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Details for anatomical structure: cell of endometrium of uterus

EndoNet ID: ENC00037

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Synonyms

cell of endometrium of uterus, ,

General information

secreting mainly carbohydrates

Links to other resources

Cytomer cy0011183

Larger structures

    Substructures

      Secreted hormones

      • Hormone: LIF

        • LIF is produced in high amounts by the human endometrium and the trophoblast itself, and LIF receptors are present on cytotrophoblast cells. [1]

        Influenced by:

        • TGF-beta type II receptor
          in cell_of_endometrium_of_uterus
          • TGF-beta1 (from 10<sup>–12</sup> to 10<sup>–8</sup>M ), -beta 2 , -beta 3 and activin A (10<sup>–10 and 10</sup>–8 M ) increases LIF secretion by human endometrial epithelium cultures. [2]
        • IL-1RI
          in cell_of_endometrium_of_uterus
          • Treatment with IL-1beta (10 <sup>–9</sup> M ) strongly stimulated LIF and IL-6 production. [2]
      • Hormone: Emap2

        • EMAP II expression is negatively regulated by PGE2. [3]
      • Hormone: PGE2

        • Expression of PGE synthase and synthesis of PGE2 were localized to glandular epithelial and endothelial cells in both basalis and functionalis regions of the human endometrium. [4]
      • Hormone: IFN-gamma

        • Endometrial large granular lymphocytes (LGLs) produce interferon-g (IFN-g), particularly when interacting with macrophages or stimulated with interleukin 12 (IL-12) and IL-2. [5]
      • Hormone: IL-11

        • IL-11 is expressed in endometrial glandular and luminal epithelium. [6]
        • IL-11 and IL-11Ralpha are also reduced in endometrium in cohorts of women with infertility and endometriosis compared with fertile women during the window of implantation. [6]
        • In contrast to LIF, IL-11 mRNA expression and immunostaining is reduced in decidua and trophoblast in women with anembryonic pregnancies that result in early abortion, compared with normal pregnancies. [6]
        • IL-11 secretion and mRNA expression by human endometrial stromal cells are stimulated by locally produced factors, relaxin and prostaglandin estradiol (E2), acting at least in part via cAMP during human endometrial stromal cell decidualization although progesterone attenuates IL-11 secretion and mRNA expression. [6]

        Influenced by:

        • progesterone receptor
          in cell_of_endometrium_of_uterus
          • Progesterone attenuates IL-11 secretion and mRNA expression. [6]
        • ER-alpha
          in cell_of_endometrium_of_uterus
          • IL-11 secretion is reduced by co-culture with estrogen and progesterone but stimulated by estrogen alone. [6]
        • Prokineticin receptor 1
          in cell_of_endometrium_of_uterus
          • In the present study, we report that PROK1 induces the expression and secretion of the cytokine IL-11 in cultured endometrial epithelial cells and first trimester decidua explants via the PK-1 receptor. [7]
      • Hormone: interleukin 6

        • In humans, IL-6 is weakly expressed during the proliferative phase, but strong immunoreactivity is present during the mid-secretory phase, predominantly in the glandular and luminal epithelial cells. [6]

        Influenced by:

        • TGF-beta type II receptor
          in cell_of_endometrium_of_uterus
          • TGF-beta 1(from 10ex–12 to 10ex–8 M ), -beta 2 , -beta 3 and activin A(10ex–10 and 10ex–8 M ) reduces IL-6 release by the human endometrial epithelium. [2]
        • IL-1RI
          in cell_of_endometrium_of_uterus
          • Treatment with IL-1beta (10 <sup>–9</sup> M ) strongly stimulated LIF and IL-6 production. [2]
      • Hormone: TGF-beta 1

        • TGF-beta 1 treatment in vitro acts directly on isolated endometrial epithelial cells, independently suppressing promatrilysin protein expression. [8]
        • TGF-b1 expression is known to be autoinductive and influenced by other growth factors in several cell types, including human endometrial stromal cells. [9]
        • In women, expression of TGF-b1, -b2 and -b3 and the type II receptor occurs in all cell types of the endometrium. [9]

        Influenced by:

        • TGF-beta type II receptor
          in cell_of_endometrium_of_uterus
          • TGF-beta 1 has been shown to decrease TGF-beta 2 and TGF-beta 3 expression while enhancing its own expression. [8]
      • Hormone: TGF-beta 2

        • TGF-beta 2 treatment in vitro acts directly on isolated endometrial epithelial cells, independently suppressing promatrilysin protein expression. [8]
        • TGF-beta 2 appears to increase expression of all three mammalian isotypes (TGF-beta 1,2,3). [8]
        • In women, expression of TGF-b1, -b2 and -b3 and the type II receptor occurs in all cell types of the endometrium. [9]
        • Within the stroma, TGF-b2 expression increases during the secretory phase. [9]
        • TGF-b2 is the progesterone- induced, stromal-derived paracrine factor that suppresses epithelial matrilysin production. [9]

        Influenced by:

        • progesterone receptor
          in cell_of_endometrium_of_uterus
          • Northern blot analysis confirmed an increase in TGF-beta 2 mRNA with progesterone treatment. [8]
      • Hormone: TGF-beta 3

        • In women, expression of TGF-b1, -b2 and -b3 and the type II receptor occurs in all cell types of the endometrium. [9]
      • Hormone: IL-1 beta

        Influenced by:

        • leptin receptor
          in cell_of_endometrium_of_uterus
          • Leptin stimulated IL-1 antagonist (IL-1Ra), IL-1beta secretion and expression of IL-1 receptor type I (IL-1R tI) in endometrial epithelial cells and endometrial stromal cells. [10]
      • Hormone: leptin

        • Endometrial leptin secretion is regulated in vitro by the human blastocyst. [11]
      • Hormone: activin A

