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Omics · study · 2026

Transection of the Cervical Sympathetic Trunk Ameliorates Pulmonary Arterial Hypertension probably by Suppressing Transcriptome Profile and calcium signaling in rat model

Listed in NCBI GEO

Pulmonary arterial hypertension (PAH) is mostly induced by excessive proliferation of pulmonary arterial smooth muscle cells (PASMCs) with undefined mechanism.

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This study investigated the function and mechanism of transection of the cervical sympathetic trunk (TCST) on the progression of monocrotaline (MCT)-induced PAH in rats and explored the underlying mechanism.A rat model of PAH was established by MCT injection. We evaluated the restoration of pulmonary architecture and hemodynamic parameters following TCST.

Transcriptome sequencing (RNA-seq) was performed to identify key regulatory genes and signaling pathways that are particularly correlated with PASMC proliferation. The identified genes and pathways were further validated in the PAH model.TCST significantly attenuated pulmonary vascular remodeling and improved hemodynamic condition, as evidenced by reduced mean pulmonary arterial pressure (mPAP), right ventricular systolic pressure (RVSP), and right ventricular hypertrophy index (RVHI) compared to the PAH+sham group.

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RNA-seq analysis revealed that TCST suppressed calcium signaling and cell proliferation pathways, with downregulated DEGs enriched in immune responses, inflammatory responses, and the calcium signaling pathway. Differential expression analysis showed downregulation of the calcium pathway genes Adra1d and Tacr1, as well as their transcriptional regulator Foxa3. Further qPCR experiments confirmed decreased levels of Adra1d, Tacr1, Plcb1, and Foxa3.

ELISA confirmed the inhibited expression of inositol trisphosphate (IP3), which directly regulate intracellular calcium concentration.We explored the mechanism of TCST in ameliorating PAH by the suppression of the Foxa3/Adra1d-Tacr1 axis involved in calcium signaling, revealing a novel link between PAH and calcium-driven vascular remodeling, and a mechanistic basis for TCST as a potential therapeutic strategy for PAH.

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Life Sciences
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RNA sequencing 65% · Sequencing 75%
Provenance · 1 source records, 9 field assertions
SourceKeyLast seenRaw
NCBI GEOGSE32827314 d agoJSON v1
FieldAssertionExtractorEvidence
access_levelsource · NCBI GEOconnector:ncbi_geo@1.0.0
concepts[field].local:field:life-sciencesmapping · NCBI GEOconnector:ncbi_geo@1.0.0
concepts[method].geo_series_type:expression-profiling-by-high-throughput-sequencingsource · NCBI GEOconnector:ncbi_geo@1.0.0/gdstype
concepts[modality].local:modality:rna-seqenrichment · NCBI GEOkeyword-concept-rules@1.0.0title+description (65%)
concepts[modality].local:modality:sequencingenrichment · NCBI GEOkeyword-concept-rules@1.0.0title+description (75%)
concepts[organism].NCBITaxon:10116source · NCBI GEOconnector:ncbi_geo@1.0.0/taxon
descriptionsource · NCBI GEOconnector:ncbi_geo@1.0.0/summary
publication_datesource · NCBI GEOconnector:ncbi_geo@1.0.0
titlesource · NCBI GEOconnector:ncbi_geo@1.0.0/title