Physiology of gamete and embryo transport through the Fallopian tube

Croxatto, Horacio B.

doi:10.1016/s1472-6483(10)61935-9

Cited by 189 publications

(165 citation statements)

References 26 publications

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“…The fallopian tube consists of distinct segments, including the fimbriated ends that lie adjacent to the ovary, the ampulla, the ampulla-isthmus junction and the isthmus portion (Croxatto, 2002). The entire length of the fallopian tube is lined with ciliated and secretory epithelial cells.…”

Section: Introductionmentioning

confidence: 99%

“…The ciliated cells are most abundant at the fimbriated/ampulla segment. The fimbriae wrap around the ovary and transport the COC into the ampulla portion (Croxatto, 2002). The secretory cells, which produce vast numbers of growth factors and glycoproteins that act in both an autocrine and paracrine manner to regulate fallopian tube cells, sperm and embryo movement and development, are mostly found in the ampulla and the ampulla-isthmus junction (Buhi et al, 2000).…”

Section: Introductionmentioning

confidence: 99%

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Human fallopian tube epithelium co-culture with murine ovarian follicles reveals crosstalk in the reproductive cycle

Zhu

Rashedi

et al. 2016

Mol. Hum. Reprod.

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STUDY QUESTION: Do interactions between human fallopian tube epithelium and murine follicles occur during an artificial reproductive cycle in a co-culture system in vitro?SUMMARY ANSWER: In a co-culture system, human fallopian tissues responded to the menstrual cycle mimetic by changes in morphology and levels of secreted factors, and increasing murine corpus luteum progesterone secretion.WHAT IS KNOWN ALREADY: The entire fallopian tube epithelium, including ciliated and secretory cells, can be regulated in the reproductive cycle. Currently, there are no in vitro culture models that can monitor fallopian tissues in real time in response to factors produced by the ovary. In addition, there are no reports on the impact of fallopian tissue on ovarian function during the menstrual cycle.STUDY DESIGN, SAMPLES/MATERIALS, METHODS: Human fallopian tissue (n = 24) was obtained by routine hysterectomies from women (aged 26-50 years, mean age = 43.6) who had not undergone exogenous hormonal treatment for at least 3 months prior to surgery. CD1 female mice were used for ovarian follicle isolation. The human fallopian epithelium layers were either co-cultured with five murine multilayer secondary follicles (150-180 μm follicles, encapsulated in one alginate gel bead) for 15 days or received stepwise steroid hormone additions for 13 days. The fallopian tissue morphology and cilia beating rate, as measured by an Andor Spinning Disk Confocal, were investigated. Oviduct-specific glycoprotein 1 (OVGP1), human insulin-like growth factor 1 (hIGF1), vascular endothelial growth factor A (VEGF-A) and interleukin 8 (IL8) as biological functional markers were measured either by ELISA or western blot to indicate dynamic changes in the fallopian epithelium during the reproductive cycle generated by mouse follicles or by stepwise steroid hormone induction. Three or four patients in each experiment were recruited for replicates. Data were presented as mean ± SD and further analyzed using one-way ANOVA followed by Tukey's multiple comparisons test. MAIN RESULTS AND THE ROLE OF CHANCE:The cultured fallopian tube epithelium responded to exogenous steroid hormone stimulation, as demonstrated by enhanced cilia beating rate (~25% increase, P = 0.04) and an increase in OVGP1 secretion (P = 0.02) in response to 1 nM estradiol (E 2 ) treatment when compared with 0.1 nM E 2 . Conversely, 10 nM progesterone plus 1 nM E 2 suppressed cilia beating rate by~30% (P = 0.008), while OVGP1 secretion was suppressed by 0.1 nM E 2 plus 50 nM progesterone (P = 0.002 versus 1 nM E 2 alone). Human fallopian tube epithelium was co-cultured with murine secondary follicles to mimic the human menstrual cycle. OVGP1 and VEGF-A secretion from fallopian tissue was similar with stepwise hormone treatment and when cultured with murine follicles. However, the secretion patterns of hIGF1 and IL8 differed in the luteal phase when comparing steroid treatment with follicle co-culture. In co-culture, hIGF1 secretion was suppressed in the luteal versus follicular phase (P = 0.005)...

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Human fallopian tube epithelium co-culture with murine ovarian follicles reveals crosstalk in the reproductive cycle

Zhu

Rashedi

et al. 2016

Mol. Hum. Reprod.

