment was given to 260 female broiler day-old chickens. Skin tearing was evaluated at the processing plant. Skin collagen and Kjeldahl-nitrogen were determined chemically. At the age of 7 wk, BW and feed efficiency were affected only in birds consuming the diet containing the highest concentration of the drug. Skin tearing increased but skin collagen concentration decreased in a dose-dependent manner. Fibroblasts were obtained by collagenase digestion from chicken skin and cultured. The cultured cells were incubated with various concentrations of halofuginone, monensin, and nicarbazin, and [3H]proline incorporation was evaluated in collagenase-digestible (representing mostly collagen) and nondigestible proteins exported by the cells into the medium. Halofuginone, at a concentration as low as 10(-11) M, inhibited incorporation of [3H]proline into collagenase-digestible proteins, but did not affect incorporation of [3H]proline into collagenase-nondigestible proteins. Even at concentrations as high as 10(-9) M, neither monensin nor nicarbazin affected collagenase-digestible proteins. The in vitro results suggest that halofuginone specifically inhibits collagen synthesis by skin fibroblasts. Results of both in vivo and in vitro trials suggest that the increase of skin tearing during processing, induced by halofuginone, is caused by direct suppression of skin collagen synthesis.

Animals↗
PubMed1991

The role of the growth plate in longitudinal bone growth.

The epiphyseal growth plate is the main site of longitudinal growth of the long bones. At this site, cartilage is formed by the proliferation and hypertrophy of cells and synthesis of the typical extracellular matrix. The formed cartilage is then calcified, degraded, and replaced by osseous tissue. Proliferation and differentiation of cartilage cells (i.e., chondrocytes) as studied mostly in culture, is regulated by various endocrine, paracrine, and autocrine agents such as growth hormone, insulin-like growth factor-I (IGF-I), transforming growth factor (TGE-beta), and vitamin D metabolites (1,25-dihydroxycholecalciferol and 24,25-dihydroxycholecalciferol). Avian chondrocyte proliferation is enhanced by agents which use adenosine 3':5'-cyclic monophosphate as a second messenger, such as parathyroid hormone or prostaglandin-E2, and is depressed by guanosine 3':5'-cyclic monophosphate agonists, such as atrial natriuretic peptide. Several of the regulating agents also affect synthesis of the main extracellular components (i.e., collagen and proteoglycans) and their transfer to the extracellular space. Cartilage calcification involves matrix vesicles secreted by the chondrocytes at a specific stage. Calcification probably involves some initial nucleation agent and participation of phosphatases. During sexual maturation, the growth plate closes by an unknown mechanism and longitudinal bone growth ceases. Disorders in the metabolism of the controlling agents or the cellular responses in growth plate may lead to several deformities classified as dysplasias. In poultry, this class of disorders is represented by chondrodystrophy and dyschondroplasia.

Animals↗
PubMed1991

Skin tearing in broilers in relation to skin collagen: effect of sex, strain, and diet.

The relationship between skin tearing and collagen in broilers was investigated in two trials in which strain and sex, and strain and diet served as factorial-arranged variables, respectively. In the first trial, males and females of three strains were examined. Both skin tearing and skin collagen were significantly influenced by strain and sex without any significant strain by sex interaction. Skin collagen, expressed as a fraction of fresh skin protein (N x 6.25) was lower and skin tearing was higher in females than in males, particularly in the most susceptible strain. In the second trial, the effects of supplementary protein or methionine and of a low-density diet were tested in females of two strains that differed in their susceptibility to skin tearing. High dietary protein reduced skin tearing and increased skin collagen. The significant diet by strain interaction resulted from the more pronounced response of the susceptible strain. Neither supplementary methionine nor feeding of low-dietary-density diet significantly affected skin tearing or skin collagen.

Animals↗
PubMed1990

Proliferation of bovine undifferentiated mammary epithelial cells in vitro is modulated by G-proteins.

