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Phytoestrogens are herbal polyphenolic compounds that exert various estrogen-like effects in animals and can be taken in easily from a foodstuff in daily life. The fallopian tube lumen, where transportation of the oocyte occurs, is lined with secretory cells and multi-ciliated epithelial cells. Recently, we showed that estrogen induces multi-ciliogenesis in the porcine fallopian tube epithelial cells (FTECs) through the activation of the estrogen receptor beta (ERβ) pathway and simultaneous inhibition of the Notch pathway. Thus, ingested phytoestrogens may induce FTEC ciliogenesis and thereby affect the fecundity. To address this issue, we added isoflavones (genistein, daidzein, or glycitin) and coumestan (coumestrol) to primary culture FTECs under air-liquid interface conditions and assessed the effects of each compound. All phytoestrogens except glycitin induced multi-ciliated cell differentiation, which followed Notch signal downregulation. On the contrary, the differentiation of secretory cells decreased slightly. Furthermore, genistein and daidzein had a slight effect on the proportion of proliferating cells exhibited by Ki67 expression. Ciliated-cell differentiation is inhibited by the ERβ antagonist, PHTPP. Thus, this study suggests that phytoestrogens can improve the fallopian tube epithelial sheet homeostasis by facilitating the genesis of multi-ciliated cells and this effect depends on the ERβ-mediated pathway.

The fallopian tube (FT) is an important reproductive organ in females. The luminal epithelium of the FT is composed of highly polarized secretory and ciliated cells. Recently, accumulating lines of evidence have suggested that the origin of high-grade serous ovarian carcinoma (HGSC) is fallopian tube epithelial cells (FTECs). Due to the lack of a high-fidelity model for FTECs in vitro, homeostasis, differentiation, as well as the transformation of FTECs are still enigmatic. In this study, we optimized the culture condition for the stable expansion of basal stem cells, as well as inducing differentiation of basal cells into polarized secretory and ciliated cells in the air-liquid interface (ALI) condition suitable for long-term culture. This storable culture method of FTECs provides a versatile platform for studying differentiation mechanisms, intercellular communication, and transformation to HGSC, as well as the physiological function of the FT in vitro.

The lumen of the fallopian tube (FT) is lined with columnar epithelium composed of secretory and ciliated cells, both of which are important for reproduction. However, the molecular mechanism regulating cell fate remains controversial. In this study, we established a primary culture system using porcine fallopian tube epithelial cells (FTECs) to study the differentiation mechanism. We found that estrogen promoted the differentiation of multi-ciliated cells (MCCs) through estrogen receptor β, following the reduction of DLL1, a ligand of Notch. Meanwhile, epidermal growth factor (EGF), a regulator of epithelial homeostasis and differentiation, suppressed ciliogenesis by the activation of Notch signaling. However, the estrogen pathway did not affect the activation of the EGF pathway. Taken together, the differentiation of MMCs in FT depends on the balance of EGF and estrogen signaling, either of which inhibits or stimulates the Notch signaling pathway respectively., Competing Interests: The authors declare no conflict of interest.

T-type calcium (Ca 2+ ) channels play important physiological functions in excitable cells including cardiomyocyte. Phosphatidylinositol-4,5-bisphosphate (PIP 2 ) has recently been reported to modulate various ion channels' function. However the actions of PIP 2 on the T-type Ca 2+ channel remain unclear. To elucidate possible effects of PIP 2 on the T-type Ca 2+ channel, we applied patch clamp method to investigate recombinant Ca V 3.1- and Ca V 3.2-T-type Ca 2+ channels expressed in mammalian cell lines with PIP 2 in acute- and long-term potentiation. Short- and long-term potentiation of PIP 2 shifted the activation and the steady-state inactivation curve toward the hyperpolarization direction of Ca V 3.1-I Ca.T without affecting the maximum inward current density. Short- and long-term potentiation of PIP 2 also shifted the activation curve toward the hyperpolarization direction of Ca V 3.2-I Ca.T without affecting the maximum inward current density. Conversely, long-term but not short-term potentiation of PIP 2 shifted the steady-state inactivation curve toward the hyperpolarization direction of Ca V 3.2-I Ca.T . Long-term but not short-term potentiation of PIP 2 blunted the voltage-dependency of current decay Ca V 3.1-I Ca.T . PIP 2 modulates Ca V 3.1- and Ca V 3.2-I Ca.T not by their current density but by their channel gating properties possibly through its membrane-delimited actions., (Copyright © 2018 Elsevier B.V. All rights reserved.)