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Aldh1a3 accelerates lung metastasis of PDAC via enhancing tumor cells - lung epithelial cells cross talk through Sema4d-Plxnb1 and Sema3a-Nrp1 signaling

ABSTRACT: In previous studies, we found that high expression of aldehyde dehydrogenase 1 family member A3 (ALDH1A3) was associated with more lymph node metastases in pancreatic ductal adenocarcinoma (PDAC). We here report in PDAC Aldh1a3 promotes lung colonization, while is dispensable in liver colonization or proliferation. Aldh1a3 upregulates the transcription of Plxnb1 and Nrp1 via accelerating acetylation at histone H3 lysine in the promoter regions of Plxnb1 and Nrp1. The enhancing signaling of Sema4d-Plxnb1 and Sema3a-Nrp1 between pancreatic cancer cells and lung epithelial cells facilitate tumor cells to colonize in the lung. Our studies have uncovered Aldh1a3 as a key regulator of semaphorin signaling. Sema4d-Plxnb1 and Sema3a-Nrp1 signaling is important for lung metastatic organotropism of PDAC, but is dispensable in liver metastasis.

ORGANISM(S): Mus musculus

PROVIDER: GSE248375 | GEO | 2026/03/02

REPOSITORIES: GEO

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Aldh1a3 accelerates lung metastasis of PDAC via enhancing tumor cells - lung epithelial cells cross talk through Sema4d-Plxnb1 and Sema3a-Nrp1 signaling

Project description:Aldh1a3 accelerates lung metastasis of PDAC via enhancing tumor cells - lung epithelial cells cross talk through Sema4d-Plxnb1 and Sema3a-Nrp1 signaling

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miR-124 acts through coREST to control the onset of Sema3A sensitivity in navigating retinal growth cones

Project description:During axon pathfinding, growth cones commonly exhibit changes in sensitivity to guidance cues that follow a strict timetable, even in the absence of pathway feedback, implicating cell-intrinsic regulation. Cellular timer mechanisms, however, are poorly understood. Here we have investigated microRNAs in the timing control of Sema3A sensitivity in retinal ganglion cell (RGC) growth cones. A developmental profiling screen identified miR-124 as a candidate timer. Loss of miR-124 delayed the onset of Sema3A sensitivity and concomitant Neuropilin-1 (NRP-1) receptor expression, and caused cell autonomous pathfinding errors. CoREST, a cofactor of a NRP1 repressor, was identified as a novel target and mediator of miR-124 for this highly specific temporal aspect of RGC growth cone responsiveness. Our findings indicate that miR-124 plays an important role in regulating the intrinsic temporal changes in RGC growth cone sensitivity and suggest that microRNAs may play a broad role as linear timers in vertebrate neuronal development. Two independent experiments were performed. One with a single sample for each of 3 stages, and the second with 2 biological replicates of each stage.

2011-12-12 | E-GEOD-33444 | biostudies-arrayexpress

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Deciphering the role of tumor cell-intrinsic Sema4D in TNBC mouse tumor using single-cell RNA sequencing

Project description:Sema4D (Semaphorin 4D, also known as CD100) is a member of the class IV semaphorin family and is predominantly expressed on the surface of lymphocytes, monocytes, macrophages, and endothelial cells. The current understanding of Sema4D function is focused on its receptor-mediated signaling activities with limited data on its intrinsic mechanisms. However, the immunological roles and functional mechanism of tumor cell-intrinsic Sema4D regulating immune escape remain largely unknown. This study employs single-cell RNA sequencing (scRNA-seq) to investigate cellular and regulatory role of Sema4d in TNBC mouse tumors.

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Smoking aggravates neovascular age-related macular degeneration via Sema4D-PlexinB1 axis-mediated activation of pericytes [scRNA-seq]

Project description:Age-related macular degeneration (AMD) is a prevalent neuroinflammation condition and the leading cause of irreversible blindness among the elderly population. Smoking significantly increases AMD risk, yet the mechanisms remain unclear. Here, we investigated the role of Sema4D-PlexinB1 axis in the progression of AMD, in which Sema4D-PlexinB1 is highly activated by smoking. Using patient-derived samples and mouse models, we discovered that smoking increased the presence of Sema4D on the surface of CD8+ T cells that migrated into the choroidal neovascularization (CNV) lesion via CXCL12-CXCR4 axis and interacted with its receptor PlexinB1 on choroidal pericytes. This led to ROR2-mediated PlexinB1 phosphorylation and pericytes activation, hence disrupted vascular homeostasis and promoted neovascularization. Inhibition of Sema4D reduced CNV and improved the benefit of anti-VEGF treatment. In conclusion, this study unveils the molecular mechanisms through which smoking exacerbates AMD pathology, and presents a potential therapeutic strategy by targeting Sema4D to augment current AMD treatments.

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Smoking aggravates neovascular age-related macular degeneration via Sema4D-PlexinB1 axis-mediated activation of pericytes [bulk RNA-seq]

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PIEZO1 promotes odontoblast-mediated reactionary dentinogenesis via Ca2+-SEMA3A axis

Project description:The odontoblasts are specialized cells responsible for dentin synthesis and nociceptive signal detection in response to external stimuli. Recent studies have shown that the mechanosensitive ion channel PIEZO1 is involved in bone formation and remodeling through the influx of calcium ions, and it is abundantly expressed in odontoblasts. However, the specific role of PIEZO1 in reactionary dentinogenesis by odontoblasts and the underlying mechanisms still remain elusive. In this study, we found intense PIEZO1 expression in the plasma membrane and cytoplasm of odontoblasts in human and mouse mandibular molars, and human odontoblast-like cells (hOBLCs). In hOBLCs, PIEZO1 positively regulated DSPP, DMP1, and COL1A1 expression through the Ca2+/PI3K-Akt/SEMA3A signaling pathway. Additionally, exogenous SEMA3A supplementation effectively reversed reduced mineralization capacity in PIEZO1-knockdown hOBLCs. In vivo, Piezo1 expression peaked at day 7 and returned to baseline at day 21 in a wild-type (WT) mice dentin injury model, with Sema3a presenting a similar expression pattern. To investigate the specific role of PIEZO1 in reactionary dentinogenesis, mice with a conditional knockout of PIEZO1 in odontoblasts were generated, and no significant differences of teeth phenotypes were observed between the control and conditional knockout (cKO) mice. Nevertheless, cKO mice exhibited reduced reactionary dentin formation, and decreased Sema3a and Dsp positive staining after dentin injury, indicating impaired dental pulp repair mediated by odontoblasts. In summary, these findings suggest that PIEZO1 enhances mineralization capacity of hOBLCs in vitro via the Ca2+/Akt/SEMA3A signaling pathway and contributes to dental pulp repair through enhancing reactionary dentinogenesis in vivo.

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Gpr97 exacerbates AKI via mediating Sema3A signaling

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2021-11-05 | E-MTAB-10122 | biostudies-arrayexpress

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