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Alpha Adrenergic Stimulation

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Godfried M. Roomans – One of the best experts on this subject based on the ideXlab platform.

  • Changes in calcium concentrations in subcellular compartments of rat submandibular gland acinar cells induced by cholinergic Stimulation.
    Histochemistry and cell biology, 1999
    Co-Authors: A.-l. Zhang, J. R. Martinez, Godfried M. Roomans
    Abstract:

    The effects of cholinergic and AlphaAdrenergic Stimulation on calcium concentrations in rat submandibular gland acinar cells were evaluated at the subcellular level by electron probe X-ray micrmicroanalysis, and the subcellular distribution of receptors for inositol 1,4,5-trisphosphate (IP(3)Rs) was investigated by electron microscopic immunohistochemistry. For measurement of calcium concentrations, experiments were carried out both in vivo and in vitro. In in vivo experiments, fragments of glands were removed and slam-frozen 3 min after intraperitoneal injection of an agonist. In in vitro experiments, the gland tissue was enzymatically dispersed, treated with an agonist in the presence or absence of extracellular Ca(2+), and slam-frozen. The frozen specimens were cut into ultrathin cryosections, which were then freeze dried. Spectra were collected from secretory granules, the perinuclear cytoplasm containing endoplasmic retireticulum (ER), and the nucleus of the acinar cells. A clear decrease in calcium content in secretory granules was observed after cholinergic Stimulation both in vivo and in vitro in the presence or absence of extracellular Ca(2+). In the presence of extracellular Ca(2+), cholinergic Stimulation following AlphaAdrenergic Stimulation reduced the calcium content in secretory granules to the same extent as cholinergic Stimulation alone. No significant changes in the calcium content of the perinuclear cytoplasm and the nucleus were noticed after cholinergic Stimulation. AlphaAdrenergic Stimulation did not significantly affect the calcium concentrations in any of the three compartments studied. IP(3)Rs were localized to ER lamellae, but not to secretory granule membranes or to nuclear membranes. Our findings suggest that: (1) in rat submandibular acini, Ca(2+) can be released from secretory granules by exposure to cholinergic, but not AlphaAdrenergic, stimuli, (2) there are, however, no IP(3)Rs present in the granular membrane and the trigger for the Ca(2+) release remains under study, and (3) the response to either type of stimulus does not involve changes in the Ca(2+) content of the nucleus or of the perinuclear cytoplasm/ER, despite the presence of IP(3)Rs in the latter structure. This may be the result of limitation in the technique used, which cannot measure changes in the proper compartment of the ER.

  • Effects of cholinergic and AlphaAdrenergic agonists on the monovalent ion content of rat submandibular gland acinar cells studied by X-ray microanalysis.
    Histochemistry and cell biology, 1997
    Co-Authors: A.-l. Zhang, J. R. Martinez, Godfried M. Roomans
    Abstract:

    The effects of cholinergic and AlphaAdrenergic Stimulation (in vivo and in vitro) on the monovalent ion content of rat submandibular gland acinar cells were evaluated at the subcellular level by X-ray micrmicroanalysis. Fragments of glands or enzymatically dispersed acini were slam-frozen and cut into ultrathin cryosections. Spectra were collected from secretory granules, nucleus, the basal cytoplasm containing endoplasmic retireticulum and the apical cytoplasm identified between secretory granules. No significant changes in Na and Cl content were observed after the isolation of acini, but the K concentration decreased compared with cells from in situ glands. The Cl and K content in all four compartments studied decreased significantly after cholinergic Stimulation both in vivo and in vitro but in a more restricted fashion after AlphaAdrenergic Stimulation. Our findings indicate that: (1) the physiological mechanisms regulating the monovalent ion composition of submandibular cells are relatively well preserved in isolated acinar cells; (2) the results from in vivo experiments are in good agreement with those from in vitro experiments; and (3) the effects of cholinergic and AlphaAdrenergic Stimulation on the K+ and Cl- efflux at the subcellular level are similar but the response is generally less with AlphaAdrenergic Stimulation.

A.-l. Zhang – One of the best experts on this subject based on the ideXlab platform.