Several cAMP-elevating agents such as cholera toxin (CT), forskolin and 3-isobutyl-1-methylxanthine (IBMX) exhibited weak mitogenic activity on bovine undifferentiated mammary epithelial cells in three-dimensional collagen culture. CT and IBMX strongly synergized with epidermal growth factor (EGF), insulin-like growth factor I (IGF-I) or both, but not with 10% fetal calf serum (FCS). Permeable cAMP analogs also synergized with IGF-I. Other hormones such as ovine prolactin, bovine growth hormone, estrogen or progesterone were not mitogenic and not synergistic with EGF, IGF-I, CT and FCS. Pertussis toxin (PT) reduced the DNA synthesis in cells cultured in the basal medium and attenuated 40-90% of the mitogenic activity stimulated by 10% FCS. PT inhibition of DNA synthesis was accompanied by ADP-ribosylation of 40 kDa and 41 kDa membrane proteins. The 41 kDa protein cross-reacted with antibodies that recognize the Gi-protein of the adenylate cyclase system, indicating the involvement of the latter in the mitogenic process. The nature of the second protein remains unknown. The present results suggest that the mitogenesis of normal mammary epithelial cells which is stimulated by IGF-I, EGF and other factors found in FCS is mediated through both cAMP-dependent and independent pathways. These pathways include PT-sensitive GTP-binding proteins.

1-Methyl-3-isobutylxanthine↗
PubMed1990

Cyclic AMP-dependent inhibition of collagen synthesis in avian epiphyseal cartilage cells: effect of chicken and human parathyroid hormone and parathyroid hormone-related peptide.

Avian cartilage cells derived from epiphyseal growth-plate and avian skin fibroblasts were cultured in vitro. Production of cAMP by cartilage cells was stimulated by the synthetic fragments (1-34) of chicken (cPTH), human (hPTH) parathyroid hormone and by parathyroid hormone-related peptide (PTHrP). The enhancement of cAMP production by any of the peptides could be blocked by the parathyroid hormone analogue (3-34)PTH, suggesting interaction with PTH specific receptors. When incubated with [3H]proline, both cell types released radiolabelled collagenase-digestible and non-digestible proteins into the medium. cPTH, hPTH, PTHrP, forskolin, prostaglandin E2 (PGE2) and 8-bromo cAMP inhibited collagen production in cartilage cells with only minor effects on non-collagenase digestible proteins. No effect of cAMP on collagen production by fibroblasts was observed. The present results provide additional evidence that avian growth-plate cartilage cells are targets for PTH, and are first to demonstrate the response of a non-mammalian system to mammalian PTHrP. The data suggest that collagen production by epiphyseal growth-plate cartilage cells is inhibited by PTH and that this inhibition is mediated by cAMP.

Animals↗
PubMed1989

Inhibition of aldosterone secretion by atrial natriuretic peptide in chicken adrenocortical cells.

Dispersed chicken adrenocortical cells were preincubated with atrial natriuretic peptide (rANP), sodium nitroprusside (SNP) or 8-bromo cyclic GMP, followed by incubations with ACTH, chicken PTH, cholera toxin or various steroid intermediates of aldosterone production. Cyclic AMP production and aldosterone secretion were evaluated, in order to determine the sites of ANP inhibition in the sequence of events leading to aldosterone secretion. Dose-dependent inhibitory effects on ACTH-stimulated aldosterone secretion by rANP and SNP were observed. Both agents appeared to stimulate cGMP production by the particulate fraction of the avian adrenocortical cells. Aldosterone production, stimulated by cyclic AMP agonists such as ACTH, chicken PTH and cholera toxin, was significantly inhibited by ANP. On the other hand, ANP did not interfere with production or degradation of cAMP. Each of the aldosterone intermediates--pregnenolone, progesterone, 11-deoxycorticosterone and corticosterone--promoted aldosterone production when included in the incubation media. Atrial natriuretic peptide and SNP inhibited aldosterone secretion when enhanced by the intermediates, by about 40-60%, but the ACTH-stimulated secretion was inhibited by over 90%. The results suggest two sites of inhibition by ANP in the pathway of aldosterone synthesis and secretion: synthesis of cholesterol or pregnenolone, and conversion of corticosterone to aldosterone. The inhibition by 8-bromo cGMP of aldosterone secretion and the similar sites of inhibition for ANP and SNP suggest that cyclic GMP mediates the inhibition in both cases.