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“…In the rat, the duration of oviductal egg transport is dependent on ovarian hormones and mating-associated signals (for review see Croxatto 2002). A single injection of oestradiol (E 2 ) on day 1 of the cycle or pregnancy shortens oviductal transport of eggs from the normal 72-96 h to less than 24 h (Ortiz et al 1979).…”

Section: Introductionmentioning

confidence: 99%

Inositol triphosphate participates in an oestradiol nongenomic signalling pathway involved in accelerated oviductal transport in cycling rats

Orihuela¹,

Parada-Bustamante²,

Zuñiga³

et al. 2006

Journal of Endocrinology

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Oestradiol (E 2 ) accelerates oviductal transport of oocytes in cycling rats through a nongenomic pathway that involves the cAMP-PKA signalling cascade. Here we examined the role of the inositol triphosphate (IP3) and mitogen-activated protein kinase (MAPK) signalling cascades in this nongenomic pathway. Oestrous rats were injected with E 2 s.c. and intrabursally (i.b) with the selective inhibitors of phospholipase C (PLC) ET-18-OCH 3 or MAPK PD98059. The number of eggs in the oviduct assessed 24 h later showed that ET-18-OCH 3 blocked E 2 -induced egg transport acceleration, whereas PD98059 had no effect. Other oestrous rats were treated with E 2 s.c. and 1, 3 or 6 h later oviducts were excised and the levels of IP3 and phosphorylated MAPK p44/42 (activated) were determined by radioreceptor assay and western blot, respectively. Oestradiol administration increased IP3 level at 1 and 6 h after treatment, whereas activated MAPK p44/42 level was unchanged. Finally, we explored whether cAMP-PKA and PLC-IP3 signalling cascades are coupled. Inhibition of adenylyl cyclase by i.b. injection of SQ 22536 blocked the increase of IP3 levels induced by E 2 , while inhibition of PLC by ET-18-OCH 3 had no effect on E 2 -induced PKA activity. Furthermore, activation of adenylyl cylase by Forskolin increased oviductal IP3 levels. Thus, activation of PLC-IP3 by E 2 requires previous stimulation of cAMP-PKA. We conclude that the nongenomic pathway utilised by E 2 to accelerate oviductal transport of oocytes in cycling rats involves successive activation of the cAMP-PKA and PLC-IP3 signalling cascades and does not require activation of MAPK. These findings clearly illustrate a nongenomic pathway triggered by E 2 that regulates a complex physiologic process accomplished by an entire organ.

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“…The rat oviduct is mainly composed of an intrinsic layer of smooth muscle fibre, and an innermost highly folded mucosa formed by epithelial and stromal cells, the endosalpinx (reviewed in Croxatto (2002)). Transport of oocytes along the oviduct depends on the interaction between the secretory activity of the epithelial cells and the contractile activity of the smooth muscle cells (Moore & Croxatto 1988a,b, Ríos et al 2007.…”

Section: Introductionmentioning

confidence: 99%

“…As smooth muscle cells are the mechanical effectors for the accelerated oocyte transport induced by E 2 in the oviduct (Croxatto 2002), this work determined the mechanism by which E 2 increases IP 3 in primary cultures of rat oviductal smooth muscle cells. Thus, we examined the effect of E 2 on the IP 3 levels in the smooth muscle cells under conditions in which protein synthesis, ER, Ga I or PLC activity were blocked by selective inhibitors.…”

Section: Introductionmentioning

confidence: 99%

Estradiol increases IP3 by a nongenomic mechanism in the smooth muscle cells from the rat oviduct

Reuquén¹,

Oróstica²,

Rojas³

et al. 2015

Reproduction

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Estradiol (E 2 ) accelerates egg transport by a nongenomic action, requiring activation of estrogen receptor (ER) and successive cAMP and IP 3 production in the rat oviduct. Furthermore, E 2 increases IP 3 production in primary cultures of oviductal smooth muscle cells. As smooth muscle cells are the mechanical effectors for the accelerated oocyte transport induced by E 2 in the oviduct, herein we determined the mechanism by which E 2 increases IP 3 in these cells. Inhibition of protein synthesis by Actinomycin D did not affect the E 2 -induced IP 3 increase, although this was blocked by the ER antagonist ICI182780 and the inhibitor of phospholipase C (PLC) ET-18-OCH 3 . Immunoelectron microscopy for ESR1 or ESR2 showed that these receptors were associated with the plasma membrane, indicating compatible localization with E 2 nongenomic actions in the smooth muscle cells. Furthermore, ESR1 but not ESR2 agonist mimicked the effect of E 2 on the IP 3 level. Finally, E 2 stimulated the activity of a protein associated with the contractile tone, calcium/ calmodulin-dependent protein kinase II (CaMKII), in the smooth muscle cells. We conclude that E 2 increases IP 3 by a nongenomic action operated by ESR1 and that involves the activation of PLC in the smooth muscle cells of the rat oviduct. This E 2 effect is associated with CaMKII activation in the smooth muscle cells, suggesting that IP 3 and CaMKII are involved in the contractile activity necessary to accelerate oviductal egg transport.Reproduction (2015) 150 331-341

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Physiology of gamete and embryo transport through the Fallopian tube

Cited by 189 publications

References 26 publications

Human fallopian tube epithelium co-culture with murine ovarian follicles reveals crosstalk in the reproductive cycle

Human fallopian tube epithelium co-culture with murine ovarian follicles reveals crosstalk in the reproductive cycle

Inositol triphosphate participates in an oestradiol nongenomic signalling pathway involved in accelerated oviductal transport in cycling rats

Estradiol increases IP3 by a nongenomic mechanism in the smooth muscle cells from the rat oviduct

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