  • Changes in calcium concentrations in subcellular compartments of rat submandibular gland acinar cells induced by cholinergic Stimulation.
    Histochemistry and cell biology, 1999
    Co-Authors: A.-l. Zhang, J. R. Martinez, Godfried M. Roomans
    Abstract:

    The effects of cholinergic and AlphaAdrenergic Stimulation on calcium concentrations in rat submandibular gland acinar cells were evaluated at the subcellular level by electron probe X-ray microanalysis, and the subcellular distribution of receptors for inositol 1,4,5-trisphosphate (IP(3)Rs) was investigated by electron microscopic immunohistochemistry. For measurement of calcium concentrations, experiments were carried out both in vivo and in vitro. In in vivo experiments, fragments of glands were removed and slam-frozen 3 min after intraperitoneal injection of an agonist. In in vitro experiments, the gland tissue was enzymatically dispersed, treated with an agonist in the presence or absence of extracellular Ca(2+), and slam-frozen. The frozen specimens were cut into ultrathin cryosections, which were then freeze dried. Spectra were collected from secretory granules, the perinuclear cytoplasm containing endoplasmic reticulum (ER), and the nucleus of the acinar cells. A clear decrease in calcium content in secretory granules was observed after cholinergic Stimulation both in vivo and in vitro in the presence or absence of extracellular Ca(2+). In the presence of extracellular Ca(2+), cholinergic Stimulation following AlphaAdrenergic Stimulation reduced the calcium content in secretory granules to the same extent as cholinergic Stimulation alone. No significant changes in the calcium content of the perinuclear cytoplasm and the nucleus were noticed after cholinergic Stimulation. AlphaAdrenergic Stimulation did not significantly affect the calcium concentrations in any of the three compartments studied. IP(3)Rs were localized to ER lamellae, but not to secretory granule membranes or to nuclear membranes. Our findings suggest that: (1) in rat submandibular acini, Ca(2+) can be released from secretory granules by exposure to cholinergic, but not AlphaAdrenergic, stimuli, (2) there are, however, no IP(3)Rs present in the granular membrane and the trigger for the Ca(2+) release remains under study, and (3) the response to either type of stimulus does not involve changes in the Ca(2+) content of the nucleus or of the perinuclear cytoplasm/ER, despite the presence of IP(3)Rs in the latter structure. This may be the result of limitation in the technique used, which cannot measure changes in the proper compartment of the ER.

  • Effects of cholinergic and AlphaAdrenergic agonists on the monovalent ion content of rat submandibular gland acinar cells studied by X-ray microanalysis.
    Histochemistry and cell biology, 1997
    Co-Authors: A.-l. Zhang, J. R. Martinez, Godfried M. Roomans
    Abstract:

    The effects of cholinergic and AlphaAdrenergic Stimulation (in vivo and in vitro) on the monovalent ion content of rat submandibular gland acinar cells were evaluated at the subcellular level by X-ray microanalysis. Fragments of glands or enzymatically dispersed acini were slam-frozen and cut into ultrathin cryosections. Spectra were collected from secretory granules, nucleus, the basal cytoplasm containing endoplasmic reticulum and the apical cytoplasm identified between secretory granules. No significant changes in Na and Cl content were observed after the isolation of acini, but the K concentration decreased compared with cells from in situ glands. The Cl and K content in all four compartments studied decreased significantly after cholinergic Stimulation both in vivo and in vitro but in a more restricted fashion after AlphaAdrenergic Stimulation. Our findings indicate that: (1) the physiological mechanisms regulating the monovalent ion composition of submandibular cells are relatively well preserved in isolated acinar cells; (2) the results from in vivo experiments are in good agreement with those from in vitro experiments; and (3) the effects of cholinergic and AlphaAdrenergic Stimulation on the K+ and Cl- efflux at the subcellular level are similar but the response is generally less with AlphaAdrenergic Stimulation.

William I. Wood – One of the best experts on this subject based on the ideXlab platform.

