Runx3 is a transcription factor that belongs to the Runx family. We studied the localization of Runx3 mRNA in the mouse uterus, and its function in the mouse endometrium using Runx3 knockout (Runx3(-/-)) mice. Runx3 mRNA was detected in the endometrial luminal epithelial cells, glandular epithelial cells and stromal cells below the epithelial cell layer on the luminal side. The uteri of Runx3(-/-) mice were smaller than those of wt mice. The endometrial layer and uterine glands of Runx3(-/-) mice were less developed than those of wild-type mice, and the endometrial stromal layer was thinner. Transforming growth factor β1 and β3 (TGFβ1 and β3) mRNA levels in endometrial stromal cells of Runx3(-/-) mice were low compared with those of wild-type mice. Estradiol-17β (E2) increased Tgfb2 mRNA levels in endometrial stromal cells of Runx3(-/-) mice, but not in those of wild-type mice. E2 increased epidermal growth factor (EGF) mRNA levels in endometrial stromal cells of wild-type mice, but did not increase those of Runx3(-/-) mice. The diminished Tgfb1 and Tgfb3 mRNA expressions may lead to the reduced proliferation of endometrial stromal cells. Alterations of E2-associated expressions of Tgfb2 and Egf mRNA in endometrial stromal cells of Runx3(-/-) mice may be associated with suppression of E2-dependent endometrial epithelial cell proliferation in Runx3(-/-) mice. Thus, Runx3 is likely to be a regulatory factor responsible for endometrial growth.
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http://dx.doi.org/10.1262/jrd.2012-066 | DOI Listing |
Sci Rep
December 2024
Department of Life Sciences, University of Siena, Siena, Italy.
The scaffold protein AMBRA1, which participates in the autophagy pathway, also promotes CD4 T cell differentiation to Tregs independent of autophagy through its interactor PP2A. Here we have investigated the role of AMBRA1 in CD8 T cell differentiation to cytotoxic T cells (CTL). AMBRA1 depletion in CD8 T cells was associated with impaired expression of the transcription factors RUNX3 and T-BET that drive CTL differentiation and resulted in impaired acquisition of cytotoxic potential.
View Article and Find Full Text PDFPLoS Genet
December 2024
Department of Molecular Genetics, Weizmann Institute of Science, Rehovot, Israel.
Epigenetics Chromatin
November 2024
Department of Microbiology, Faculty of Science, Chulalongkorn University, Bangkok, 10330, Thailand.
Background: To avoid exaggerated inflammation, innate immune cells adapt to become hypo-responsive or "tolerance" in response to successive exposure to stimuli, which is a part of innate immune memory. Polycomb repressive complex 2 (PRC2) mediates the transcriptional repression by catalyzing histone H3 lysine 27 trimethylation (H3K27me3) but little is known about its role in lipopolysaccharide (LPS)-induced tolerance in macrophages.
Result: We examined the unexplored roles of EED, a component of the PRC2, in LPS tolerant macrophages.
BMJ Open Respir Res
November 2024
Department of Pediatrics, Yantaishan Hospital, Yantai, Shandong, China
Purpose: Our research aimed to evaluate whether proto-oncogene serine/threonine-protein kinase Pim-1 (Pim1) inactivation could attenuate asthma by promoting runt-related transcription factor 3 (Runx3) expression and explore the underlying molecular mechanism.
Method: Phorbol 12-myristate 13-acetate (PMA, 50 nM) was used to induce inflammation in BEAS-2B human airway epithelial cells. ELISA and immunofluorescence double staining confirmed inflammation modelling and differential expression of Pim1 and Runx3.
Theranostics
September 2024
Organ Transplantation Center, Affiliated Hospital of Qingdao University, Qingdao, China.
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