CRH inhibits NF-κB signaling in human melanocytes
Open accessAbstract
Corticotropin releasing hormone (CRH), a messenger of stress at the central level, is expressed in the epidermis where it operates within local equivalent of hypothalamo-pituitary axis. CRH inhibits NF-kappaB activity in human immortalized epidermal (PIG1) melanocytes. In melanocytes CRH stimulates pro-opiomelanocortin (POMC) mRNA and adrenocorticotropin (ACTH) peptide production. Knockdown of POMC levels by transfecting cells with antisense oligonucleotides blocks the effect of CRH on NF-kappaB signaling indicating that the above inhibition is indirect, e.g. through activation of POMC. We suggest that induction of POMC by CRH serves as a feedback mechanism to self-restrict inflammatory response in the skin.
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Locally produced POMC-derived peptides and locally produced glucocorticoids can counteract pro-inflammatory activities.
“These proinflammatory activities can be counteracted by locally produced POMC derived peptides [73, 129, 173] and by locally produced glucocorticoids [1, 73].”
From Steroidogenesis in the skin: Implications for local immune functions (2013) · cites this paper as [173]
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References 51 · Cited by 45
- Authors
- Zbytek, B., Pfeffer, L. M., & Slominski, A. T.
- Affiliations
- University of Tennessee Health Science Center (US)
- Corresponding author
- Slominski, Andrzej T.
- Venue
- Peptides
- Publisher
- Elsevier BV
- Published
- 2006-12
- Volume
- 27
- Issue
- 12
- Pages
- 3276-3283
- ISSN
- 0196-9781 (ISSN-L)
- PMC
- PMC1839005
- OpenAlex
- W2012717006
- Cited by
- 45
- References
- 51
- Citations by year
- 2025: 1 · 2024: 2 · 2023: 1 · 2022: 4 · 2021: 1 · 2020: 3 · 2019: 1 · 2018: 1 · 2017: 2 · 2016: 3 · 2015: 3 · 2013: 5 · 2012: 6
- FWCI
- 1.04
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Peptides (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health (1s10rr013725-01)
- National Cancer Institute (R01CA073753, R01CA133322, CA 73753)
- National Institute of Arthritis and Musculoskeletal and Skin Diseases (AR-052190, AR 047079, R01AR052190, R01AR047079)
- National Center for Research Resources (S10 RR13725-01)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › NF-κB Signaling Pathways
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuropeptides and Animal Physiology
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Keywords
- corticotropin-releasing factor, NF-κB signaling, melanocytes, proopiomelanocortin, ACTH, epidermis, hypothalamic-pituitary-adrenal axis, stress response, inflammation modulation, antisense oligonucleotide knockdown
- MeSH terms
- Cell Line, Transformed, Corticotropin-Releasing Hormone, Humans, Melanocytes, Signal Transduction, NF-kappa B
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