  • cardiotrophin 1 activates a distinct form of cardiac muscle cell hypertrophy assembly of sarcomeric units in series via gp130 leukemia inhibitory factor receptor dependent pathways
    Journal of Biological Chemistry, 1996
    Co-Authors: Kai C Wollert, Christopher C Glembotski, Tetsuya Taga, Mikiyoshi Saito, Masashi Narazaki, Tadamitsu Kishimoto, Ann B Vernallis, John K. Heath, Diane Pennica, William I. Wood
    Abstract:

    Cardiotrophin-1 (CT-1) was recently isolated by expression cloning based on its ability to induce an increase in cell size in neonatal rat ventricular cardiomyocytes. Sequence similarity data suggested that CT-1 is a novel member of a family of structurally related cytokines sharing the receptor component gp130. The present study documents that gp130 is required for CT-1 signaling in cardiomyocytes, by demonstrating that a monoclonal anti-gp130 antibody completely inhibits c-fos induction by CT-1. Similarly, a leukemia inhibitory factor receptor subunit beta (LIFRbeta) antagonist effectively blocks the CT-1 induction of c-fos, indicating a requirement for LIFRbeta in the hypertrophic response, as well. Upon Stimulation with CT-1, both gpl30 and the LIFRbeta are tyrosine-phosphorylated, providing further evidence that CT-1 signals through the gp130/LIFRbeta heterodimer in cardiomyocytes. CT-1 induces a hypertrophic response in cardiomyocytes that is distinct from the phenotype seen after AlphaAdrenergic Stimulation, both with regard to cell morphology and gene exprexpression pattern. Stimulation with CT-1 results in an increase in cardiac cell size that is characterized by an increase in cell length but no significant change in cell width. Confocal laser microscopy of CT-1 stimulated cells reveals the assembly of sarcomeric units in series rather than in parallel, as seen after AlphaAdrenergic Stimulation. CT-1 induces a distinct pattern of immediate early genes, and up-regulates the atrial natriuretic factor (ANF) gene, but does not affect skeletal Alphaactin or myosin light chain-2v expression. As evidenced by nuclear run-on transcription assays, both CT-1 and AlphaAdrenergic Stimulation lead to an increase in ANF gene transcription. Transient transfection analyses document that, in contrast to AlphaAdrenergic Stimulation, the CT-1 responsive cis-regulatory elements are located outside of the proximal 3 kilobase pairs of the ANF 5′-flanking region. These studies indicate that CT-1 can activate a distinct form of myocardial cell hypertrophy, characterized by the promotion of sarcomere assembly in series, via gpl30/LIFRbeta-dependent signaling pathways.

  • Cardiotrophin-1 Activates a Distinct Form of Cardiac Muscle Cell Hypertrophy ASSEMBLY OF SARCOMERIC UNITS IN SERIES VIA gp130/LEUKEMIA INHIBITORY FACTOR RECEPTOR-DEPENDENT PATHWAYS
    The Journal of biological chemistry, 1996
    Co-Authors: Kai C Wollert, Christopher C Glembotski, Tetsuya Taga, Mikiyoshi Saito, Masashi Narazaki, Tadamitsu Kishimoto, Ann B Vernallis, John K. Heath, Diane Pennica, William I. Wood
    Abstract:

    Cardiotrophin-1 (CT-1) was recently isolated by expression cloning based on its ability to induce an increase in cell size in neonatal rat ventricular cardiomyocytes. Sequence similarity data suggested that CT-1 is a novel member of a family of structurally related cytokines sharing the receptor component gp130. The present study documents that gp130 is required for CT-1 signaling in cardiomyocytes, by demonstrating that a monoclonal anti-gp130 antibody completely inhibits c-fos induction by CT-1. Similarly, a leukemia inhibitory factor receptor subunit beta (LIFRbeta) antagonist effectively blocks the CT-1 induction of c-fos, indicating a requirement for LIFRbeta in the hypertrophic response, as well. Upon Stimulation with CT-1, both gpl30 and the LIFRbeta are tyrosine-phosphorylated, providing further evidence that CT-1 signals through the gp130/LIFRbeta heterodimer in cardiomyocytes. CT-1 induces a hypertrophic response in cardiomyocytes that is distinct from the phenotype seen after AlphaAdrenergic Stimulation, both with regard to cell morphology and gene exprexpression pattern. Stimulation with CT-1 results in an increase in cardiac cell size that is characterized by an increase in cell length but no significant change in cell width. Confocal laser microscopy of CT-1 stimulated cells reveals the assembly of sarcomeric units in series rather than in parallel, as seen after AlphaAdrenergic Stimulation. CT-1 induces a distinct pattern of immediate early genes, and up-regulates the atrial natriuretic factor (ANF) gene, but does not affect skeletal Alphaactin or myosin light chain-2v expression. As evidenced by nuclear run-on transcription assays, both CT-1 and AlphaAdrenergic Stimulation lead to an increase in ANF gene transcription. Transient transfection analyses document that, in contrast to AlphaAdrenergic Stimulation, the CT-1 responsive cis-regulatory elements are located outside of the proximal 3 kilobase pairs of the ANF 5′-flanking region. These studies indicate that CT-1 can activate a distinct form of myocardial cell hypertrophy, characterized by the promotion of sarcomere assembly in series, via gpl30/LIFRbeta-dependent signaling pathways.

