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HIP-55/DBNL-dependent regulation of adrenergic receptor mediates the ERK1/2 proliferative pathway
Ning Liu1, Rui Xing, Chengzhi Yang
1Central Laboratory, Jilin University Second Hospital, Changchun 130041, China.
Abstract:
The activation of β-adrenergic receptors (β-ARs) plays a key role in regulating cardiac function. However, the detailed regulatory mechanisms of β-AR-induced fibrosis are still unclear. We used a proteomics approach to analyze the changes in protein expression patterns in cardiac fibrosis with β-AR stimulation. HIP-55 (also called debrin-like; DBNL) was revealed as a novel regulator in the signaling regulatory network with β-AR activation. Further studies of both HIP-55-overexpressed and -deficient cardiac fibroblasts indicated that HIP-55 negatively regulated β-AR-activated cardiac fibroblast proliferation and the proliferative signaling pathway may be associated with the extracellular signal-regulated protein kinase (ERK) activation. Our data provide a new mechanistic insight into the role of HIP-55 in β-AR-induced cardiac fibroblast proliferation and suggest a new treatment strategy for proliferative disorders.
Insights
Beta-adrenergic receptors (β-ARs) impact heart function, but their role in fibrosis is unclear. HIP-55 protein was identified as a key regulator, inhibiting β-AR-activated cardiac fibroblast proliferation via the ERK pathway.
Area of Science:
- Cardiology
- Molecular Biology
- Proteomics
Background:
- Beta-adrenergic receptors (β-ARs) are crucial for cardiac function.
- Mechanisms underlying β-AR-induced cardiac fibrosis remain incompletely understood.
Purpose of the Study:
- To investigate the role of protein expression changes in β-AR-stimulated cardiac fibrosis.
- To identify novel regulators in β-AR signaling pathways within cardiac fibroblasts.
Main Methods:
- Proteomics analysis to identify differentially expressed proteins in cardiac fibrosis.
- Investigated HIP-55 (debrin-like; DBNL) function in cardiac fibroblasts using overexpression and deficiency models.
- Examined the involvement of the extracellular signal-regulated protein kinase (ERK) pathway.
Main Results:
- HIP-55 was identified as a novel regulator in the β-AR signaling network.
- HIP-55 negatively regulates the proliferation of cardiac fibroblasts stimulated by β-AR.
- HIP-55's inhibitory effect on proliferation is linked to the ERK signaling pathway.
Conclusions:
- HIP-55 plays a significant role in modulating β-AR-induced cardiac fibroblast proliferation.
- The findings offer new mechanistic insights into cardiac fibrosis regulation.
- HIP-55 presents a potential therapeutic target for proliferative cardiac disorders.
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