Vasohibin Expression in the Bovine Corpus Luteum: Regulation by VEGF and Prostaglandin F2 alpha.

Shirasuna, Koumei; Sasahara, Kiemi; Akabane, Y.; Matsui, Motozumi; Meidan, Rina; Shimizu, Takashi; Miyamoto, Akio

doi:10.1093/biolreprod/81.s1.545

Cited by 3 publications

(6 citation statements)

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“…Whereas uterine PGF 2a has been clearly linked to luteolysis (Schams & Berisha 2004), it is a debatable point whether luteal PGF 2a had a luteolytic effect in the present study. However, changes in luteal mRNA expressions in ovaries of the LPS group do not resemble changes observed after exogenous PGF 2a treatment in cows, including decreased mRNA expressions of PTGFR, steroidogenic (STAR, HSD3B) and angiogenic factors (VEGF, FGF2), and increased vasoactive factor EDN1 mRNA expression (Shirasuna et al 2010). In the present study, there were no significant differences in these parameters between control and LPS ovaries, except for a temporary increase in VEGFA 121 , indicating a non-specific response to LPS challenge.…”

Section: Discussionmentioning

confidence: 63%

“…In bovine endometrial cells, PGE 2 and PGF 2a production were elevated after LPS challenge (Herath et al 2006), in association with extended luteal phases and premature regression of the CL, respectively (Opsomer et al 2000). The predominant effect (luteotropic or luteolytic) was dependent on PGE 2 to PGF 2a ratio (Herath et al 2006) and luteal phase (Shirasuna et al 2010), with PGE 2 primarily controlling the early and PGF 2a the mid-and late luteal phases, respectively. In the present study using mid-luteal CL, increased mRNA expression of PGFS in the LPS group compared to the control group might have contributed to lower P 4 concentrations after hCG challenge in LPS-treated ovaries.…”

Section: Discussionmentioning

confidence: 96%

“…During physiological luteolysis in cattle, PGF 2a is released from the endometrium as well as the CL (Shirasuna et al 2004). Furthermore, gene expressions of steroidogenic, angiogenic, and vasoactive factors in luteal tissue provided relevant information regarding functionality of the bovine CL (Miyamoto et al 2009, Shirasuna et al 2010. The proinflammatory cytokine TNFA is present in bovine luteal cells, as well as in immune cells (mainly macrophages; Sakumoto et al 2011), and is capable of reducing P 4 secretion, increasing PGF 2a production, and inducing apoptosis in luteal cell cultures (Okuda & Sakumoto 2003, Skarzynski et al 2005.…”

Section: Introductionmentioning

confidence: 99%

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Lipopolysaccharide enhances apoptosis of corpus luteum in isolated perfused bovine ovaries in vitro

Lüttgenau¹,

Möller²,

Kradolfer³

et al. 2016

Reproduction

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Lipopolysaccharide (LPS), the endotoxin of Gram-negative bacteria, has detrimental effects on the structure and function of bovine corpus luteum (CL) in vivo. The objective was to investigate whether these effects were mediated directly by LPS or via LPS-induced release of PGF 2a . Bovine ovaries with a mid-cycle CL were collected immediately after slaughter and isolated perfused for 240 min. After 60 min of equilibration, LPS (0.5 mg/ml) was added to the medium of five ovaries, whereas an additional six ovaries were not treated with LPS (control). After 210 min of perfusion, all ovaries were treated with 500 iu of hCG. In the effluent perfusate, concentrations of progesterone (P 4 ) and PGF 2a were measured every 10 and 30 min, respectively. Punch biopsies of the CL were collected every 60 min and used for RT-qPCR to evaluate mRNA expression of receptors for LPS (TLR2, -4) and LH (LHCGR); the cytokine TNFA; steroidogenic (STAR, HSD3B), angiogenic (VEGFA 121 , FGF2), and vasoactive (EDN1) factors; and factors of prostaglandin synthesis (PGES, PGFS, PTGFR) and apoptosis (CASP3, -8, -9). Treatment with LPS abolished the hCG-induced increase in P 4 (P%0.05); however, there was a tendency (PZ0.10) for increased release of PGF 2a at 70 min after LPS challenge. Furthermore, mRNA abundance of TLR2, TNFA, CASP3, CASP8, PGES, PGFS, and VEGFA 121 increased (P%0.05) after LPS treatment, whereas all other factors remained unchanged (PO0.05).In conclusion, reduced P 4 responsiveness to hCG in LPS-treated ovaries in vitro was not due to reduced steroidogenesis, but was attributed to enhanced apoptosis. However, an impact of luteal PGF 2a could not be excluded.

