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Identification of circulating miRNA molecular signature for erectile dysfunction in type 2 diabetes

ABSTRACT: Identification of circulating miRNA molecular signature for erectile dysfunction in type 2 diabetes

PROVIDER: PRJNA754377 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15442109.fastq.gz	Fastqsanger.gz
	SRR15442110.fastq.gz	Fastqsanger.gz
	SRR15442111.fastq.gz	Fastqsanger.gz
	SRR15442112.fastq.gz	Fastqsanger.gz
	SRR15442113.fastq.gz	Fastqsanger.gz

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Project description:Background: Erectile dysfunction (ED) is a common complication of diabetes mellitus (DM), and because of its complex neurovascular etiology, the associated molecular pathogenic mechanisms are not fully understood. This study investigated the important functions and potential molecular regulatory roles of CELF2 in DMED. Methods: An in vitro HUVEC model with CELF2 overexpression was successfully established via transfection with a CELF2-overexpressing lentiviral vector. The effects of CELF2 overexpression on cell proliferation and angiogenesis were assessed via CCK-8 and angiogenesis assays. RNA sequencing was employed to evaluate the gene expression profiles and alternative splicing events regulated by CELF2. An RNA-sequencing assay was performed to evaluate gene expression profiles and alternative splicing genes in HUVECs overexpressing CELF2, and an integration analysis was combined with GSE146078 data to detect potential target genes related to DMED. Results: The expression of genes related to angiogenesis and the immune response significantly increased with CELF2 overexpression, and the four hub genes associated with alternative splicing in aging and angiogenesis were CXCL2, CXCL10, IL-1A and IL-6. Conclusions: CELF2 appears to be a key factor in DMED, influencing gene expression and alternative splicing related to angiogenesis and immune responses. The identified hub genes (CXCL2, CXCL10, IL-1A, and IL-6) are closely related to DMED and warrant further investigation to understand the underlying mechanisms and potential therapeutic implications. Keywords: Diabetes mellitus; Erectile dysfunction; RBPs; CELF2; RNA sequencing

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Project description:Phosphodiesterase type 5 inhibitors (PDE5is) are the primary therapeutic option for erectile dysfunction. However, 30% of patients do not respond to PDE5is treatment, making the quest for a new treatment modality a central endeavor. Here, we found a new pathway in erectile function control, mechano-regulated YAP/TAZ activate Adrenomedullin transcription, which sustains smooth muscle cells (SMCs) relaxation to maintain the erection. We first found that penile erection stretches the SMCs, dominating YAP/TAZ activity. Subsequently, we showed that YAP/TAZ plays a vital role in erectile function and penile rehabilitation using genetic lesions and several animal models. The mechanism relies on the regulation of Adrenomedullin on penile SMCs contraction, which we identify here as a direct YAP/TAZ transcript. Notably, conventional PDE5is targeting NO-cGMP signaling do not cure YAP/TAZ deficient ED. In contrast, by activating YAP/TAZ-Adrenomedullin cascade, mechano-stimulation improved erectile function, including PDE5is non-responders in both experimental models and clinical trials. Our studies lay the groundwork for exploring mechano-YAP/TAZ-Adrenomedullin as prospective targets in the treatment of ED

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Gene expression profile on the penile tissue of erectile dysfunction (ED) in cavernous nerve injury (CNI) RAT model

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