Exendin-4 inhibits interleukin-1β-induced iNOS expression at the protein level, but not at the transcriptional and posttranscriptional levels, in RINm5F β-cells
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Cytokines such as interleukin-1β (IL-1β) stimulate inducible nitric oxide synthase (iNOS) expression and nitric oxide overproduction leading to β-cell damage. Meanwhile, glucagon-like peptide-1 (GLP-1) and its potent analog exendin-4 (EX-4) were well known for β-cell proliferation. However, the protective mechanisms of GLP-1 in β-cells exposed to cytokines were not fully elucidated. Therefore, the effects of EX-4 on the IL-1β-induced iNOS gene expression were investigated employing RINm5F β-cells. EX-4 inhibited IL-1β-induced iNOS protein expression and nitrite production. However, northern blot and promoter analyses showed that EX-4 failed to inhibit IL-1β-induced iNOS mRNA expression and iNOS promoter activity. By electrophoretic mobility shift assay (EMSA), EX-4 did not alter the binding activity of NF-κB to the iNOS promoter. Consistent with the EMSA result, EX-4 did not inhibit nuclear translocation of p65. We also tested the effect of EX-4 on iNOS mRNA stability. Actinomycin D chase experiments showed that EX-4 did not affect the decay rate of iNOS mRNA and the promoter assay using the construct containing 3′-untranslated region of iNOS showed that EX-4 did not alter the stability of iNOS mRNA. Meanwhile, forskolin significantly inhibited IL-1β-induced iNOS protein, which was reversed by H-89, a protein kinase A (PKA) inhibitor. Moreover, EX-4 pretreatment restored IL-1β-induced decrease in cAMP toward control level. Additionally, the cycloheximide chase study demonstrated that EX-4 significantly accelerated iNOS protein degradation. We therefore concluded that EX-4 inhibited IL-1β-induced iNOS protein and nitrite production via cAMP/PKA system irrespective of both transcriptional and posttranscriptional mechanisms of iNOS gene, and this inhibitory effect of EX-4 appears to be regulated at posttranslational level.
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Binding of GLP-1 or GLP-1RAs to these receptors can activate the cAMP/PKA signaling pathway, affecting key transcription factors like NF-κB.
“Binding of GLP-1 or GLP-1RAs to these receptors can activate the cAMP/PKA signaling pathway, affecting key transcription factors like NF-κB.287,288”
From Glucagon-like peptide-1 receptor: mechanisms and advances in therapy (2024) · cites this paper as [288]
The Introduction says GLP-1 and exendin-4 activate cAMP/PKA signaling. But the section “Effects of EX-4 on IL-1b-induced NF-kB activation” reports that exendin-4 did not reduce NF-κB binding or inhibit p65 nuclear translocation in RINm5F cells. Thus, the paper's tested NF-κB effect is contrary to the claim, despite supporting the cAMP/PKA portion. (LLM, conf=0.88)
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Chang, S., Cho, J. M., Kim, D., Jang, H., Ko, S., Jo, Y., & Kim, M. (2011) · Journal of Cellular Biochemistry · doi:10.1002/jcb.24024 · Cited by 7 · see citing works
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Unis, A. (2013) · American Journal of Pharmacology and Toxicology · doi:10.3844/ajptsp.2013.107.119 · Cited by 2 · see citing works
Niu, B., Li, C., Su, H., Li, Q., He, Q., Liu, L., Xue, Y., Shen, T., & Xia, X. (2017) · Experimental and Therapeutic Medicine · doi:10.3892/etm.2017.4803 · Cited by 2 · see citing works
Exendin-4 Exacerbates Burn-Induced Mortality in Mice by Switching to Th2 Response
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The impact of glucotoxicity on pancreatic β-cell function
Muhammed, S. J. (2012) · Lund University Publications (Lund University)
GLP-1 Can Protect Proinflammatory Cytokines Induced Beta Cell Apoptosis through the Ubiquitination
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Chang, S.-Y., Yongjun, K. O., & Myung-Jun, K. I. M. (2026) · Journal of Nutritional Science and Vitaminology · doi:10.3177/jnsv.72.424
Self-citation
- Authors
- Kang, J.-H., Chang, S.-Y., Jang, H.-J., Kim, D.-B., Ryu, G. R., Ko, S. H., Jeong, I.-K., Jo, Y.-H., & Kim, M.-J.
- Affiliations
- Catholic University of Korea (KR)
- Kyung Hee University (KR)
- ORCID
- Venue
- Journal of Endocrinology
- Publisher
- Bioscientifica
- Published
- 2009-04-27
- Volume
- 202
- Issue
- 1
- Pages
- 65-75
- ISSN
- 0022-0795 (ISSN-L)
- 1479-6805
- OpenAlex
- W2141082261
- Cited by
- 30
- References
- 72
- Citations by year
- 2025: 2 · 2024: 2 · 2023: 3 · 2022: 1 · 2017: 1 · 2016: 1 · 2015: 3 · 2013: 3 · 2012: 4
- FWCI
- 4.72
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Endocrinology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Korean Diabetes Association
- Catholic University of Korea
- College of Medicine, Catholic University of Korea
- Topics
- Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Treatment and Management
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Endoplasmic Reticulum Stress and Disease
- Keywords
- exendin-4, IL-1β, inducible nitric oxide synthase, beta-cell protection, cAMP/PKA signaling, nitrite production, NF-κB, glucagon-like peptide-1
- MeSH terms
- Exenatide, Cyclic AMP, Animals, Cell Line, Hypoglycemic Agents, Nitric Oxide, Peptides, Promoter Regions, Genetic, Protein Processing, Post-Translational, RNA, Messenger, Transcription, Genetic, Venoms, Gene Expression Regulation, Enzymologic, NF-kappa B, RNA Stability, Insulin-Secreting Cells, Rats, Nitric Oxide Synthase Type II, Interleukin-1beta
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