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Transforming growth factor β signaling in uterine development and function.

Li Q - J Anim Sci Biotechnol (2014)

Bottom Line: Mounting evidence supports its important role in female reproduction and development.By drawing on mouse and human studies as a main source, this review focuses on the recent progress on understanding TGFβ signaling in the uterus.The review also considers the involvement of dysregulated TGFβ signaling in pathological conditions that cause pregnancy loss and fertility problems in women.

View Article: PubMed Central - PubMed

Affiliation: Department of Veterinary Integrative Biosciences, College of Veterinary Medicine and Biomedical Sciences, Texas A&M University, College Station, TX 77843 USA.

ABSTRACT
Transforming growth factor β (TGFβ) superfamily is evolutionarily conserved and plays fundamental roles in cell growth and differentiation. Mounting evidence supports its important role in female reproduction and development. TGFBs1-3 are founding members of this growth factor family, however, the in vivo function of TGFβ signaling in the uterus remains poorly defined. By drawing on mouse and human studies as a main source, this review focuses on the recent progress on understanding TGFβ signaling in the uterus. The review also considers the involvement of dysregulated TGFβ signaling in pathological conditions that cause pregnancy loss and fertility problems in women.

No MeSH data available.


Related in: MedlinePlus

Major functions of TGFβ superfamily signaling in the female reproduction. TGFβ superfamily signaling regulates a variety of reproductive processes including follicular development (e.g., TGFβs, GDF9, BMP15, activins, and AMH), ovulation (e.g., GDF9), oocyte competence (e.g., GDF9 and BMP15), decidualization (e.g., BMP2 and NODAL), implantation (e.g., ALK2-mediated signaling), pregnancy (e.g., BMPR2-mediated signaling), embryonic development (e.g., TGFβs, activins, follistatin, BMP2, and BMP4), and uterine development (TGFBR1-mediated signaling).
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Fig2: Major functions of TGFβ superfamily signaling in the female reproduction. TGFβ superfamily signaling regulates a variety of reproductive processes including follicular development (e.g., TGFβs, GDF9, BMP15, activins, and AMH), ovulation (e.g., GDF9), oocyte competence (e.g., GDF9 and BMP15), decidualization (e.g., BMP2 and NODAL), implantation (e.g., ALK2-mediated signaling), pregnancy (e.g., BMPR2-mediated signaling), embryonic development (e.g., TGFβs, activins, follistatin, BMP2, and BMP4), and uterine development (TGFBR1-mediated signaling).

Mentions: TGFβ superfamily is evolutionarily conserved and plays fundamental roles in cell growth and differentiation. The signal transduction and biological functions of this signaling pathway have been extensively investigated [2, 4, 8, 9, 25]. TGFβ superfamily signaling is essential for female reproduction (Figure 2), and dysregulation of TGFβ signaling may cause catastrophic consequences, leading to reproductive diseases and cancers [26–33].Figure 2


Transforming growth factor β signaling in uterine development and function.

Li Q - J Anim Sci Biotechnol (2014)

Major functions of TGFβ superfamily signaling in the female reproduction. TGFβ superfamily signaling regulates a variety of reproductive processes including follicular development (e.g., TGFβs, GDF9, BMP15, activins, and AMH), ovulation (e.g., GDF9), oocyte competence (e.g., GDF9 and BMP15), decidualization (e.g., BMP2 and NODAL), implantation (e.g., ALK2-mediated signaling), pregnancy (e.g., BMPR2-mediated signaling), embryonic development (e.g., TGFβs, activins, follistatin, BMP2, and BMP4), and uterine development (TGFBR1-mediated signaling).
© Copyright Policy - open-access
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC4255921&req=5

Fig2: Major functions of TGFβ superfamily signaling in the female reproduction. TGFβ superfamily signaling regulates a variety of reproductive processes including follicular development (e.g., TGFβs, GDF9, BMP15, activins, and AMH), ovulation (e.g., GDF9), oocyte competence (e.g., GDF9 and BMP15), decidualization (e.g., BMP2 and NODAL), implantation (e.g., ALK2-mediated signaling), pregnancy (e.g., BMPR2-mediated signaling), embryonic development (e.g., TGFβs, activins, follistatin, BMP2, and BMP4), and uterine development (TGFBR1-mediated signaling).
Mentions: TGFβ superfamily is evolutionarily conserved and plays fundamental roles in cell growth and differentiation. The signal transduction and biological functions of this signaling pathway have been extensively investigated [2, 4, 8, 9, 25]. TGFβ superfamily signaling is essential for female reproduction (Figure 2), and dysregulation of TGFβ signaling may cause catastrophic consequences, leading to reproductive diseases and cancers [26–33].Figure 2

Bottom Line: Mounting evidence supports its important role in female reproduction and development.By drawing on mouse and human studies as a main source, this review focuses on the recent progress on understanding TGFβ signaling in the uterus.The review also considers the involvement of dysregulated TGFβ signaling in pathological conditions that cause pregnancy loss and fertility problems in women.

View Article: PubMed Central - PubMed

Affiliation: Department of Veterinary Integrative Biosciences, College of Veterinary Medicine and Biomedical Sciences, Texas A&M University, College Station, TX 77843 USA.

ABSTRACT
Transforming growth factor β (TGFβ) superfamily is evolutionarily conserved and plays fundamental roles in cell growth and differentiation. Mounting evidence supports its important role in female reproduction and development. TGFBs1-3 are founding members of this growth factor family, however, the in vivo function of TGFβ signaling in the uterus remains poorly defined. By drawing on mouse and human studies as a main source, this review focuses on the recent progress on understanding TGFβ signaling in the uterus. The review also considers the involvement of dysregulated TGFβ signaling in pathological conditions that cause pregnancy loss and fertility problems in women.

No MeSH data available.


Related in: MedlinePlus