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Section: Discussionmentioning

confidence: 63%

Section: Discussionmentioning

confidence: 96%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Lipopolysaccharide enhances apoptosis of corpus luteum in isolated perfused bovine ovaries in vitro

Lüttgenau¹,

Möller²,

Kradolfer³

et al. 2016

Reproduction

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“…Following treatment with PGF2, luteal VEGF protein levels decreased within 2 hours, followed by a reduction in the expression of mRNA encoding ANGPT1 and VEGF (Neuvians et al, 2004;Tanaka et al, 2004). By contrast, ANGPT2 mRNA and protein levels rapidly increased following PGF2 administration (Berisha et al, 2010;Shirasuna et al, 2010;Tanaka et al, 2004). Likewise, PGF2 induced expression of TGFB1 (Hou et al, 2008) and TNF (Henkes et al, 2008) in luteal tissue.…”

Section: Fig 7 Tgfb1 Causes Loss Of Ve-cadherin From Cellular Junctmentioning

confidence: 99%

“…The expression of angiogenic factors, such as vascular endothelial growth factor (VEGF) (Berisha et al, 2010;Neuvians et al, 2004;Shirasuna et al, 2010), the angiopoietins (ANPGT1 and ANGPT2) (Berisha et al, 2010;Shirasuna et al, 2010;Tanaka et al, 2004) and cytokines such as TGFB1 (Hou et al, 2008) and TNF (Henkes et al, 2008), is acutely regulated during regression of the corpus luteum. Angiopoietins play a role in stabilization of capillaries; an elevated ratio of ANGPT2 : ANGPT1 decreases capillary stabilization, which, together with a low level of VEGF, results in blood vessel destabilization and regression (Yancopoulos et al, 2000).…”

Section: Fig 7 Tgfb1 Causes Loss Of Ve-cadherin From Cellular Junctmentioning

confidence: 99%

TGFB1 disrupts the angiogenic potential of microvascular endothelial cells of the corpus luteum

Maroni

Davis

2011

Journal of Cell Science

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SummaryCyclical formation and regression of the ovarian corpus luteum is required for reproduction. During luteal regression, the microvasculature of the corpus luteum is extensively disrupted. Prostaglandin F2, a primary signal for luteal regression, induces the expression of transforming growth factor 1 (TGFB1) in the corpus luteum. This study determined the actions of TGFB1 on microvascular endothelial cells isolated from the bovine corpus luteum (CLENDO cells). We hypothesized that TGFB1 participates in the disruption of the microvasculature during luteal regression. TGFB1 activated the canonical SMAD signaling pathway in CLENDO cells. TGFB1 (1 ng/ml) significantly reduced both basal and fetal-calf-serum-stimulated DNA synthesis, without reducing cell viability. TGFB1 also significantly reduced CLENDO cell transwell migration and disrupted the formation of capillary-like structures when CLENDO cells were plated on Matrigel. By contrast, CLENDO cells plated on fibrillar collagen I gels did not form capillary-like structures and TGFB1 induced cell death. Additionally, TGFB1 caused loss of VE-cadherin from cellular junctions and loss of cellcell contacts, and increased the permeability of confluent CLENDO cell monolayers. These studies demonstrate that TGFB1 acts directly on CLENDO cells to limit endothelial cell function and suggest that TGFB1 might act in the disassembly of capillaries observed during luteal regression.

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Possible action of vasohibin-1 as an inhibitor in the regulation of vascularization of the bovine corpus luteum

et al. 2012

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The development of the corpus luteum (CL), which secretes large amounts of progesterone to establish pregnancy, is accompanied by active angiogenesis, vascularization, and lymphangiogenesis. Negative feedback regulation is a critical physiological mechanism. Vasohibin-1 (VASH1) was recently discovered as a novel endothelium-derived negative feedback regulator of vascularization. We therefore investigated the expression of VASH1 in the bovine CL. Expression of VASH1 mRNA and protein was predominantly localized to luteal endothelial cells (LECs). VASH1 expression in the CL was constant through the early to late luteal phases and decreased during CL regression relating with the action of luteolytic prostaglandin F 2a in vivo. To investigate the role of VASH1, we determined whether VASH1 treatment affects angiogenesis and/or lymphangiogenesis using LECs and lymphatic endothelial cells (LyECs) in vitro. Vascular endothelial growth factor A (VEGFA) stimulated the expression of VASH1 in LECs but not in LyECs, and VASH1 completely blocked VEGFA-induced formation of capillary-like tube structures of LECs and LyECs in vitro. In summary, VASH1 is predominantly located on LECs in the bovine CL and inhibits the angiogenic and lymphangiogenic actions of VEGFA. Bovine CL therefore has a VEGFA-VASH1 system that may be involved in regulation of luteal function, especially in the development of the CL. The results indicate that VASH1 has the potential to act as a negative feedback regulator of angiogenesis and lymphangiogenesis in the CL in cows.

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Vasohibin Expression in the Bovine Corpus Luteum: Regulation by VEGF and Prostaglandin F2 alpha.

Cited by 3 publications

References 0 publications

Lipopolysaccharide enhances apoptosis of corpus luteum in isolated perfused bovine ovaries in vitro

Lipopolysaccharide enhances apoptosis of corpus luteum in isolated perfused bovine ovaries in vitro

TGFB1 disrupts the angiogenic potential of microvascular endothelial cells of the corpus luteum

Possible action of vasohibin-1 as an inhibitor in the regulation of vascularization of the bovine corpus luteum

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