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Slc39a2-mediated Zinc Homeostasis Modulates Innate Immune Signaling in Phenylephrine-induced Cardiomyocyte Hypertrophy

ABSTRACT: Slc39a2-mediated Zinc Homeostasis Modulates Innate Immune Signaling in Phenylephrine-induced Cardiomyocyte Hypertrophy

PROVIDER: PRJNA734256 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14699664.fastq.gz	Fastqsanger.gz
	SRR14699665.fastq.gz	Fastqsanger.gz
	SRR14699666.fastq.gz	Fastqsanger.gz
	SRR14699667.fastq.gz	Fastqsanger.gz
	SRR14699668.fastq.gz	Fastqsanger.gz

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Slc39a2-mediated Zinc Homeostasis Modulates Innate Immune Signaling in Phenylephrine-induced Cardiomyocyte Hypertrophy

Project description:Zinc dyshomeostasis has been involved in the pathogenesis of cardiac hypertrophy; however, the dynamic regulation of intracellular zinc and its downstream signaling in cardiac hypertrophy remain largely unknown. Here we screened ZIP (SLC39) family members that were responsible for zinc uptake in a phenylephrine (PE)-induced cardiomyocyte hypertrophy model. We found that Slc39a2 was the only member that was altered at mRNA level by PE treatment in neonatal rat ventricular myocytes (NRVMs), but its protein level was not affected. Zincpyr1 staining showed a significant decrease in zinc uptake after PE treatment or after Slc39a2 knockdown in NRVMs, indicating an inhibition of its transport activity during hypertrophy. Slc39a2 deficiency caused spontaneous hypertrophy in NRVMs, and further exacerbated the hypertrophic responses after PE treatment. RNA sequencing analysis confirmed a largely aggravated pro-hypertrophic transcriptome reprogramming after Slc39a2 knockdown. Interestingly, the innate immune pathways, including NOD signaling, TOLL-like receptor, NFB, and IRFs, were substantially enriched after Slc39a2 knockdown. Whereas IRF7, the most sensitive among all IRFs, did not mediate the effect of Slc39a2 in hypertrophy, pro-hypertrophy phosphorylations of NFB and STAT3 were significantly enhanced after Slc39a2 knockdown, in parallel with degradation of IkBα protein. Our data demonstrate that SLC39A2-mediated zinc homeostasis contributes to the remodeling of innate immune signaling in cardiomyocyte hypertrophy, and provide novel insights into the pathogenesis of heart failure and its treatment.

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Project description:Pathological growth of cardiomyocytes during hypertrophy is characterized by excess protein synthesis; however, the regulatory mechanism remains largely unknown. Using a neonatal rat ventricular myocyte (NRVMs) model, here we find that the expression of nucleosome assembly protein 1 like 5 (Nap1l5) is upregulated in phenylephrine (PE)-induced hypertrophy. Knockdown of Nap1l5 expression by siRNA significantly blocks cell size enlargement and pathological gene induction after PE treatment. In contrast, Adenovirus-mediated Nap1l5 overexpression significantly aggravates the pro-hypertrophic effects of PE on NRVMs. RNA-seq analysis reveals that Nap1l5 knockdown reverses the pro-hypertrophic transcriptome reprogramming after PE treatment. Whereas immune response is dominantly enriched in the upregulated genes, oxidative phosphorylation, cardiac muscle contraction and ribosome related pathways are remarkably enriched in the down-regulated genes. Although PRC2 and PRC1 are involved in Nap1l5-mediated gene regulation, Nap1l5 does not directly alter the levels of global histone methylations. However, puromycin incorporation assay shows that Nap1l5 is both necessary and sufficient to drive the increased protein synthesis rate in cardiomyocyte hypertrophy. This is attributable to a direct regulation of ribosome assembly by Nap1l5. Our findings demonstrate a previously unrecognized role of Nap1l5 in translation control during cardiac hypertrophy.

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