Christopher C Glembotski – One of the best experts on this subject based on the ideXlab platform.

  • cardiotrophin 1 activates a distinct form of cardiac muscle cell hypertrophy assembly of sarcomeric units in series via gp130 leukemia inhibitory factor receptor dependent pathways
    Journal of Biological Chemistry, 1996
    Co-Authors: Kai C Wollert, Christopher C Glembotski, Tetsuya Taga, Mikiyoshi Saito, Masashi Narazaki, Tadamitsu Kishimoto, Ann B Vernallis, John K. Heath, Diane Pennica, William I. Wood
    Abstract:

    Cardiotrophin-1 (CT-1) was recently isolated by expression cloning based on its ability to induce an increase in cell size in neonatal rat ventricular cardiomyocytes. Sequence similarity data suggested that CT-1 is a novel member of a family of structurally related cytokines sharing the receptor component gp130. The present study documents that gp130 is required for CT-1 signaling in cardiomyocytes, by demonstrating that a monoclonal anti-gp130 antibody completely inhibits c-fos induction by CT-1. Similarly, a leukemia inhibitory factor receptor subunit beta (LIFRbeta) antagonist effectively blocks the CT-1 induction of c-fos, indicating a requirement for LIFRbeta in the hypertrophic response, as well. Upon Stimulation with CT-1, both gpl30 and the LIFRbeta are tyrosine-phosphorylated, providing further evidence that CT-1 signals through the gp130/LIFRbeta heterodimer in cardiomyocytes. CT-1 induces a hypertrophic response in cardiomyocytes that is distinct from the phenotype seen after AlphaAdrenergic Stimulation, both with regard to cell morphology and gene expression pattern. Stimulation with CT-1 results in an increase in cardiac cell size that is characterized by an increase in cell length but no significant change in cell width. Confocal laser microscopy of CT-1 stimulated cells reveals the assembly of sarcomeric units in series rather than in parallel, as seen after AlphaAdrenergic Stimulation. CT-1 induces a distinct pattern of immediate early genes, and up-regulates the atrial natriuretic factor (ANF) gene, but does not affect skeletal Alpha-actin or myosin light chain-2v expression. As evidenced by nuclear run-on transcription assays, both CT-1 and AlphaAdrenergic Stimulation lead to an increase in ANF gene transcription. Transient transfection analyses document that, in contrast to AlphaAdrenergic Stimulation, the CT-1 responsive cis-regulatory elements are located outside of the proximal 3 kilobase pairs of the ANF 5′-flanking region. These studies indicate that CT-1 can activate a distinct form of myocardial cell hypertrophy, characterized by the promotion of sarcomere assembly in series, via gpl30/LIFRbeta-dependent signaling pathways.