Adrenal Cortex↗
PubMed1989

Modulation of responsiveness of the adenylate cyclase system in avian chondroprogenitor cells by pertussis toxin, PTH, and PGE2.

Chondroprogenitor cells, derived from avian tibia epiphyseal growth plate, were cultured in vitro. Incubation of these cells with pertussis toxin augmented their cAMP response to parathyroid hormone (PTH), attenuated the response to forskolin, but did not modify the response to PGE2. Pertussis toxin modulation of the cAMP response was accompanied by ADP ribosylation of two proteins with molecular weights of 39 and 40 kD. Using specific antibodies, the 39 kD protein was identified as the inhibitory guanine nucleotide binding protein (Gi) of the adenylate cyclase system. The other ADP-ribosylated protein has not been identified. Preincubation of the chondroprogenitor cells with PTH or PGE2 resulted in time-dependent heterologous desensitization of the cAMP response to a second challenge of either hormone. The cells did not recover from the densitization for at least 18 h after removal of the hormones. PTH and PGE2 treatment did not affect the cAMP response to forskolin and cholera toxin. The PTH-dependent cAMP production was also not altered by forskolin treatment. PTH homologous desensitization was not affected by pertussis toxin treatment, but the heterologous desensitization due to PGE2 was significantly attenuated. These results suggest that exposure of chondroprogenitor cells to PTH and PGE2 results in heterologous desensitization of the cAMP response. The desensitization is not due to changes in the adenylate cyclase activity. The pertussis toxin-sensitive G proteins are involved in the PTH heterologous rather than homologous desensitization of the cAMP response.

Adenosine Diphosphate Ribose↗
PubMed1989

Renal and adrenal adenosine 3',5'-monophosphate production and corticosteroid secretion in response to synthetic chicken parathyroid hormone-(1-34).

The activity of synthetic chicken (c) PTH-(1-34) amide was tested in dispersed chicken and rat kidney and adrenocortical cells. In the adrenal cells the effect of intact cPTH was also evaluated. In chicken kidney cells, the time- and dose-response patterns of cAMP production were similar for cPTH-(1-34) amide and human (h) PTH-(1-34), whereas rat kidney cells were considerably more sensitive to hPTH-(1-34) than to cPTH-(1-34) amide. The agonist effects of both hPTH-(1-34) and cPTH-(1-34) amide in kidney cells were inhibited by the bovine PTH-(3-34) analog. In chicken adrenocortical cells, cPTH-(1-34) amide stimulated cAMP production and steroid secretion. This action of the peptide was inhibited by bovine PTH-(3-34) and hPTH-(1-34), which by themselves showed no agonist effects. The maximal response of steroid secretion to cPTH-(1-34) amide was significantly lower than that to ACTH, but intact cPTH (supplied as a semipurified parathyroid extract) stimulated steriodogenesis to the same extent as ACTH. In rat adrenocortical cells, intact cPTH stimulated both cAMP formation and steriodogenesis, but cPTH-(1-34) amine showed no agonist effect. The action of the intact hormone in the rat adrenal could be inhibited by cPTH-(1-34) amide. The present results demonstrate the interaction of cPTH-(1-34) with kidney and adrenocortical cells of either chicken or rat. The cAMP and steroidogenic responses of the adrenocortical cells to PTH appear to be dependent (completely in the rat and partially in the chicken) on some sequence beyond the 1-34 region.

Adrenal Cortex Hormones↗
PubMed1989

Atrial natriuretic peptide and sodium nitroprusside stimulate cyclic GMP accumulation by avian skin fibroblasts and epiphyseal growth-plate chondroprogenitor cells.

