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Dynamic modeling of folliculogenesis signaling pathways in the presence of miRNAs expression
BACKGROUND: TEK signaling plays a very important role in folliculogenesis. It activates Ras/ERK/MYC, PI3K/AKT/mTORC1 and ovarian steroidogenesis activation pathways. These are the main pathways for cell growth, differentiation, migration, adhesion, proliferation, survival and protein synthesis. RESU...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5735818/ https://www.ncbi.nlm.nih.gov/pubmed/29258623 http://dx.doi.org/10.1186/s13048-017-0371-y |
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author | Bahrami, Abolfazl Miraie-Ashtiani, Seyed Reza Sadeghi, Mostafa Najafi, Ali Ranjbar, Reza |
author_facet | Bahrami, Abolfazl Miraie-Ashtiani, Seyed Reza Sadeghi, Mostafa Najafi, Ali Ranjbar, Reza |
author_sort | Bahrami, Abolfazl |
collection | PubMed |
description | BACKGROUND: TEK signaling plays a very important role in folliculogenesis. It activates Ras/ERK/MYC, PI3K/AKT/mTORC1 and ovarian steroidogenesis activation pathways. These are the main pathways for cell growth, differentiation, migration, adhesion, proliferation, survival and protein synthesis. RESULTS: TEK signaling on each of the two important pathways where levels of pERK, pMYC, pAkt, pMCL1 and pEIF4EBP1 are increased in dominant follicles and pMYC is decreased in dominant follicles. Over activation of ERK and MYC which are the main cell growth and proliferation and over activation of Akt, MCl1, mTORC1 and EIF4EBP1 which are the main cell survival and protein synthesis factors act as promoting factors for folliculogenesis. In case of over expression of hsa-miR-30d-3p and hsa-miR-451a, MYC activity level is considerably increased in subordinate follicles. Our simulation results show that in the presence of has-miR-548v and bta-miR-22-3p, downstream factors of pathways are inhibited. CONCLUSIONS: Our work offers insight into the design of natural biological procedures and makes predictions that can guide further experimental studies on folliculogenesis pathways. Moreover, it defines a simple signal processing unit that may be useful for engineering synthetic biology and genes circuits to carry out cell-based computation. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s13048-017-0371-y) contains supplementary material, which is available to authorized users. |
format | Online Article Text |
id | pubmed-5735818 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-57358182017-12-21 Dynamic modeling of folliculogenesis signaling pathways in the presence of miRNAs expression Bahrami, Abolfazl Miraie-Ashtiani, Seyed Reza Sadeghi, Mostafa Najafi, Ali Ranjbar, Reza J Ovarian Res Research BACKGROUND: TEK signaling plays a very important role in folliculogenesis. It activates Ras/ERK/MYC, PI3K/AKT/mTORC1 and ovarian steroidogenesis activation pathways. These are the main pathways for cell growth, differentiation, migration, adhesion, proliferation, survival and protein synthesis. RESULTS: TEK signaling on each of the two important pathways where levels of pERK, pMYC, pAkt, pMCL1 and pEIF4EBP1 are increased in dominant follicles and pMYC is decreased in dominant follicles. Over activation of ERK and MYC which are the main cell growth and proliferation and over activation of Akt, MCl1, mTORC1 and EIF4EBP1 which are the main cell survival and protein synthesis factors act as promoting factors for folliculogenesis. In case of over expression of hsa-miR-30d-3p and hsa-miR-451a, MYC activity level is considerably increased in subordinate follicles. Our simulation results show that in the presence of has-miR-548v and bta-miR-22-3p, downstream factors of pathways are inhibited. CONCLUSIONS: Our work offers insight into the design of natural biological procedures and makes predictions that can guide further experimental studies on folliculogenesis pathways. Moreover, it defines a simple signal processing unit that may be useful for engineering synthetic biology and genes circuits to carry out cell-based computation. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s13048-017-0371-y) contains supplementary material, which is available to authorized users. BioMed Central 2017-12-19 /pmc/articles/PMC5735818/ /pubmed/29258623 http://dx.doi.org/10.1186/s13048-017-0371-y Text en © The Author(s). 2017 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated. |
spellingShingle | Research Bahrami, Abolfazl Miraie-Ashtiani, Seyed Reza Sadeghi, Mostafa Najafi, Ali Ranjbar, Reza Dynamic modeling of folliculogenesis signaling pathways in the presence of miRNAs expression |
title | Dynamic modeling of folliculogenesis signaling pathways in the presence of miRNAs expression |
title_full | Dynamic modeling of folliculogenesis signaling pathways in the presence of miRNAs expression |
title_fullStr | Dynamic modeling of folliculogenesis signaling pathways in the presence of miRNAs expression |
title_full_unstemmed | Dynamic modeling of folliculogenesis signaling pathways in the presence of miRNAs expression |
title_short | Dynamic modeling of folliculogenesis signaling pathways in the presence of miRNAs expression |
title_sort | dynamic modeling of folliculogenesis signaling pathways in the presence of mirnas expression |
topic | Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5735818/ https://www.ncbi.nlm.nih.gov/pubmed/29258623 http://dx.doi.org/10.1186/s13048-017-0371-y |
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