Dataset Information

The physiological basis with uterine myometrium contractions from electro-mechanical/hormonal myofibril function to the term and preterm labor.

ABSTRACT:

Background

Most labor-related problems can be attributed to the uterine myometrium muscle, as this irritable tissue must suppress its irritability potential during pregnancy. Unfortunately, fewer studies have investigated the causes of this lack of suppression in preterm labor.

Methods

We conducted a scoping narrative review using three online databases (PubMed, Scopus, and Science Direct).

Results

The review focused on ion channel functions in the myometrium, including sodium channels [Na K-ATPase, Na-activated K channels (Slo2), voltage-gated (SCN) Na⁺, Na⁺ leaky channels, nonselective (NALCN) channels], potassium channels [KATP (Kir6) channels, voltage-dependent K channels (Kv4, Kv7, and Kv11), twin-pore domain K channels (TASK, TREK), inward rectifier Kir7.1, Ca²⁺-activated K⁺ channels with large (KCNMA1, Slo1), small (KCNN1-3), intermediate (KCNN4) conductance], and calcium channels [L-Type and T-type Ca²⁺ channels, calcium-activated chloride channels (CaCC)], as well as hyperpolarization-activated cation channels. These channels' functions are associated with hormonal effects such as oxytocin, estrogen/progesterone, and local prostaglandins.

Conclusion

Electromechanical/hormonal activity and environmental autocrine factors can serve as the primary practical basis for premature uterine contractions in term/preterm labor. Our findings highlight the significance of.1.the amplitude rate of hyperpolarization and the frequency of contractions,2.changes in the estrogen/progesterone ratio,3.Prostaglandins E/F involvement in initiating potential spikes and the increase of intracytoplasmic Ca²⁺.This narrative study highlights the range of hyperpolarization and the frequency of myometrium contractions as crucial factors. The synchronized complex progress of estrogen to progesterone ratio and prostaglandins plays a significant role in initiating potential spikes and increasing intracytoplasmic Ca²⁺, which further influences the contraction process during labor. Insights into myometrium physiology gained from this study may pave the way for much-needed new treatments to reduce problems associated with normal and preterm labor.

SUBMITTER: Zangeneh FZ

PROVIDER: S-EPMC10687101 | biostudies-literature | 2023 Nov

REPOSITORIES: biostudies-literature

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Publications

The physiological basis with uterine myometrium contractions from electro-mechanical/hormonal myofibril function to the term and preterm labor.

Zangeneh Farideh Zafari FZ Hantoushzadeh Sedighe S

Heliyon 20231119 11

<h4>Background</h4>Most labor-related problems can be attributed to the uterine myometrium muscle, as this irritable tissue must suppress its irritability potential during pregnancy. Unfortunately, fewer studies have investigated the causes of this lack of suppression in preterm labor.<h4>Methods</h4>We conducted a scoping narrative review using three online databases (PubMed, Scopus, and Science Direct).<h4>Results</h4>The review focused on ion channel functions in the myometrium, including sod ...[more]

PMID: 38034762

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Project description:BackgroundPreterm birth is now recognized as the primary cause of infant mortality worldwide. Interplay between hormonal and inflammatory signaling in the uterus modulates the onset of contractions; however, the relative contribution of each remains unclear. In this study we aimed to characterize temporal transcriptome changes in the uterus preceding term labor and preterm labor (PTL) induced by progesterone withdrawal or inflammation in the mouse and compare these findings with human data.MethodsMyometrium was collected at multiple time points during gestation and labor from three murine models of parturition: (1) term gestation; (2) PTL induced by RU486; and (3) PTL induced by lipopolysaccharide (LPS). RNA was extracted and cDNA libraries were prepared and sequenced using the Illumina HiSeq 2000 system. Resulting RNA-Seq data were analyzed using multivariate modeling approaches as well as pathway and causal network analyses and compared against human myometrial transcriptome data.ResultsWe identified a core set of temporal myometrial gene changes associated with term labor and PTL in the mouse induced by either inflammation or progesterone withdrawal. Progesterone withdrawal initiated labor without inflammatory gene activation, yet LPS activation of uterine inflammation was sufficient to override the repressive effects of progesterone and induce a laboring phenotype. Comparison of human and mouse uterine transcriptomic datasets revealed that human labor more closely resembles inflammation-induced PTL in the mouse.ConclusionsLabor in the mouse can be achieved through inflammatory gene activation yet these changes are not a requisite for labor itself. Human labor more closely resembles LPS-induced PTL in the mouse, supporting an essential role for inflammatory mediators in human "functional progesterone withdrawal." This improved understanding of inflammatory and progesterone influence on the uterine transcriptome has important implications for the development of PTL prevention strategies.

Project description:The mechanisms used to coordinate uterine contractions are not known. We develop a new model based on the proposal that there is a maximum distance to which action potentials can propagate in the uterine wall. This establishes "regions", where one action potential burst can rapidly recruit all the tissue. Regions are recruited into an organ-level contraction via a stretch-initiated contraction mechanism (myometrial myogenic response). Each uterine contraction begins with a regional contraction, which slightly increases intrauterine pressure. Higher pressure raises tension throughout the uterine wall, which initiates contractions of more regions and further increases pressure. The positive feedback synchronizes regional contractions into an organ-level contraction. Cellular automaton (CA) simulations are performed with Mathematica. Each "cell" is a region that is assigned an action potential threshold. An anatomy sensitivity factor converts intrauterine pressure to regional tension through the Law of Laplace. A regional contraction occurs when regional tension exceeds regional threshold. Other input variables are: starting and minimum pressure, burst and refractory period durations, enhanced contractile activity during an electrical burst, and reduced activity during the refractory period. Complex patterns of pressure development are seen that mimic the contraction patterns observed in laboring women. Emergent behavior is observed, including global synchronization, multiple pace making regions, and system memory of prior conditions. The complex effects of nifedipine and oxytocin exposure are simulated. The force produced can vary as a nonlinear function of the number of regions. The simulation directly links tissue-level physiology to human labor. The concept of a uterine pacemaker is re-evaluated because pace making activity may occur well before expression of a contraction. We propose a new classification system for biological CAs that parallels the 4-class system of Wolfram. However, instead of classifying the rules, biological CAs should classify the set of input values for the rules that describe the relevant biology.

Dataset Information

The physiological basis with uterine myometrium contractions from electro-mechanical/hormonal myofibril function to the term and preterm labor.

Background

Methods

Results

Conclusion

Publications

The physiological basis with uterine myometrium contractions from electro-mechanical/hormonal myofibril function to the term and preterm labor.

Similar Datasets

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