<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Hamshaw I</submitter><funding>Wellcome Trust</funding><pagination>1285779</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC10752971</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>14</volume><pubmed_abstract>Preterm birth is the leading cause of infant morbidity and mortality. There has been an interest in developing prostaglandin F&lt;sub>2α&lt;/sub> (PGF&lt;sub>2α&lt;/sub>) antagonists as a new treatment for preterm birth, although much of the rationale for their use is based on studies in rodents where PGF&lt;sub>2α&lt;/sub> initiates labour by regressing the corpus luteum and reducing systemic progesterone concentrations. How PGF&lt;sub>2α&lt;/sub> antagonism would act in humans who do not have a fall in systemic progesterone remains unclear. One possibility, in addition to an acute stimulation of contractions, is a direct alteration of the myometrial smooth muscle cell state towards a pro-labour phenotype. In this study, we developed an immortalised myometrial cell line, MYLA, derived from myometrial tissue obta</pubmed_abstract><journal>Frontiers in pharmacology</journal><pubmed_title>PGF&lt;sub>2α&lt;/sub> induces a pro-labour phenotypical switch in human myometrial cells that can be inhibited with PGF&lt;sub>2α&lt;/sub> receptor antagonists.</pubmed_title><pmcid>PMC10752971</pmcid><funding_grant_id>200870/Z/16/Z</funding_grant_id><pubmed_authors>Blanks AM</pubmed_authors><pubmed_authors>Hamshaw I</pubmed_authors><pubmed_authors>Baxter L</pubmed_authors><pubmed_authors>Wever WJ</pubmed_authors><pubmed_authors>Pinton P</pubmed_authors><pubmed_authors>Ferguson GD</pubmed_authors><pubmed_authors>Stark R</pubmed_authors><pubmed_authors>Alam MT</pubmed_authors><pubmed_authors>Straube A</pubmed_authors><pubmed_authors>Sen A</pubmed_authors><pubmed_authors>Yue Y</pubmed_authors><pubmed_authors>Yin J</pubmed_authors></additional><is_claimable>false</is_claimable><name>PGF&lt;sub>2α&lt;/sub> induces a pro-labour phenotypical switch in human myometrial cells that can be inhibited with PGF&lt;sub>2α&lt;/sub> receptor antagonists.</name><description>Preterm birth is the leading cause of infant morbidity and mortality. There has been an interest in developing prostaglandin F&lt;sub>2α&lt;/sub> (PGF&lt;sub>2α&lt;/sub>) antagonists as a new treatment for preterm birth, although much of the rationale for their use is based on studies in rodents where PGF&lt;sub>2α&lt;/sub> initiates labour by regressing the corpus luteum and reducing systemic progesterone concentrations. How PGF&lt;sub>2α&lt;/sub> antagonism would act in humans who do not have a fall in systemic progesterone remains unclear. One possibility, in addition to an acute stimulation of contractions, is a direct alteration of the myometrial smooth muscle cell state towards a pro-labour phenotype. In this study, we developed an immortalised myometrial cell line, MYLA, derived from myometrial tissue obta</description><dates><release>2023-01-01T00:00:00Z</release><publication>2023</publication><modification>2025-04-20T09:26:35.587Z</modification><creation>2025-04-20T09:26:35.587Z</creation></dates><accession>S-EPMC10752971</accession><cross_references><pubmed>38155905</pubmed><doi>10.3389/fphar.2023.1285779</doi></cross_references></HashMap>