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MicroRNA-637/661 ameliorate hypoxic induced pulmonary arterial hypertension by targeting TRIM29 signaling pathway

ABSTRACT: microRNA-637/661 ameliorate hypoxic induced pulmonary arterial hypertension by targeting TRIM29 signaling pathway

PROVIDER: PRJNA1144819 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR30147187_1.fastq.gz	Fastqsanger.gz
	SRR30147187_2.fastq.gz	Fastqsanger.gz
	SRR30147188_1.fastq.gz	Fastqsanger.gz
	SRR30147188_2.fastq.gz	Fastqsanger.gz
	SRR30147189_1.fastq.gz	Fastqsanger.gz

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microRNA-637/661 ameliorate hypoxic-induced pulmonary arterial hypertension by targeting TRIM29 signaling pathway.

Project description:The pathogenesis of pulmonary arterial hypertension (PAH) is closely linked to the abnormal proliferation of pulmonary artery smooth muscle cells. Studies have demonstrated that microRNAs play pivotal roles in the progression of pulmonary hypertension. We found that microRNA-637 (miR-637) and microRNA-661 (miR-661) are expressed at low levels in the serum of PAH patients. Moreover, the overexpression of miR-637 or miR-661 inhibited human pulmonary artery smooth muscle cell (HPASMC) proliferation and migration in hypoxic culture. Mechanistically, we overexpressed these two microRNAs in HPASMCs, and the RNA-sequencing (RNA-seq) results demonstrated that TRIM29 mRNA was suppressed, indicating that TRIM29 is a substrate. TRIM29 accumulates in the serum of patients with PAH and promotes cell proliferation and migration by activating AKT/mTOR signalling. In addition, overexpression of miR-637 or miR-661 reversed TRIM29-mediated HPASMC proliferation and migration. This study revealed that miR-637 and miR-661 are able to inhibit the proliferation ability of HPASMCs under hypoxic conditions through targeting TRIM29, suggesting that the microRNA-637/661/TRIM29 axis may act as a target for PAH treatment.

| S-EPMC11564567 | biostudies-literature

microRNA-637/661 ameliorate hypoxic induced pulmonary arterial hypertension by targeting TRIM29 signaling pathway

Project description:To investigate the synergistic effect of miR637/miR661 in PAH regulation, we overexpressed these two microRNAs in HPASMC cells cultured in a low oxygen environment.We then performed the RNA-seq assay to analysis gene expression profiles.

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Project description:Transcriptional profiling of human normal-like breast cells MCF10A comparing control MCF10A cells transfected with a pLenti6/BLOCK-iT™-DEST vector with MCF10A cells transfected with a pLenti6/BLOCK-iT™-DEST vector containing TRIM29 shRNA targeting nucleotides 1265–1285 of the TRIM29 open reading frame (ORF, NM_012101). Transcriptional profiling of human breast cancer cells MCF7 comparing control MCF7 cells transfected with a pLenti6.2/N-LumioTM/V5-DEST vector with MCF7 cells transfected with a pLenti6.2/N-LumioTM/V5-DEST vector containing TRIM29 full-length cDNA (ORF, NM_012101). Two-condition experiment, MCF10A-vector control vs. MCF10A-TRIM29 shRNA cells; MCF7-vector control vs. MCF7-TRIM29 cells.

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Project description:Prostate adenocarcinoma (PRAD) is the second most common cause of cancer-related deaths in men. In PRAD, high variability in DNA methylation and a high rate of large genomic rearrangements is often observed. To elucidate the reasons behind such high variance, we integrated DNA methylation, RNA-seq, and copy number alterations datasets from The Cancer Genome Atlas (TCGA) focusing on PRAD and subsequently employed weighted gene co-expression network analysis (WGCNA). Our results show that only a single cluster of co-expressed genes is associated with genomic and epigenomic instability. Within this cluster, TP63 and TRIM29 are key transcription regulators and are downregulated in PRAD. We revealed that TP63 regulates the level of enhancer methylation in prostate basal epithelium cells. TRIM29 forms a complex with TP63 and together regulate the expression of genes specific to the prostate basal epithelium. Moreover, TRIM29 binds DNA repair proteins and prevents formation of the TMPRSS2:ERG gene fusion typically observed in PRAD. Therefore, the study shows that TRIM29 and TP63 are important regulators maintaining the identity of the basal epithelium under physiological conditions. Finally, we uncover the role of TRIM29 in PRAD development.

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