Adrenergic Signaling in Health and Disease

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cell Signaling".

Deadline for manuscript submissions: closed (31 December 2022) | Viewed by 3111

Special Issue Editors


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Guest Editor
Department of Biology, University of Pisa, Pisa, Italy
Interests: animal models; retinal diseases; retinal function; angiogenesis; inflammation; hypoxia-inducible factor 1; vascular endothelial growth factor; β2 adrenoceptor signaling; β3 adrenoceptor function
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Co-Guest Editor
Department of Biology, University of Pisa, Pisa, Italy
Interests: neurodegeneration; neoangiogenesis; retinal ganglion cells; neurovascular unit; glaucoma; diabetic retinopathy; optic neuropathy; retinitis pigmentosa; pattern electroretinogram
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Adrenoceptors are central mediators in the sympathetic nervous system, triggering the body’s ability to react to acute stress. Cathecolamines, released under stress conditions, bind to and activate α1-adrenoceptors, α2-adrenoceptors, and β-adrenoceptors to mediate cell-specific responses to adrenergic stimuli. The role of adrenergic system has been widely associated with the regulation of cardiovascular functions, with α- and β-adrenoceptors displaying opposite activity and representing crucial therapeutic targets for cardiovascular diseases. However, a relevant role of adrenoceptors is also increasingly emerging in several other tissues and organs such as the brain, retina, lungs, adipose tissue, kidney, urinary bladder, etc., in which altered adrenoceptor function is involved in clinically relevant disorders. In this respect, targeting specific α- and β-adrenoceptors subtypes has also become the subject of interest for the treatment of neurological, respiratory, metabolic, and urologic conditions. Novel insights into the α- and β-adrenoceptor signaling, and the relative ligands selectivity and specificity, represent the new frontier for the characterization of adrenergic system function from systemic to cell-specific levels in health and disease.

This Special Issue aims at providing a comprehensive overview of recent findings, broadening the knowledge on the adrenoceptor system and its potential role in physiology and disease. In particular, we invite you to provide original research articles investigating novel mechanistic insights into adrenoceptor function, as well as to summarize the current state of the art. Manuscripts providing translational value will be particularly welcome.

Prof. Paola Bagnoli
Guest Editor
Dr. Rosario Amato
co-Guest Editor

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Keywords

  • animal models
  • sympathetic regulation
  • adrenoceptor-associated diseases
  • adrenoceptor localization and function
  • signaling pathways
  • potential ligands

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Published Papers (1 paper)

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Research

21 pages, 2629 KiB  
Article
HIF-1-Dependent Induction of β3 Adrenoceptor: Evidence from the Mouse Retina
by Rosario Amato, Francesco Pisani, Emiliano Laudadio, Maurizio Cammalleri, Martina Lucchesi, Silvia Marracci, Luca Filippi, Roberta Galeazzi, Maria Svelto, Massimo Dal Monte and Paola Bagnoli
Cells 2022, 11(8), 1271; https://doi.org/10.3390/cells11081271 - 8 Apr 2022
Cited by 14 | Viewed by 2710
Abstract
A major player in the homeostatic response to hypoxia is the hypoxia-inducible factor (HIF)-1 that transactivates a number of genes involved in neovessel proliferation in response to low oxygen tension. In the retina, hypoxia overstimulates β-adrenoceptors (β-ARs) which play a key role in [...] Read more.
A major player in the homeostatic response to hypoxia is the hypoxia-inducible factor (HIF)-1 that transactivates a number of genes involved in neovessel proliferation in response to low oxygen tension. In the retina, hypoxia overstimulates β-adrenoceptors (β-ARs) which play a key role in the formation of pathogenic blood vessels. Among β-ARs, β3-AR expression is increased in proliferating vessels in concomitance with increased levels of HIF-1α and vascular endothelial growth factor (VEGF). Whether, similarly to VEGF, hypoxia-induced β3-AR upregulation is driven by HIF-1 is still unknown. We used the mouse model of oxygen-induced retinopathy (OIR), an acknowledged model of retinal angiogenesis, to verify the hypothesis of β3-AR transcriptional regulation by HIF-1. Investigation of β3-AR regulation over OIR progression revealed that the expression profile of β3-AR depends on oxygen tension, similar to VEGF. The additional evidence that HIF-1α stabilization decouples β3-AR expression from oxygen levels further indicates that HIF-1 regulates the expression of the β3-AR gene in the retina. Bioinformatics predicted the presence of six HIF-1 binding sites (HBS #1-6) upstream and inside the mouse β3-AR gene. Among these, HBS #1 has been identified as the most suitable HBS for HIF-1 binding. Chromatin immunoprecipitation-qPCR demonstrated an effective binding of HIF-1 to HBS #1 indicating the existence of a physical interaction between HIF-1 and the β3-AR gene. The additional finding that β3-AR gene expression is concomitantly activated indicates the possibility that HIF-1 transactivates the β3-AR gene. Our results are indicative of β3-AR involvement in HIF-1-mediated response to hypoxia. Full article
(This article belongs to the Special Issue Adrenergic Signaling in Health and Disease)
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