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Experimental and bioinformatic analysis of cultured Bovine Endometrial Cells (BEND) responding to interferon tau (IFNT).

Palma-Vera SE, Einspanier R - Reprod. Biol. Endocrinol. (2016)

Bottom Line: Bioinformatic analyses detected that PLA2G4A was associated to IRF-1 and IRF-6, while ESR1, PR and PTGS2 were associated to only IRF-6.All genes exhibit one motif per IRF, except miR-106a that had three binding sites for IRF-6.Future studies will use these data to detect new IFNT regulatory mechanisms in the endometrium.

View Article: PubMed Central - PubMed

Affiliation: Institute of Veterinary Biochemistry, Freie Universität Berlin, Oertzenweg 19b, 14163, Berlin, Germany.

ABSTRACT

Background: In ruminants, embryo implantation depends on progesterone (P4) and interferon tau (IFNT) controlling endometrial function. IFNT antagonizes bovine endometrial cells (BEND) response to phorbol 12,13-dibutyrate (PDBU) through posttranscriptional regulation of gene expression. We have previously described microRNAs (miRNAs) profiles in bovine endometrium, detecting miR-106a, relevant for embryo maternal communication. In this study, we investigated the expression miR-106a and genes for prostaglandin-endoperoxide synthase 2 (PTGS2), phospholipase A2, group IVA (PLA2G4A), estrogen receptor 1 (ESR1) and progesterone receptor (PR) in response to IFNT in BEND cells and searched for interferon responsive factors (IRFs) binding sites in their promoter genomic regions. The aim of this study was to unravel the molecular mechanisms involved in IFNT signalling and its regulation of miR-106a.

Findings: PTGS2 showed increased expression under PDBU, which was antagonized by IFNT. IFNT induced expression of PR and miR-106a and downregulation of ESR1 and PR. Bioinformatic analyses detected that PLA2G4A was associated to IRF-1 and IRF-6, while ESR1, PR and PTGS2 were associated to only IRF-6. All genes exhibit one motif per IRF, except miR-106a that had three binding sites for IRF-6.

Conclusions: We report the IFNT regulatory effect on miR-106a expression through IRF-6 in bovine endometrial cells. We identified a set of potential binding sites for IRF-1 and IRF-6 within the bovine genome. A set of candidate gene regions could be characterized where IFNT can act via IRFs to regulate the expression of proteins and miRNAs. Future studies will use these data to detect new IFNT regulatory mechanisms in the endometrium.

No MeSH data available.


Related in: MedlinePlus

Normalized fold change expression of miR-106a for BEND cells. Expression was normalized to a stable unregulated miRNA (bta-miR-99a-5p). For each experiment, six biological replicates were used
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Fig2: Normalized fold change expression of miR-106a for BEND cells. Expression was normalized to a stable unregulated miRNA (bta-miR-99a-5p). For each experiment, six biological replicates were used

Mentions: An overall significant effect was detected on the expression of miR-106a (Fig. 2). This effect was most likely due to the activity of IFNT, which increased the expression of miR-106a approximately 30 % when applied alone. Also, when IFNT was applied with P4 and PDBU plus P4, a similar increment was detected. The only treatment group where the regulatory effect of IFNT was not observed when IFNT was added in combination with PDBU. This indicates that PDBU might counter-regulate the activity of IFNT and P4 ameliorates this effect.Fig. 2


Experimental and bioinformatic analysis of cultured Bovine Endometrial Cells (BEND) responding to interferon tau (IFNT).

Palma-Vera SE, Einspanier R - Reprod. Biol. Endocrinol. (2016)

Normalized fold change expression of miR-106a for BEND cells. Expression was normalized to a stable unregulated miRNA (bta-miR-99a-5p). For each experiment, six biological replicates were used
© Copyright Policy - OpenAccess
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC4835850&req=5

Fig2: Normalized fold change expression of miR-106a for BEND cells. Expression was normalized to a stable unregulated miRNA (bta-miR-99a-5p). For each experiment, six biological replicates were used
Mentions: An overall significant effect was detected on the expression of miR-106a (Fig. 2). This effect was most likely due to the activity of IFNT, which increased the expression of miR-106a approximately 30 % when applied alone. Also, when IFNT was applied with P4 and PDBU plus P4, a similar increment was detected. The only treatment group where the regulatory effect of IFNT was not observed when IFNT was added in combination with PDBU. This indicates that PDBU might counter-regulate the activity of IFNT and P4 ameliorates this effect.Fig. 2

Bottom Line: Bioinformatic analyses detected that PLA2G4A was associated to IRF-1 and IRF-6, while ESR1, PR and PTGS2 were associated to only IRF-6.All genes exhibit one motif per IRF, except miR-106a that had three binding sites for IRF-6.Future studies will use these data to detect new IFNT regulatory mechanisms in the endometrium.

View Article: PubMed Central - PubMed

Affiliation: Institute of Veterinary Biochemistry, Freie Universität Berlin, Oertzenweg 19b, 14163, Berlin, Germany.

ABSTRACT

Background: In ruminants, embryo implantation depends on progesterone (P4) and interferon tau (IFNT) controlling endometrial function. IFNT antagonizes bovine endometrial cells (BEND) response to phorbol 12,13-dibutyrate (PDBU) through posttranscriptional regulation of gene expression. We have previously described microRNAs (miRNAs) profiles in bovine endometrium, detecting miR-106a, relevant for embryo maternal communication. In this study, we investigated the expression miR-106a and genes for prostaglandin-endoperoxide synthase 2 (PTGS2), phospholipase A2, group IVA (PLA2G4A), estrogen receptor 1 (ESR1) and progesterone receptor (PR) in response to IFNT in BEND cells and searched for interferon responsive factors (IRFs) binding sites in their promoter genomic regions. The aim of this study was to unravel the molecular mechanisms involved in IFNT signalling and its regulation of miR-106a.

Findings: PTGS2 showed increased expression under PDBU, which was antagonized by IFNT. IFNT induced expression of PR and miR-106a and downregulation of ESR1 and PR. Bioinformatic analyses detected that PLA2G4A was associated to IRF-1 and IRF-6, while ESR1, PR and PTGS2 were associated to only IRF-6. All genes exhibit one motif per IRF, except miR-106a that had three binding sites for IRF-6.

Conclusions: We report the IFNT regulatory effect on miR-106a expression through IRF-6 in bovine endometrial cells. We identified a set of potential binding sites for IRF-1 and IRF-6 within the bovine genome. A set of candidate gene regions could be characterized where IFNT can act via IRFs to regulate the expression of proteins and miRNAs. Future studies will use these data to detect new IFNT regulatory mechanisms in the endometrium.

No MeSH data available.


Related in: MedlinePlus