ArticleBiological trace element research2013
Dietary selenium influences calcium release and activation of MLCK in uterine smooth muscle of rats.
Article in Biological trace element research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed, 18 citations in OpenAlex.
- Porcine Sapovirus-Induced Tight Junction Dissociation via Activation of RhoA/ROCK/MLC Signaling Pathway.Journal of virology · 2021Article
- Rotavirus-Induced Early Activation of the RhoA/ROCK/MLC Signaling Pathway Mediates the Disruption of Tight Junctions in Polarized MDCK Cells.Scientific reports · 2018Article
- Selenium Deficiency Facilitates Inflammation Through the Regulation of TLR4 and TLR4-Related Signaling Pathways in the Mice Uterus.Inflammation · 2015Article
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Authors and funding
10 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
We sought to elucidate the effects of different concentrations of dietary selenium on calcium ion release, MLCK levels, and muscle contraction in the uterine smooth muscle of rats. The selenium (Se) content of blood and of uterine smooth muscle tissues was detected by fluorescence spectrophotometry. Ca(2+) content was measured by atomic absorption spectroscopy. Calmodulin (CaM) and MLCK RNA and protein levels were analyzed by quantitative real-time polymerase chain reaction and Western blot, respectively. Dietary Se intake increased the Se levels in the blood and in uterine smooth muscle tissues and increased the Ca(2+) concentration in uterine smooth muscle tissues. The addition of Se also promoted CaM expression and enhanced MLCK activation in uterine smooth muscle tissues. In conclusion, Ca(2+), CaM, and MLCK were regulated by Se in uterine smooth muscle; Se plays a major role in regulating smooth muscle contraction in the uterus.
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