        • Activin A is expressed and produced by both the embryo and the human endometrial epithelium during the menstrual cycle. [2]
        • In early pregnancy, activin A may facilitate implantation, because of its ability to promote cytotrophoblast differentiation towards an invasive phenotype and to stimulate the production of paracrine or endocrine agents involved in invasion such as placental hormones. [2]
        • Activin A is a candidate paracrine agent for promotion of stromal cell decidualization. [12]
        • Activin betaA and betaB subunits are produced by human endometrium, predominantly by epithelial cells in non-pregnant endometrium. [12]
      • Hormone: inhibin alpha

        • The strong expression of the inhibin-alpha subunit is co-expressed with activin-beta subunits in epithelial and stromal cells. [12]
      • Hormone: TGF-beta 4

        • Expression:Mesenchymal cells of the endometrial stroma. Transiently expressed before and during menstrual bleeding. [13]
      • Hormone: sFRP-4

      • Hormone: CTGF

      • Hormone: VEGF-165

        • VEGF stimulates capillary endothelial mitogenesis and morphogenesis in endometrium. [14]

        Influenced by:

        • ER-alpha
          in cell_of_endometrium_of_uterus
          • 17beta-estradiol (E2) directly regulates VEGF gene transcription in endometrial cells. [14]
          • A 2-fold increase in steady-state VEGF mRNA was evident after 15 h of E2. [14]
        • ER-beta
          in cell_of_endometrium_of_uterus
          • A 2-fold increase in steady-state VEGF mRNA was evident after 15 h of E2. [14]
          • 17beta-estradiol (E2) directly regulates VEGF gene transcription in endometrial cells. [14]
      • Hormone: TNF-alpha

        • Is increased in the endometrium of women with menorrhagia. [15]
      • Hormone: TIMP-4

      • Hormone: uteroglobin

      • Hormone: FGF-1 isoform 1

      • Hormone: VCAM1 soluble form

      • Hormone: FAM3A

      Receptors

      • Receptor: leptin receptor

        Influences:

        • IL-1 beta
          • Leptin stimulated IL-1 antagonist (IL-1Ra), IL-1beta secretion and expression of IL-1 receptor type I (IL-1R tI) in endometrial epithelial cells and endometrial stromal cells. [10]
      • Receptor: LIFR

      • Receptor: CRF-R1

      • Receptor: ER-alpha

        Influences:

        • IL-11
          • IL-11 secretion is reduced by co-culture with estrogen and progesterone but stimulated by estrogen alone. [6]
        • VEGF-165
          • 17beta-estradiol (E2) directly regulates VEGF gene transcription in endometrial cells. [14]
          • A 2-fold increase in steady-state VEGF mRNA was evident after 15 h of E2. [14]
      • Receptor: ER-beta

        Influences:

        • VEGF-165
          • A 2-fold increase in steady-state VEGF mRNA was evident after 15 h of E2. [14]
          • 17beta-estradiol (E2) directly regulates VEGF gene transcription in endometrial cells. [14]
      • Receptor: progesterone receptor

        Influences:

        • IL-11
          • Progesterone attenuates IL-11 secretion and mRNA expression. [6]
        • TGF-beta 2
          • Northern blot analysis confirmed an increase in TGF-beta 2 mRNA with progesterone treatment. [8]
      • Receptor: CD40

      • Receptor: EP1

      • Receptor: EP4

      • Receptor: EP2

      • Receptor: IL6ST

      • Receptor: IL-11Ralpha

      • Receptor: IL-6R

      • Receptor: TGF-beta type II receptor

        Influences:

        • TGF-beta 1
          • TGF-beta 1 has been shown to decrease TGF-beta 2 and TGF-beta 3 expression while enhancing its own expression. [8]
        • LIF
          • TGF-beta1 (from 10<sup>–12</sup> to 10<sup>–8</sup>M ), -beta 2 , -beta 3 and activin A (10<sup>–10 and 10</sup>–8 M ) increases LIF secretion by human endometrial epithelium cultures. [2]
        • interleukin 6
          • TGF-beta 1(from 10ex–12 to 10ex–8 M ), -beta 2 , -beta 3 and activin A(10ex–10 and 10ex–8 M ) reduces IL-6 release by the human endometrial epithelium. [2]
      • Receptor: IL-1RI

        Influences:

        • LIF
          • Treatment with IL-1beta (10 <sup>–9</sup> M ) strongly stimulated LIF and IL-6 production. [2]
        • interleukin 6
          • Treatment with IL-1beta (10 <sup>–9</sup> M ) strongly stimulated LIF and IL-6 production. [2]
      • Receptor: ALK4

      • Receptor: activin receptor type 2B

        Induced phenotype:

        • cell differentiation
          • Human endometrium expresses activin A recpetor type I and type II. Thereby, it is a target for activin A, which stimulates stromal cell differentiation along with the expression and secretion of markers of endometrial receptivity. [16]
      • Receptor: ACTRIIA

        Induced phenotype:

        • cell differentiation
          • Human endometrium expresses activin A recpetor type I and type II. Thereby, it is a target for activin A, which stimulates stromal cell differentiation along with the expression and secretion of markers of endometrial receptivity. [16]
      • Receptor: TGFR-3

      • Receptor: TGF-beta type I receptor

      • Receptor: thrombospondin receptor

      • Receptor: basigin

      • Receptor: Prokineticin receptor 1

        • PROKR1 localizes to the glandular and luminal epithelium, endothelial, and stromal cells in the functional layer of the endometrium [17]

        Influences:

        • IL-11
          • In the present study, we report that PROK1 induces the expression and secretion of the cytokine IL-11 in cultured endometrial epithelial cells and first trimester decidua explants via the PK-1 receptor. [7]
      Reference