Effects of luteinizing hormone and human chorionic gonadotropin on corpus luteum cells in a spheroid cell culture system

Walz, Andrea; Keck, Christoph; Weber, Holger; Kissel, Casey; Pietrowski, Detlef

doi:10.1002/mrd.20325

Cited by 27 publications

(17 citation statements)

References 38 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…This builds on in vivo observations where GnRH antagonist inhibited the post-ovulatory peak in proliferation by 90% in primates . However, hCG, but not LH, stimulated sprout formation in endothelial-granulosa spheroids (Walz et al 2005). In the current study, it is unclear whether LH acted on endothelial cells directly or by acting on luteal cells to stimulate the production of angiogenic factors.…”

Section: Discussionmentioning

confidence: 99%

A novel physiological culture system that mimics luteal angiogenesis

Robinson¹,

Hammond²,

Mann³

et al. 2008

Reproduction

View full text Add to dashboard Cite

Luteal inadequacy is a major cause of poor embryo development and infertility. Angiogenesis, the formation of new blood vessels, is an essential process underpinning corpus luteum (CL) development and progesterone production. Thus, understanding the factors that regulate angiogenesis during this critical time is essential for the development of novel strategies to alleviate luteal inadequacy and infertility. This study demonstrates the development of a physiologically relevant primary culture system that mimics luteal angiogenesis. This system incorporates all luteal cell types (e.g. endothelial, steroidogenic cells, fibroblasts and pericytes). Using this approach, endothelial cells, identified by the specific marker von Willebrand factor (VWF), start to form clusters on day 2, which then proliferate and develop thread-like structures. After 9 days in culture, these tubule-like structures lengthen, thicken and form highly organized intricate networks resembling a capillary bed. Development of the vasculature was promoted by coating wells with fibronectin, as determined by image analysis (P!0.001). Progesterone production increased with time and was stimulated by LH re-enforcing the physiological relevance of the model in mimicking in vivo luteal function. LH also increased the area stained positively for VWF by twofold (P!0.05). Development of this endothelial cell network was stimulated by fibroblast growth factor 2 and vascular endothelial growth factor A, which increased total area of VWF positive staining on day 9, both independently (three-to fourfold; P!0.01) and in combination (tenfold; P!0.001). In conclusion, the successful development of endothelial cell networks in vitro provides a new opportunity to elucidate the physiological control of the angiogenic process in the developing CL. Reproduction (2008) 135 405-413

show abstract

Section: Discussionmentioning

confidence: 99%

A novel physiological culture system that mimics luteal angiogenesis

Robinson¹,

Hammond²,

Mann³

et al. 2008

Reproduction

View full text Add to dashboard Cite

show abstract

“…The endothelial cells were assumed to be one of the important sites for the BFB with the stricter permselectivity in the PCO syndrome than that in normal animal ovaries (Powers et al 1995, Zhou et al 2007b. Morphological changes during follicular development always depend on dynamic cellular rearrangements in the living animal ovaries, partly regulated by cell-cell adhesion molecules (Bazzoni & Dejana 2004, Walz et al 2005). One of the major intercellular junctions is the tight junction, which is the most apical junction of epithelial and endothelial cells completely sealing their intercellular spaces, and occludin and claudins are the major molecules of the tight junctions (Dejana 2004, Schneeberger & Lynch 2004.…”

Section: Discussionmentioning

confidence: 99%

Permselectivity of blood follicle barriers in mouse ovaries of the mifepristone-induced polycystic ovary model revealed by in vivo cryotechnique

Zhou

Ohno²,

Terada³

et al. 2008

Reproduction

View full text Add to dashboard Cite

Despite the potential association of polycystic ovary (PCO) syndrome with hemodynamic changes, follicular microenvironment and the involvement of blood follicle barriers (BFB), a histopathological examination has been hampered by artifacts caused by conventional preparation methods. In this study, mouse ovaries of a mifepristone-induced PCO model were morphologically and immunohistochemically examined by in vivo cryotechnique (IVCT), which prevents those technical artifacts. Ovarian specimens of PCO model mice were prepared by IVCT or the conventional perfusion fixation after s.c. injection of mifepristone. Their histology and immunolocalization of plasma proteins, including albumin (molecular mass, 69 kDa), immunoglobulin G (IgG, 150 kDa), inter-a-trypsin inhibitor (ITI, 220 kDa), fibrinogen (340 kDa), and IgM (900 kDa), were examined. In the PCO model, enlarged blood vessels with abundant blood flow were observed in addition to cystic follicles with degenerative membrana granulosa. The immunolocalization of albumin and IgM in the PCO model were similar to those in normal mice. Albumin immunolocalized in the blood vessels, interstitium or follicles, and IgM was mostly restricted within the blood vessels. In contrast, immunolocalization of IgG, ITI, and fibrinogen changed in the PCO model. Both IgG and ITI were clearly blocked by follicular basement membranes, and hardly observed in the membrana granulosa, though fibrinogen was mostly observed within blood vessels. These findings suggest that increased blood flow and enhanced selectivity of molecular permeation through the BFB are prominent features in the PCO ovaries, and changes in hemodynamic conditions and permselectivity of BFB are involved in the pathogenesis and pathophysiology of PCO syndrome. Reproduction (2008) 136 599-610

show abstract

“…Development of ascites is a consequence of dysregulated endothelial function leading to increased vascular permeability of peritoneal vessels [4]. Under physiological conditions, vascular permeability is mediated by strictly regulated opening and closure of cell-cell-junctions [5][6][7]. For that reason, any disturbance of junctional organization might result in dysregulated vascular function leading to pathological conditions by modifying the regular structure of the vessel wall [8].…”

Section: Introductionmentioning

confidence: 99%