ArticleJournal of molecular histology2025
TGF-β signaling regulates gene expression, phagocytosis, and cell proliferation and supports glial cell survival in primary rat mixed glial cell cultures.
Article in Journal of molecular histology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
1 citing paper in PubMed.
- TGF‑β1 in obstructive sleep apnea: linking intermittent hypoxia, upper‑airway remodeling, and systemic comorbidities.Sleep & breathing = Schlaf & Atmung · 2026Review
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
Glial cells, including astrocytes, microglia, and oligodendrocytes, play an important role in the repair of damaged central nervous system tissue. In our previous study, we showed that transforming growth factor-beta (TGF-β) signaling occurs in glial cells in the hippocampus after ischemia. However, the functional significance of TGF-β signaling in the hippocampus after ischemia remains unclear. In the present study, transcriptome analysis was performed to comprehensively examine the TGF-β signaling-induced gene expression changes in primary cultured rat mixed glial cells. TGF-β1 upregulated 287 genes and downregulated 272 genes. Representative genes upregulated by TGF-β1 included genes encoding extracellular matrix-related proteins. Conversely, representative genes downregulated by TGF-β1 included genes encoding proteins related to immune response. These results suggest the diverse effects of TGF-β1 on gene expression. Since genes downregulated by TGF-β1 included genes involved in cell phagocytosis, proliferation, and survival, the effects of TGF-β1 and -β2 on cell phagocytosis, proliferation, and survival were investigated in mixed glial cells. TGF-β1 and -β2 suppressed astrocyte and microglial proliferation, and promoted and suppressed astrocyte and microglial phagocytosis, respectively. Additionally, TGF-β1 or -β2 canceled the serum-free culture-induced increase in the ratio of TUNEL-labeled microglia and oligodendrocytes. Furthermore, the culture in a medium containing the TGF-β signaling inhibitor SB525334 reduced glial cell survival and increased the expressions of genes encoding cell death-related molecules. Our study results suggest that TGF-β contributes to postischemic brain tissue repair by regulating glial cell gene expression, phagocytosis, and proliferation, and supporting glial cell survival.
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Identifiers
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.