Chondroprogenitor cells derived from avian tibia epiphyseal growth plate, and skin fibroblasts were cultured in vitro. In the fibroblasts, human (1-28) and rat (5-28) atrial natriuretic peptide (ANP) stimulated cyclic GMP (cGMP) production in a dose-dependent manner without affecting cAMP. Sodium nitroprusside also stimulated cGMP accumulation by chondroprogenitor cells and fibroblasts, but the maximum cGMP accumulation elicited by sodium nitroprusside was much lower than that obtained with ANP. The effects of ANP and sodium nitroprusside on chondroprogenitor cells and skin fibroblasts were additive. Human ANP increased cGMP production by the particulate fraction prepared either from chondroprogenitor cells or fibroblasts. Sodium nitroprusside, at concentrations of up to 1 mmol/l, did not affect cGMP production by the particulate fraction prepared from either cell type. The present study provides additional evidence that avian growth-plate chondroprogenitor cells and skin fibroblasts are targets for ANP. ANP and nitroprusside activate different guanylate cyclase isoenzymes--the particulate and soluble forms of the enzyme respectively. The data suggest that most of the guanylate cyclase activity in these cells is localized in the particulate fraction.

1-Methyl-3-isobutylxanthine↗
PubMed1988

Nucleotide sequence of cloned cDNAs encoding chicken preproparathyroid hormone.

In order to characterize an avian parathyroid hormone gene, a lambda gt10 cDNA library constructed from chicken parathyroid gland mRNA was screened with a human preproparathyroid hormone (preproPTH) cDNA probe. Nucleotide sequence analysis of three independent clones confirmed that they encoded chicken preproPTH. This analysis, complemented by primer extension and Northern blot analysis of mRNA, demonstrated a 5'-untranslated region for chicken preproPTH of 127 nucleotides, a coding region of 357 nucleotides, and a 3'-untranslated region of approximately 2500 nucleotides. The coding sequence predicts a mature chicken PTH of 88 amino acids in contrast to the 84 amino acids of the mammalian hormones. Comparison of the avian and the mammalian hormones shows striking homology in the region of amino acids 1-32. The middle and carboxyl-terminal portions of chicken PTH, however, differ considerably from the mammalian hormones and include deletions of sequences conserved in mammalian PTH and insertions of novel peptide sequences. Comparison of the avian and mammalian structures suggests potential alterations of the mammalian sequences that may lead to altered bioactivity and/or hormone metabolism.

Amino Acid Sequence↗
PubMed1988

Inhibition of the proliferation of Nb2 cells by femtomolar concentrations of cholera toxin and partial reversal of the effect by 12-O-tetradecanoyl-phorbol-13-acetate.

One hour of exposure to cholera toxin is sufficient to elicit a significant delay in the initiation of DNA synthesis and cell division in lactogenic hormone-dependent Nb2-11C lymphoma cells. The inhibitory effect occurs already at very low concentrations of cholera toxin (5-50 fM), at which it is not accompanied by a detectable increase in intracellular cAMP, or ADP-ribosylation of the alpha subunit of Gs, the stimulatory guanine nucleotide binding protein of adenylate cyclase; IBMX, the phosphodiesterase inhibitor, acts synergistically to cholera toxin, indicating that a minute increase in cAMP may be sufficient for the inhibition. This indication is substantiated by the finding that dibutyryl cAMP also inhibits cell proliferation. Phorbol diester reverses partially the inhibitory activity of cholera toxin. It is most likely that this effect does not result from blocking the increase in cAMP, but rather from some subsequent, yet unidentified, events. The inhibitory effect of cholera toxin is not dependent on the concentration of the proliferation-stimulating lactogenic hormone and cannot be abolished or reduced by excess of the hormone. Cholera toxin also inhibits the autonomous proliferation of a lactogenic hormone-independent cell line (Nb2-SP); however, in this case the inhibition is not affected by TPA.

Animals↗