  • Cardiotrophin-1 Activates a Distinct Form of Cardiac Muscle Cell Hypertrophy ASSEMBLY OF SARCOMERIC UNITS IN SERIES VIA gp130/LEUKEMIA INHIBITORY FACTOR RECEPTOR-DEPENDENT PATHWAYS
    The Journal of biological chemistry, 1996
    Co-Authors: Kai C Wollert, Christopher C Glembotski, Tetsuya Taga, Mikiyoshi Saito, Masashi Narazaki, Tadamitsu Kishimoto, Ann B Vernallis, John K. Heath, Diane Pennica, William I. Wood
    Abstract:

    Cardiotrophin-1 (CT-1) was recently isolated by expression cloning based on its ability to induce an increase in cell size in neonatal rat ventricular cardiomyocytes. Sequence similarity data suggested that CT-1 is a novel member of a family of structurally related cytokines sharing the receptor component gp130. The present study documents that gp130 is required for CT-1 signaling in cardiomyocytes, by demonstrating that a monoclonal anti-gp130 antibody completely inhibits c-fos induction by CT-1. Similarly, a leukemia inhibitory factor receptor subunit beta (LIFRbeta) antagonist effectively blocks the CT-1 induction of c-fos, indicating a requirement for LIFRbeta in the hypertrophic response, as well. Upon Stimulation with CT-1, both gpl30 and the LIFRbeta are tyrosine-phosphorylated, providing further evidence that CT-1 signals through the gp130/LIFRbeta heterodimer in cardiomyocytes. CT-1 induces a hypertrophic response in cardiomyocytes that is distinct from the phenotype seen after AlphaAdrenergic Stimulation, both with regard to cell morphology and gene expression pattern. Stimulation with CT-1 results in an increase in cardiac cell size that is characterized by an increase in cell length but no significant change in cell width. Confocal laser microscopy of CT-1 stimulated cells reveals the assembly of sarcomeric units in series rather than in parallel, as seen after AlphaAdrenergic Stimulation. CT-1 induces a distinct pattern of immediate early genes, and up-regulates the atrial natriuretic factor (ANF) gene, but does not affect skeletal Alpha-actin or myosin light chain-2v expression. As evidenced by nuclear run-on transcription assays, both CT-1 and AlphaAdrenergic Stimulation lead to an increase in ANF gene transcription. Transient transfection analyses document that, in contrast to AlphaAdrenergic Stimulation, the CT-1 responsive cis-regulatory elements are located outside of the proximal 3 kilobase pairs of the ANF 5′-flanking region. These studies indicate that CT-1 can activate a distinct form of myocardial cell hypertrophy, characterized by the promotion of sarcomere assembly in series, via gpl30/LIFRbeta-dependent signaling pathways.

  • the Alpha Adrenergic Stimulation of atrial natriuretic factor expression in cardiac myocytes requires calcium influx protein kinase c and calmodulin regulated pathways
    Journal of Biological Chemistry, 1991
    Co-Authors: C A Sei, C E Irons, Amy B Sprenkle, Patrick M Mcdonough, Joan Heller Brown, Christopher C Glembotski
    Abstract:

    Abstract It has been shown recently that AlphaAdrenergic agonists can stimulate atrial natriuretic factor (ANF) expression in ventricular cardiac myocytes; however, little is known about the intracellular signals mediating this activation. The present study focused on the potential roles of calcium-regulated kinases and calcium influx in the AlphaAdrenergic Stimulation of ANF gene expression in ventricular myocardial cell cultures. Myocardial cells maintained for 48 h in serum-free medium supplemented with phenylephrine (PE) possessed up to 15-fold higher levels of ANF peptide and ANF mRNA than control cells. The removal of PE, or the addition of nifedipine, resulted in a rapid decline in ANF expression, suggesting that the sustained elevation of some intracellular messenger (e.g. calcium and/or phospholipid hydrolysis products) was required for the Adrenergic response. The calcium channel agonist BAY K 8644 was capable of increasing ANF expression in a nifedipine-sensitive manner; however, unlike PE, it did not stimulate phosphoinositide hydrolysis. The protein kinase C inhibitor, H7, caused an approximate 75% reduction in PE-stimulated ANF expression, but had no effect on BAY K-stimulated expression. W7, a calcium/calmodulin inhibitor, completely blocked the effects of both PE and BAY K 8644. The addition of either H7 or W7 24 h after the PE addition resulted in a decline of ANF expression. These results indicate that AlphaAdrenergic agonists augment ANF gene expression through at least two pathways, one that is H7-sensitive, perhaps involving the sustained activation of protein kinase C, and the other that is W7-sensitive, perhaps involving the sustained activation of calmodulin-regulated kinases. Further, it appears that BAY K 8644-mediated increases in ANF expression are independent of protein kinase C activation and dependent on calmodulin-regulated events.

