Sarah England
Washington University in St Louis, MO·Physiology
For most of pregnancy, the uterus stays relatively calm, with weak and uncoordinated contractions. Near term, contractions become stronger, more frequent and synchronized enough to deliver the baby.
- Fields
Physiology
Medicine & Clinical Research
Biophysics
- Topics
uterine contractility
myometrium
smooth muscle
- Grants
- 1 known grant, through Aug 2027
What they work on
- Measure the activity of the NALCN/SLO2.1 complex, a sodium leak channel paired with a sodium-activated potassium channel, in mouse uterine smooth muscle cells across pregnancy.
- Determine how NALCN/SLO2.1 activity affects calcium levels inside uterine smooth muscle cells and the strength of uterine contractions.
- Identify additional proteins that bind the NALCN/SLO2.1 complex in uterine smooth muscle cells and test how they change its function.
More about the research
Labor that starts too early or too late carries risks. Yet the molecular switch behind this transition is unknown, which makes it hard to design drugs that prevent preterm labor or help start labor. A key driver is a gradual change in the electrical charge across the membrane of uterine smooth muscle cells (myometrial smooth muscle cells, or MSMCs). As the inside becomes less negative, the muscle becomes easier to excite and contract.
Why it matters
Preterm labor and post-term pregnancy pose risks to mothers and babies, and current tools for controlling uterine contractions are limited. Defining the NALCN/SLO2.1 channel complex could point to future drugs. Activating the complex could keep the uterus relaxed and prevent preterm labor, while inhibiting it could help induce labor.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
David Aaron Jacobson
Vanderbilt University, TN·Physiology
Determine how the calcium pump PMCA1 and sodium/calcium exchanger NCX1 control β-cell calcium removal and insulin secretion, and how diabetes alters them, using β-cell knockout mice and human pseudoislets with shRNA knockdown.
Kirk Campbell
University of Pennsylvania, PA·Physiology
Define how Hippo-YAP signaling regulates the calcium-activated potassium channel KCa3.1 in podocytes, including whether nuclear YAP protects the actin cytoskeleton by repressing the KCNN4 gene that encodes it.
Romulo Hurtado
Weill Medical College of Cornell University, NY·Physiology
Define the transcriptional signaling mechanisms required for formation of HCN channel-expressing pacemaker cells and for functional peristalsis in the upper urinary tract, using a mutant mouse that lacks these pacemakers but has normal smooth muscle.
The school
Washington University in St Louis: 97 labs on PI Pages, $1.2B a year on research, 365 research doctorates a year.
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