Mode Switch of Ca2 + Oscillation-Mediated Uterine Peristalsis and Associated Embryo Implantation Impairments in Mouse Adenomyosis

article OA: gold CC0 ⤵ 9 in-corpus citations
AI-generated summary by claude@2026-06, 2026-06-09

Adenomyotic mouse uteri exhibit a Ca2+ oscillation and peristalsis mode switch from bursts to spikes, alongside oxytocin hyperresponsiveness in neonates, leading to impaired embryo implantation.

One-sentence paraphrase of the abstract; not a substitute for reading it. No clinical advice. How this works

AI-generated deep summary by claude@2026-06, 2026-06-09

This paper studied how uterine peristalsis and underlying intracellular Ca2+ oscillations differ between control and tamoxifen-induced mouse adenomyosis, using precision-cut uterine slice preparations that preserve in vivo architecture and allow imaging of Ca2+ dynamics. In neonatal (day 14) and adult (day 55) control mice, peristalsis occurred as bursts with multiple peaks linked to intracellular Ca2+ oscillations, whereas in adenomyotic uteri peristalsis and Ca2+ oscillations shifted to spikes with single peaks and smaller amplitudes, without changes in oscillation/peristalsis peak frequency. The estimated peristaltic force and total Ca2+ raised were reduced in adenomyosis, and neonatal adenomyotic uteri—but not adult—showed hyperresponsiveness to oxytocin; embryo implantation was decreased in adult adenomyotic mice, with fertility impairment associated with these motility changes. This paper is centrally about adenomyosis — it demonstrates a burst-to-spike mode switch in Ca2+ oscillations and uterine peristalsis in a mouse model linked to impaired embryo implantation.

Read from the paper's body, not the abstract. Not a substitute for reading the paper. No clinical advice. How this works

Abstract

Adenomyosis is a debilitating gynecological disease of the uterus with no medicinal cure. The tissue injury and repair hypothesis for adenomyosis suggests that uterine hyperperistalsis or dysperistalsis plays a pivotal role in establishing adenomyotic lesions. However, specific impairments in uterine peristalsis and the underlying cellular signals for these changes in adenomyosis remain elusive. Here, we report a precision-cut uterine slice preparation that preserves in vivo uterine architecture and generates peristalsis similar to that seen in the whole uterus. We found that uterine peristalsis in neonatal mice at day 14 and adult mice at day 55 presents as bursts with multiple peaks induced by intracellular Ca 2+ oscillations. Using a mouse model of adenomyosis induced by tamoxifen, a selective estrogen receptor modulator, we discovered that uterine peristalsis and Ca 2+ oscillations from adenomyotic uteri on days 14 and 55 become spikes (single peaks) with smaller amplitudes. The peak frequency of Ca 2+ oscillations or peristalsis does not show a difference between control and adenomyotic mice. However, both the estimated force generated by uterine peristalsis and the total Ca 2+ raised by Ca 2+ oscillations are smaller in uteri from adenomyotic mice. Uteri from adenomyotic mice on day 14, but not on day 55, exhibit hyperresponsiveness to oxytocin. Embryo implantations are decreased in adenomyotic adult mice. Our results reveal a mode switch from bursts to spikes (rather than an increased peak frequency) of uterine Ca 2+ oscillations and peristalsis and concurrent hyperresponsiveness to oxytocin in the neonatal stage are two characteristics of adenomyosis. These characteristics may contribute to embryo implantation impairments and decreased fertility in adenomyosis.

My notes (saved in your browser only)

Condition tags

adenomyosis

Citation neighborhood

Papers in the corpus that this work cites (lower rings, blue) and that cite this one (upper rings, green). Dot size scales with the paper's in-corpus citation count — bigger dot = more influential within the endo/adeno field. Click a dot to open that paper. [ expand to 2 hops ] — adds papers reached through this work's immediate citers/citees. Heavier; up to 60 extra dots.

References (100)

Cited by (9)

SciLite annotations

organisms 91
mus sp. mus sp. transgenic mice mus sp. mus sp. transgenic mice homo heidelbergensis humans human transgenic mice mus sp. transgenic mice mus sp. mus sp. mus sp. mus sp. mus sp. rodents rodents multicellular animals rodents mus sp. mus sp. rodents mus sp. mus sp. mus sp. mus sp. peanut mus sp. mus sp. mus sp. mus sp. mus sp. mus sp. transgenic mice naine d'afrique de l'ouest transgenic mice transgenic mice transgenic mice transgenic mice mus sp. mus sp. mus sp. mus sp. mus sp. mus sp. mus sp. mus sp. mus sp. mus sp. mus sp. mus sp. transgenic mice mus sp. mus sp. mus sp. mus sp. mus sp. transgenic mice +31 more
chemicals 59
tamoxifen 2-pyrrolyl group 2-acylglycerol 18:0 estrogen calcium tamoxifen 2-acylglycerol 18:0 2-pyrrolyl group water calcium tamoxifen tamoxifen tamoxifen lecithin tamoxifen carbon dioxide salt agarose agarose silicone macromolecule 2-acylglycerol 18:0 calcein am argon alexa fluor 488 haematoxylin haematoxylin 2-pyrrolyl group hexose + c4h5n3o2 tamoxifen tamoxifen tamoxifen tamoxifen tamoxifen tamoxifen tamoxifen tamoxifen tamoxifen tamoxifen tamoxifen hexose + c4h5n3o2 2-pyrrolyl group calcium calcium 2-pyrrolyl group calcium oxytocin photon tamoxifen tamoxifen tamoxifen 2-pyrrolyl group tamoxifen tamoxifen tamoxifen tamoxifen tamoxifen tamoxifen 2-acylglycerol 18:0 argon

Source provenance

europepmc
last seen: 2026-06-04T01:30:01.192114+00:00
openalex
last seen: 2026-06-10T17:14:06.276822+00:00
pubmed
last seen: 2026-05-13T22:24:08.918168+00:00
scilite
last seen: 2026-05-18T04:25:29.313245+00:00
License: CC0 · commercial use OK