Activation of phospholipase D by 8‐Br‐cAMP occurs through novel pathway involving Src, Ras, and ERK in human endometrial stromal cells

Yoon, Mee-Sup; Koo, Jun Bon; Hwang, Jin Ho; Lee, Ki Sung; Han, Joong‐Soo

doi:10.1016/j.febslet.2005.09.034

Cited by 22 publications

(20 citation statements)

References 37 publications

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“…Furthermore, it was shown that 8-bromo-cAMP stimulated PLD activity after activation of ERK 1/2 in primary cells of rat endometrium (38), supporting the hypothesis that PLD is downstream of ERK in that system. The mechanism whereby S1P activates PI3K and ERK 1/2 most likely involves an interaction of S1P with its Gi protein-coupled receptors, because preincubation of cells with PTX before treatment with S1P abolished the activation of these two pathways.…”

Section: Discussionmentioning

confidence: 50%

Sphingosine-1-phosphate stimulates aldosterone secretion through a mechanism involving the PI3K/PKB and MEK/ERK 1/2 pathways

Brizuela

Rábano

Gangoiti

et al. 2007

Journal of Lipid Research

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We reported recently that sphingosine-1-phosphate (S1P) is a novel regulator of aldosterone secretion in zona glomerulosa cells of adrenal glands and that phospholipase D (PLD) is implicated in this process. We now show that S1P causes the phosphorylation of protein kinase B (PKB) and extracellularly regulated kinases 1/2 (ERK 1/2), which is an indication of their activation, in these cells. These effects are probably mediated through the interaction of S1P with the Gi protein-coupled receptors S1P1/3, as pretreatment with pertussis toxin or with the S1P1/3 antagonist VPC 23019 completely abolished the phosphorylation of these kinases. Inhibitors of phosphatidylinositol 3-kinase (PI3K) or mitogen-activated protein kinase kinase (MEK) blocked S1P-stimulated aldosterone secretion. This inhibition was only partial when the cells were incubated independently with inhibitors of each pathway. However, aldosterone output was completely blocked when the cells were pretreated with LY 294002 and PD 98059 simultaneously. These inhibitors also blocked PLD activation, which indicates that this enzyme is downstream of PI3K and MEK in this system. We propose a working model for S1P in which stimulation of the PI3K/PKB and MEK/ERK pathways leads to the stimulation of PLD and aldosterone secretion.-Brizuela, L., M. Rábano, P. Gangoiti, N. Narbona, J. M. Macarulla, M. Trueba, and A. Gómez-Muñ oz. Sphingosine-1-phosphate stimulates aldosterone secretion through a mechanism involving the PI3K/PKB and MEK/ERK 1/2 pathways. J. Lipid Res.

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Section: Discussionmentioning

confidence: 50%

Sphingosine-1-phosphate stimulates aldosterone secretion through a mechanism involving the PI3K/PKB and MEK/ERK 1/2 pathways

Brizuela

Rábano

Gangoiti

et al. 2007

Journal of Lipid Research

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“…Indeed, IGF-I activates SRC in mouse endometrial cells [68]. In addition, SRC is activated by the cAMP/ PKA signaling pathway in hESCs [76].…”

Section: D]pyrimidine (Pp1) and 4-amino-5-(4-chlorophenyl)-7-(t-butylmentioning

confidence: 99%

Molecular and Cellular Mechanisms for Differentiation and Regeneration of the Uterine Endometrium

2008

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Abstract. The human endometrium undergoes cyclical changes including proliferation, differentiation, tissue breakdown, and shedding (menstruation) throughout a woman's reproductive life. The postovulatory rise in ovarian progesterone induces profound remodeling and differentiation of the estradiol-primed endometrium. This change, termed decidualization, is crucial for embryo implantation and maintenance of the pregnancy. To date, activation and crosstalk of cAMP-and progesterone-mediated signaling pathways have emerged as key cellular events to drive integrated changes at both the transcriptome and the proteome levels. This results in the induction and maintenance of the decidual phenotype and function. Our recent series of studies highlights the critical role of SRC kinase activation (v-src sarcoma viral oncogene homolog) and STAT5 (signal transducer and activator of transcription 5) phosphorylation in decidualization. After separation of the functional layer of the differentiated endometrium that follows progesterone withdrawal, i.e., menstruation, the basal layer of the endometrium, under the influence of estradiol, regrows and initiates a unique form of angiogenesis and regenerates a new functional layer. The molecular and cellular mechanisms for this process remain elusive, mainly because of difficulties in reproducing menstrual tissue breakdown, shedding, and subsequent tissue regeneration in vitro. We have recently developed a "humanized" mouse model in which a functional human endometrium is reconstituted. It may be used as an in vivo experimental tool for the study of endometrial angiogenesis and regeneration. This model may also be used to identify and test new therapeutic strategies for endometriosis, endometrial cancer, implantation failure, and infertility related to endometrial dysfunction.

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“…For instance, TSC and PLD are both modulated by mitogens (e.g., serum and insulin) [40][41][42][43][44][45][46] and TNFα. 15,47 The Ras-Raf-MEK-Erk pathway inhibits TSC2 via phosphorylation by either Erk 48,49 or a downstream kinase Rsk, 50 at the same time PLD activation by Ras [51][52][53][54] or Erk 54,55 has also been suggested. Most recently, our studies have uncovered a direct interaction between Rheb and PLD1.…”

Section: Pld1 As An Effector Of Rheb In Mtorc1 Signalingmentioning

confidence: 99%

mTOR signaling: PLD takes center stage

Sun¹,

Chen

2008

Cell Cycle

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Activation of phospholipase D by 8‐Br‐cAMP occurs through novel pathway involving Src, Ras, and ERK in human endometrial stromal cells

Cited by 22 publications

References 37 publications

Sphingosine-1-phosphate stimulates aldosterone secretion through a mechanism involving the PI3K/PKB and MEK/ERK 1/2 pathways

Sphingosine-1-phosphate stimulates aldosterone secretion through a mechanism involving the PI3K/PKB and MEK/ERK 1/2 pathways

Molecular and Cellular Mechanisms for Differentiation and Regeneration of the Uterine Endometrium

mTOR signaling: PLD takes center stage

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