Luteinizing hormone increases platelet-derived growth factor-D gene expression in human granulosa–luteal cells

Hwu, Yuh Ming; Li, Sheng Hsiang; Lee, Robert Kuo Kuang; Lin, Ming Huei; Tsai, Yu Hui; Yeh, Tien Shun

doi:10.1016/j.fertnstert.2009.05.064

Cited by 8 publications

(5 citation statements)

References 22 publications

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“…In testicular Leydig cells and in ovarian granulosa cells, both human chorionic gonadotropin (hCG) and LH increase C/EBPb levels (Sterneck et al 1997, Nalbant et al 1998. The same treatment, however, represses PDGFRA expression in human granulosa-luteal cells (Hwu et al 2009) in agreement with a repressing role for C/EBPb in Pdgfra expression. Immature and mature Leydig cells isolated from 20-to 70-day-old rats exclusively express C/EBPb (Nalbant et al 1998).…”

Section: Discussionmentioning

confidence: 92%

Transcription of platelet-derived growth factor receptor in Leydig cells involves specificity protein 1 and 3

Bergeron¹,

Bagu²,

Tremblay

2011

Journal of Molecular Endocrinology

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Platelet-derived growth factor (PDGF) A is secreted by Sertoli cells and acts on Leydig precursor cells, which express the receptor PDGFRA, triggering their differentiation into steroidogenically active Leydig cells. There is, however, no information regarding the molecular mechanisms that govern Pdgfra expression in Leydig cells. In this study, we isolated and characterized a 2 . 2 kb fragment of the rat Pdgfra 5 0 -flanking sequence in the TM3 Leydig cell line, which endogenously expresses Pdgfra. A series of 5 0 progressive deletions of the Pdgfra promoter was generated and transfected in TM3 cells. Using this approach, two regions (K183/K154 and K154/K105), each conferring 46% of Pdgfra promoter activity, were identified. To better define the regulatory elements, trinucleotide mutations spanning the K154/K105 region were introduced by site-directed mutagenesis in the context of the K2 . 2 kb Pdgfra promoter.Mutations that altered the TCCGAGGGAAAC sequence at K138 bp significantly decreased Pdgfra promoter activity in TM3 cells. Several proteins from TM3 nuclear extracts were found to bind to this G(C/A) motif in electromobility shift assay. Two of the proteins were identified as the transcription factors SP1 and SP3. Using transient transfections of TM3 Leydig cells, SP1 and SP3 were found to activate the Pdgfra promoter by threefold. The SP1/SP3-dependent activation of the Pdgfra promoter was severely blunted when the G(C/A) motif was mutated. Our study provides new insights into the regulatory mechanisms of Pdgfra transcription in Leydig cells, which includes a role for the transcription factors SP1 and SP3.

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Section: Discussionmentioning

confidence: 92%

Transcription of platelet-derived growth factor receptor in Leydig cells involves specificity protein 1 and 3

Bergeron¹,

Bagu²,

Tremblay

2011

Journal of Molecular Endocrinology

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“…PDGF signaling has been proposed as one of the factors involved in early folliculogenesis (Nilsson et al, ; Sleer and Taylor, ; Pinkas et al, ) since PDGFRβ has been detected in granulosa cells of primordial follicles from adults (Pinkas et al, ). Indeed, luteinizing hormone significantly increases PDGFD mRNA levels but suppresses PDGFB mRNA in human granulosa‐luteal cells (Hwu et al, ). While PDGF concentrations in FF from OHSS patients are reported to be comparable to those of ascites fluid (Hwu et al, ; Chen et al, ), the decrease in PDGF levels found in the present work imply a distinct vascular etiology is underlying PCOS—one that may be related to the altered early folliculogenesis observed in PCOS patients.…”

