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Wireless Electrical-Molecular Quantum Signalling for Cancer Cell Induced Death

ABSTRACT: Wireless Electrical-Molecular Quantum Signalling for Cancer Cell Induced Death

PROVIDER: PRJNA975960 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24731228_1.fastq.gz	Fastqsanger.gz
	SRR24731228_2.fastq.gz	Fastqsanger.gz
	SRR24731229_1.fastq.gz	Fastqsanger.gz
	SRR24731229_2.fastq.gz	Fastqsanger.gz
	SRR24731230_1.fastq.gz	Fastqsanger.gz

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Project description:Background: Electrical stimulation (ES) has been established as a reliable and beneficial approach in therapeutic rehabilitation, exhibiting negligible side effects. Nevertheless, research focusing on the application of ES for cardiac hypertrophy remains limited, as it fails to provide an enduring remedy for chronic diseases. Battery-free implants have been surgically placed on the surface of the vagus nerve in rats, and wireless ES has been applied for four weeks to observe potential alterations in cardiac hypertrophy. Methods: In this investigation, vagal ES, characterized by its wireless, battery-free, and fully implantable nature, was utilized to treat cardiac hypertrophy. The vagus nerve at the stimulation site was carefully embedded within an envelope, sealed securely using multiple bioabsorbable sutures. Subsequently, a cardiac hypertrophy model was induced in rats via abdominal aortic coarctation for four weeks. A comprehensive array of experimental techniques was employed, encompassing qRT-PCR, Western blotting, transmission electron microscopy, HE staining, WGA staining, Masson’s staining, immunohistochemistry, and immunofluorescence. Results: The findings of this investigation demonstrated that ES markedly attenuates cardiac hypertrophy. Metabolomic analysis revealed a notable reduction in lactate levels within myocardial tissue following ES. Proteomic analysis of myocardial tissues indicated a substantial decrease in the expression of autophagy and mitophagy-related proteins after ES. Additionally, ChIP-seq results identified BCL2 interacting protein 3 (Bnip3) as a binding partner for H3K18 lactylation (H3K18la), exploring its role in modulating mitophagy. Mechanistically, it was shown that ES reduced lactate accumulation through the upregulation of monocarboxylate transporter 4 (MCT4) by decreasing norepinephrine (NE) levels. Furthermore, ES reversed cardiac hypertrophy by diminishing H3K18la levels, thus inhibiting BNIP3 protein expression. Conclusion: Continuous ES effectively reduces intracellular lactate by lowering NE levels within myocardial tissue, inhibiting mitophagy mediated by H3K18la.This pathway assists in diminishing cardiac hypertrophy, emphasizing the critical involvement of the afferent vagal pathway in regulating cardiac hypertrophy.

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Wireless Electrical-Molecular Quantum Signalling for Cancer Cell Induced Death

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