International Journal of Molecular Sciences

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Special Issue Editor

Prof. Dr. Hiroshi Takemori

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Guest Editor

Department of Chemistry and Biomolecular Science, Faculty of Engineering, Gifu University, Yanagido 1-1, Gifu 501-1193, Japan
Interests: CREB; SIK; CRTC; melanogenesis; inflammation; live imaging; exosome

Special Issue Information

Dear Colleagues,

cAMP, a signal transducer, plays important roles in a variety of cells and tissues in response to extracellular stimulants. While cAMP signaling is evolutionarily conserved in eukaryotes, it is also highly diverse and involved in the regulation of morphogenesis to behavior, skin color, and circadian rhythms. Dysregulation of cAMP signaling is linked to the development of various diseases, e.g., diabetes, cardiovascular disease, respiratory disease, autoimmune disease, neurological disorder, and aging. cAMP signaling modulates gene expression, translation, and protein degradation via the actions of protein kinase A (PKA) and exchange protein directly activated by cAMP (Epac). In addition, it is important that feedback mechanisms of cAMP signaling, e.g., phosphodiesterase, phosphatase, and the transcriptional repressor, regulate homeostasis of the above biological actions. Moreover, in coordination with Ca²⁺ signaling, cAMP signaling is found to moderate exosome production and release, which explains the involvement of cAMP signaling in new mechanisms for intra- and extracellular communications.

This special issue will focus on downstream phenomena and regulatory mechanisms of cAMP signaling, especially in vertebrates, including newly discovered mechanisms. With regard to diseases, we will focus on pathogenesis in which impairments in cAMP signaling play important roles.

Prof. Dr. Hiroshi Takemori
Guest Editor

Manuscript Submission Information

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Keywords

cAMP
transcription
metabolism
development
stress response
cell–cell communication

Published Papers (2 papers)

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Research

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17 pages, 1832 KiB

Open AccessArticle

The Role of Cyclic Adenosine Monophosphate (cAMP) in Modulating Glucocorticoid Receptor Signaling and Its Implications on Glucocorticoid-Related Collagen Loss

by Wesuk Kang, Dabin Choi, Jiyun Roh, Yearim Jung, Yoojeong Ha, Suhjin Yang and Taesun Park

Int. J. Mol. Sci. 2023, 24(12), 10180; https://doi.org/10.3390/ijms241210180 - 15 Jun 2023

Cited by 1 | Viewed by 1619

Abstract

Glucocorticoid receptors (GRs) play a pivotal role in the stress response of the body, but overactivation can disrupt normal physiological functions. This study explores the role of cyclic adenosine monophosphate (cAMP) in GR activation and the associated mechanisms. We initially used the human embryonic kidney 293 cell line (HEK293) and found that cAMP enhancement, using forskolin and 3-isobutyl-1-methylxanthine (IBMX), did not alter glucocorticoid signaling under normal conditions, as evidenced by glucocorticoid response element (GRE) activity and the translocation of GR. However, in stressful conditions induced by dexamethasone, a synthetic glucocorticoid, cAMP was found to lessen glucocorticoid signaling within a short time frame but amplify it over an extended period in HEK293 cells. Bioinformatic analysis revealed that cAMP upregulation triggers the extracellular signal-regulated kinase (ERK) pathway, which influences GR translocation and ultimately regulates its activity. This stress-modulating function of cAMP was also investigated in the Hs68 dermal fibroblast line, known for its susceptibility to glucocorticoids. We found that cAMP enhancement via forskolin reduces GRE activity and reverses collagen loss in Hs68 cells exposed to dexamethasone. These findings underline the context-specific role of cAMP signaling in managing glucocorticoid signaling and its potential therapeutic application in treating stress-related pathological conditions like skin aging characterized by collagen reduction. Full article

(This article belongs to the Special Issue cAMP Signaling: Function and Implication in Diseases)

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Review

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20 pages, 1464 KiB

Open AccessReview

Therapeutic Targets and Precision Medicine in COPD: Inflammation, Ion Channels, Both, or Neither?

by Graeme B. Bolger

Int. J. Mol. Sci. 2023, 24(24), 17363; https://doi.org/10.3390/ijms242417363 - 11 Dec 2023

Cited by 1 | Viewed by 1701

Abstract

The development of a wider range of therapeutic options is a key objective in drug discovery for chronic obstructive pulmonary disease (COPD). Fundamental advances in lung biology have the potential to greatly expand the number of therapeutic targets in COPD. The recently reported successful Phase 3 clinical trial of the first biologic agent for COPD, the monoclonal antibody dupilumab, adds additional support to the importance of targeting inflammatory pathways in COPD. However, numerous other cellular mechanisms are important targets in COPD therapeutics, including airway remodeling, the CFTR ion channel, and mucociliary function. Some of these emerging targets can be exploited by the expanded use of existing COPD drugs, such as roflumilast, while targeting others will require the development of novel molecular entities. The identification of additional therapeutic targets and agents has the potential to greatly expand the value of using clinical and biomarker data to classify COPD into specific subsets, each of which can be predictive of an enhanced response to specific subset(s) of targeted therapies. The author reviews established and emerging drug targets in COPD and uses this as a framework to define a novel classification of COPD based on therapeutic targets. This novel classification has the potential to enhance precision medicine in COPD patient care and to accelerate clinical trials and pre-clinical drug discovery efforts. Full article

(This article belongs to the Special Issue cAMP Signaling: Function and Implication in Diseases)

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