98%
921
2 minutes
20
Neurotrophins and inflammatory mediators are known to influence endometrial function, but their interplay in luminal epithelial cells remains poorly characterized. In this study, sheep endometrial luminal epithelial cells (SELECs) were treated with nerve growth factor (NGF), lipopolysaccharide (LPS), or both, and the effects on gene expression and prostaglandin secretion were evaluated. NGF stimulation alone induced a clear transcriptional activation of , neurotrophic receptor tyrosine kinase 1 (), p75 neurotrophin receptor (), cyclooxygenase 2 (), and steroidogenic acute regulatory protein (). LPS treatment selectively increased Toll-like receptor 4 (), , and insulin-like growth factor binding protein 6 (). Combined NGF and LPS treatment did not enhance the transcriptional response beyond that induced by NGF alone, except for . However, co-treatment resulted in a modest increase in prostaglandin production, particularly prostaglandin F2α (PGF2α), but not prostaglandin E2 (PGE2), compared to single treatments, suggesting a possible post-transcriptional modulation rather than a transcriptional synergy. These findings indicate that NGF acts as the primary transcriptional driver in SELECs, while LPS contributes selectively and may enhance prostaglandin output. The observed increase in prostaglandin production may involve post-transcriptional mechanisms, although this remains to be confirmed.
Download full-text PDF |
Source |
---|---|
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC12295654 | PMC |
http://dx.doi.org/10.3390/ijms26146862 | DOI Listing |
Int J Mol Sci
July 2025
Department of Veterinary Medicine, University of Perugia, Via San Costanzo 4, 06126 Perugia, Italy.
Neurotrophins and inflammatory mediators are known to influence endometrial function, but their interplay in luminal epithelial cells remains poorly characterized. In this study, sheep endometrial luminal epithelial cells (SELECs) were treated with nerve growth factor (NGF), lipopolysaccharide (LPS), or both, and the effects on gene expression and prostaglandin secretion were evaluated. NGF stimulation alone induced a clear transcriptional activation of , neurotrophic receptor tyrosine kinase 1 (), p75 neurotrophin receptor (), cyclooxygenase 2 (), and steroidogenic acute regulatory protein ().
View Article and Find Full Text PDFCells
June 2025
Department of Microbiology, College of Medicine, Konyang University, Daejeon 32992, Republic of Korea.
In this study, we investigated the potential of a three-mushroom complex extract (GMK) to inhibit neuronal cell death induced by the activation of AMPA and NMDA receptors following glutamate treatment in NGF-differentiated PC12 neuronal cells. GMK significantly mitigated glutamate-induced excitotoxic neuronal apoptosis by reducing the elevated expression of BAX, a critical regulator of apoptosis, and restoring BCL2 levels. These neuroprotective effects were associated with redox regulation, as evidenced by the upregulation of SOD, CAT, and GSH levels, and the downregulation of MDA levels.
View Article and Find Full Text PDFBiol Psychiatry Glob Open Sci
September 2025
Wits Integrated Molecular Physiology Research Initiative, Wits Health Consortium Ltd., Department of Physiology, School of Biomedical Sciences, Faculty of Health Sciences, University of the Witwatersrand, Johannesburg, South Africa.
Background: Neuroinflammation is linked to the development of depression. Exposure to the proinflammatory endotoxin lipopolysaccharide (LPS) is associated with a depressive-like phenotype in rodents. However, acute LPS exposure may reflect sickness behavior, and thus the molecular mechanisms and neurobehavioral changes associated with chronic neuroinflammation warrant investigation.
View Article and Find Full Text PDFJCI Insight
November 2024
Division of Spine Surgery, Department of Orthopedics, The Third Affiliated Hospital, Southern Medical University, Academy of Orthopedics, Guangdong Province, Guangzhou, China.
Soft tissue trauma can cause immune system disturbance and neuropathological invasion, resulting in heterotopic ossification (HO) due to aberrant chondrogenic differentiation of mesenchymal stem cells (MSCs). However, the molecular mechanisms behind the interaction between the immune and nervous systems in promoting HO pathogenesis are unclear. In this study, we found that mast cell-specific deletion attenuated localized tissue inflammation, with marked inhibition of HO endochondral osteogenesis.
View Article and Find Full Text PDFNeurol Res
December 2024
Department of Basic Sciences, Division of Biochemistry and Molecular Biology, Faculty of Veterinary Medicine, Shahid Chamran University of Ahvaz, Ahvaz, Iran.
Introduction: Astrocytes, specialized glial cells, are essential for maintaining the central nervous system homeostasis. Inflammatory conditions can disrupt neurotrophic factors and receptor expression in astrocytes, leading to potential central nervous system damage. Itaconate, recently identified for its anti-inflammatory properties, was investigated in this study for its effects on neurotrophic factors in LPS-stimulated primary rat astrocytes.
View Article and Find Full Text PDF