J. R. Martinez – One of the best experts on this subject based on the ideXlab platform.

  • Changes in calcium concentrations in subcellular compartments of rat submandibular gland acinar cells induced by cholinergic Stimulation.
    Histochemistry and cell biology, 1999
    Co-Authors: A.-l. Zhang, J. R. Martinez, Godfried M. Roomans
    Abstract:

    The effects of cholinergic and AlphaAdrenergic Stimulation on calcium concentrations in rat submandibular gland acinar cells were evaluated at the subcellular level by electron probe X-ray microanalysis, and the subcellular distribution of receptors for inositol 1,4,5-trisphosphate (IP(3)Rs) was investigated by electron microscopic immunohistochemistry. For measurement of calcium concentrations, experiments were carried out both in vivo and in vitro. In in vivo experiments, fragments of glands were removed and slam-frozen 3 min after intraperitoneal injection of an agonist. In in vitro experiments, the gland tissue was enzymatically dispersed, treated with an agonist in the presence or absence of extracellular Ca(2+), and slam-frozen. The frozen specimens were cut into ultrathin cryosections, which were then freeze dried. Spectra were collected from secretory granules, the perinuclear cytoplasm containing endoplasmic reticulum (ER), and the nucleus of the acinar cells. A clear decrease in calcium content in secretory granules was observed after cholinergic Stimulation both in vivo and in vitro in the presence or absence of extracellular Ca(2+). In the presence of extracellular Ca(2+), cholinergic Stimulation following AlphaAdrenergic Stimulation reduced the calcium content in secretory granules to the same extent as cholinergic Stimulation alone. No significant changes in the calcium content of the perinuclear cytoplasm and the nucleus were noticed after cholinergic Stimulation. AlphaAdrenergic Stimulation did not significantly affect the calcium concentrations in any of the three compartments studied. IP(3)Rs were localized to ER lamellae, but not to secretory granule membranes or to nuclear membranes. Our findings suggest that: (1) in rat submandibular acini, Ca(2+) can be released from secretory granules by exposure to cholinergic, but not AlphaAdrenergic, stimuli, (2) there are, however, no IP(3)Rs present in the granular membrane and the trigger for the Ca(2+) release remains under study, and (3) the response to either type of stimulus does not involve changes in the Ca(2+) content of the nucleus or of the perinuclear cytoplasm/ER, despite the presence of IP(3)Rs in the latter structure. This may be the result of limitation in the technique used, which cannot measure changes in the proper compartment of the ER.

  • Effects of cholinergic and AlphaAdrenergic agonists on the monovalent ion content of rat submandibular gland acinar cells studied by X-ray microanalysis.
    Histochemistry and cell biology, 1997
    Co-Authors: A.-l. Zhang, J. R. Martinez, Godfried M. Roomans
    Abstract:

    The effects of cholinergic and AlphaAdrenergic Stimulation (in vivo and in vitro) on the monovalent ion content of rat submandibular gland acinar cells were evaluated at the subcellular level by X-ray microanalysis. Fragments of glands or enzymatically dispersed acini were slam-frozen and cut into ultrathin cryosections. Spectra were collected from secretory granules, nucleus, the basal cytoplasm containing endoplasmic reticulum and the apical cytoplasm identified between secretory granules. No significant changes in Na and Cl content were observed after the isolation of acini, but the K concentration decreased compared with cells from in situ glands. The Cl and K content in all four compartments studied decreased significantly after cholinergic Stimulation both in vivo and in vitro but in a more restricted fashion after AlphaAdrenergic Stimulation. Our findings indicate that: (1) the physiological mechanisms regulating the monovalent ion composition of submandibular cells are relatively well preserved in isolated acinar cells; (2) the results from in vivo experiments are in good agreement with those from in vitro experiments; and (3) the effects of cholinergic and AlphaAdrenergic Stimulation on the K+ and Cl- efflux at the subcellular level are similar but the response is generally less with AlphaAdrenergic Stimulation.