Section: Discussionmentioning

confidence: 99%

“…Indeed, luteinizing hormone significantly increases PDGFD mRNA levels but suppresses PDGFB mRNA in human granulosa‐luteal cells (Hwu et al, ). While PDGF concentrations in FF from OHSS patients are reported to be comparable to those of ascites fluid (Hwu et al, ; Chen et al, ), the decrease in PDGF levels found in the present work imply a distinct vascular etiology is underlying PCOS—one that may be related to the altered early folliculogenesis observed in PCOS patients. The concomitant reduction in PDGF levels and elevation in ovarian VEGF concentrations in PCOS patients are in agreement with changes reported for Pdgfb and Pdgfrb knock‐out mice, which possess elevated VEGF levels at late gestation (Hellstrom et al, ).…”

Section: Discussionmentioning

confidence: 99%

Platelet‐derived growth factor BB and DD and angiopoietin1 are altered in follicular fluid from polycystic ovary syndrome patients

Scotti

Parborell

Irusta

et al. 2014

Molecular Reproduction Devel

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Polycystic ovary syndrome (PCOS) is the most common endocrinological pathology among women of reproductive age, and is characterized by abnormalities in ovarian angiogenesis, among other features. Consistent with this association, follicular fluid (FF) concentration and ovarian expression of vascular endothelial growth factor (VEGF) are increased in PCOS patients. In this study, we examined the protein levels of platelet-derived growth factor (PDGF) BB and DD (PDGFBB and PDGFDD), angiopoietin 1 and 2 (ANGPT1 and ANGPT2), and their soluble receptor sTIE2 in FF from PCOS and control patients undergoing assisted reproductive techniques. We also analyzed the effect of FF from PCOS and control patients on tight and adherens junction protein expression in an endothelial cell line. PDGFBB and PDGFDD were significantly lower whereas ANGPT1 concentration was significantly higher in FF from PCOS patients than from control patients. No changes were found in the concentration of ANGPT2 or sTIE2. Expression of claudin-5 was significantly increased in endothelial cells incubated for 24 hr in the presence of FF from PCOS versus from control patients, while vascular-endothelial cadherin, β-catenin, and zonula occludens 1 expression were unchanged. The changes observed in the levels of PDGF isoforms and ANGPT1 may prevent VEGF-induced vascular permeability in the PCOS ovary by regulating endothelial-cell-junction protein levels. Restoring the levels of angiogenic factors may provide new insights into PCOS treatment and the prevention of ovarian hyperstimulation syndrome in affected women.

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“…AMH inhibits primordial follicle growth, acting as an inhibitory factor during early stages of folliculogenesis (Durlinger et al, 2002a). Luteinizing hormone (LH) has been described as one of the regulators of PDGF synthesis in human luteinized granulosa cells since it is able to increase mRNA levels of pdgfd and to decrease mRNA levels of pdgfb (Hwu et al, 2009). In this sense, we have demonstrated that ovarian concentration of PDGFB and PDGFD are decreased in a rat OHSS model, suggesting a role of these proteins in the pathogenesis of OHSS (Scotti et al, 2013).…”

Section: Introductionmentioning

confidence: 99%

Local administration of platelet-derived growth factor B (PDGFB) improves follicular development and ovarian angiogenesis in a rat model of Polycystic Ovary Syndrome

Pietro

Scotti

Irusta

et al. 2016

Molecular and Cellular Endocrinology

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Luteinizing hormone increases platelet-derived growth factor-D gene expression in human granulosa–luteal cells

Cited by 8 publications

References 22 publications

Transcription of platelet-derived growth factor receptor in Leydig cells involves specificity protein 1 and 3

Transcription of platelet-derived growth factor receptor in Leydig cells involves specificity protein 1 and 3

Platelet‐derived growth factor BB and DD and angiopoietin1 are altered in follicular fluid from polycystic ovary syndrome patients

Local administration of platelet-derived growth factor B (PDGFB) improves follicular development and ovarian angiogenesis in a rat model of Polycystic Ovary Syndrome

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