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Details for anatomical structure: acidophil somatotroph cell of anterior pituitary

EndoNet ID: ENC00002

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Synonyms

acidophil somatotroph cell of anterior pituitary, chromophil cell, Endocrinocytus acidophilus

General information

secreting growth hormone (HGH)

Links to other resources

Cytomer cy0011193

Larger structures

    Substructures

      Secreted hormones

      • Hormone: angiotensin II

      • Hormone: galanin

      • Hormone: motilin

      • Hormone: TRH

      • Hormone: IGF-1

      • Hormone: GH

        • GH secretion is regulated by indirect negative feedback mechanisms via autocrine actions of GH at the pituitary. [2]

        Influenced by:

        • sst5
          in acidophil_somatotroph_cell_of_anterior_pituitary
          • SSTR2 and SSTR5 mediate suppression of GH and TSH secretion. [3]
          • SRIF and CST similarly inhibited (p < 0.05) spontaneous GH secretion of about 90%. [4]
          • Somatostatin induced inhibition of GH secretion is mediated through (SSTR) 2 and 5. [5]
        • GHS-R1
          in acidophil_somatotroph_cell_of_anterior_pituitary
        • GHRH-R
          in acidophil_somatotroph_cell_of_anterior_pituitary
        • IGF-1R
          in acidophil_somatotroph_cell_of_anterior_pituitary
        • sst2
          in acidophil_somatotroph_cell_of_anterior_pituitary
          • SSTR2 and SSTR5 mediate suppression of GH and TSH secretion. [3]
          • SRIF and CST similarly inhibited (p < 0.05) spontaneous GH secretion of about 90%. [4]
          • Somatostatin induced inhibition of GH secretion is mediated through (SSTR) 2 and 5. [5]
        • CXCR1
          in acidophil_somatotroph_cell_of_anterior_pituitary
          • CINC/gro stiumaletes GH secretion from anterior pituitary monolayer cultures in a concentration-dependent manner with a substantial lag time. [6]
        • leptin receptor
          in acidophil_somatotroph_cell_of_anterior_pituitary
          • Leptin-deficient patients although exhibited normal height, presented decreased GH response to ITT and physical exercise, whereas leptin-resitant patients subjects have significant growth delay during early childhood and decreased GH secretion. [7]
        • GHS-R1
          in hypothalamus
          • GHS-R 1a mediates the classical GH-releasing effect [8]

      Receptors

      • Receptor: GHS-R1

        Influences:

        • GH
      • Receptor: GHRH-R

        Induced phenotype:

        • Growth hormone deficiency
          • One cause of growth hormone deficiency is a mutation in the GHRH-R gene. [9]
        • dwarfism

        Influences:

        • GH
      • Receptor: sst2

        Influences:

        • GH
          • SSTR2 and SSTR5 mediate suppression of GH and TSH secretion. [3]
          • SRIF and CST similarly inhibited (p < 0.05) spontaneous GH secretion of about 90%. [4]
          • Somatostatin induced inhibition of GH secretion is mediated through (SSTR) 2 and 5. [5]
      • Receptor: sst5

        Influences:

        • GH
          • SSTR2 and SSTR5 mediate suppression of GH and TSH secretion. [3]
          • SRIF and CST similarly inhibited (p < 0.05) spontaneous GH secretion of about 90%. [4]
          • Somatostatin induced inhibition of GH secretion is mediated through (SSTR) 2 and 5. [5]
      • Receptor: leptin receptor

        Influences:

        • GH
          • Leptin-deficient patients although exhibited normal height, presented decreased GH response to ITT and physical exercise, whereas leptin-resitant patients subjects have significant growth delay during early childhood and decreased GH secretion. [7]
      • Receptor: IGF-1R

        Induced phenotype:

        • cell growth
          • Insulin-like growth factor-1 mediates regulatory effects on cell growth by activation of IGF-1 receptor. [10]
        • positive regulation of cell proliferation
          • Insulin-like growth factor-1 stimulates proliferation of cells , required for sustained growth of many cells. [11]
        • negative regulation of apoptosis
          • Insulin-like growth factor-1 protects cells from apoptosis. [12]
        • transformation
          • Insulin-like growth factor-1 is required for transformation and maintenance of transformed state. [13]

        Influences:

        • GH
      • Receptor: orexin receptor 1

      • Receptor: CXCR1

        Influences:

        • GH
          • CINC/gro stiumaletes GH secretion from anterior pituitary monolayer cultures in a concentration-dependent manner with a substantial lag time. [6]
      Reference