Back to Search
Start Over
CXCL10/CXCR3 signaling mediates inhibitory action by interferon-gamma on CRF-stimulated adrenocorticotropic hormone (ACTH) release
- Source :
- Cell and Tissue Research. 364:395-404
- Publication Year :
- 2015
- Publisher :
- Springer Science and Business Media LLC, 2015.
-
Abstract
- Secretion of hormones by the anterior pituitary gland can be stimulated or inhibited by paracrine factors that are produced during inflammatory reactions. The inflammation cytokine interferon-gamma (IFN-γ) is known to inhibit corticotropin-releasing factor (CRF)-stimulated adrenocorticotropin (ACTH) release but its signaling mechanism is not yet known. Using rat anterior pituitary, we previously demonstrated that the CXC chemokine ligand 10 (CXCL10), known as interferon-γ (IFN-γ) inducible protein 10 kDa, is expressed in dendritic cell-like S100β protein-positive (DC-like S100β-positive) cells and that its receptor CXCR3 is expressed in ACTH-producing cells. DC-like S100β-positive cells are a subpopulation of folliculo-stellate cells in the anterior pituitary. In the present study, we examine whether CXCL10/CXCR3 signaling between DC-like S100β-positive cells and ACTH-producing cells mediates inhibition of CRF-activated ACTH-release by IFN-γ, using a CXCR3 antagonist in the primary pituitary cell culture. We found that IFN-γ up-regulated Cxcl10 expression via JAK/STAT signaling and proopiomelanocortin (Pomc) expression, while we reconfirmed that IFN-γ inhibits CRF-stimulated ACTH-release. Next, we used a CXCR3 agonist in primary culture to analyze whether CXCL10 induces Pomc-expression and ACTH-release using a CXCR3 agonist in the primary culture. The CXCR3 agonist significantly stimulated Pomc-expression and inhibited CRF-induced ACTH-release, while ACTH-release in the absence of CRF did not change. Thus, the present study leads us to an assumption that CXCL10/CXCR3 signaling mediates inhibition of the CRF-stimulated ACTH-release by IFN-γ. Our findings bring us to an assumption that CXCL10 from DC-like S100β-positive cells acts as a local modulator of ACTH-release during inflammation.
- Subjects :
- Male
0301 basic medicine
Agonist
endocrine system
medicine.medical_specialty
Pro-Opiomelanocortin
Receptors, CXCR3
Histology
Corticotropin-Releasing Hormone
medicine.drug_class
medicine.medical_treatment
S100 Calcium Binding Protein beta Subunit
Adrenocorticotropic hormone
CXCR3
Pathology and Forensic Medicine
Interferon-gamma
03 medical and health sciences
Paracrine signalling
Adrenocorticotropic Hormone
Anterior pituitary
Pituitary Gland, Anterior
Internal medicine
medicine
Animals
CXCL10
Rats, Wistar
Cells, Cultured
Inflammation
Chemistry
hemic and immune systems
Cell Biology
Rats
Chemokine CXCL10
030104 developmental biology
Endocrinology
Cytokine
medicine.anatomical_structure
Corticotropic cell
Rats, Transgenic
hormones, hormone substitutes, and hormone antagonists
Signal Transduction
Subjects
Details
- ISSN :
- 14320878 and 0302766X
- Volume :
- 364
- Database :
- OpenAIRE
- Journal :
- Cell and Tissue Research
- Accession number :
- edsair.doi.dedup.....c57cd8d290d6c9f7aff141c3317cf41f