Adenosine receptors are involved in the upregulation of HO-1 and pAMPK in IL-1beta-stimulated gingival fibroblasts

McKay Blatter, University of the Pacific Arthur A. Dugoni School of Dentistry
Dallin Montierth, University of the Pacific Arthur A. Dugoni School of Dentistry
Ana Carolina Morandini, University of the Pacific Arthur A. Dugoni School of Dentistry
Erivan S. Ramos-Junior, University of the Pacific Arthur A. Dugoni School of Dentistry

This work was supported by Research Enhancement Award to ACM [Award 03-Activity 117] from the Arthur A. Dugoni School of Dentistry.

Introduction/Context/Diagnosis

BACKGROUND: Heme oxygenase-1 (HO-1) has been linked to many physiological and pathological processes through its ability to regulate the host inflammatory response. Activation of adenosine monophosphate–activated protein kinase (AMPK) has been linked to reduced systemic oxidative stress through antioxidant defense pathways, preventing alveolar bone loss. We aimed to investigate if both HO-1 and AMPK would be modulated by the effects elicited by adenosine signaling in human gingival fibroblasts under inflammatory conditions (IL-1b stimulation).

 

Adenosine receptors are involved in the upregulation of HO-1 and pAMPK in IL-1beta-stimulated gingival fibroblasts

BACKGROUND: Heme oxygenase-1 (HO-1) has been linked to many physiological and pathological processes through its ability to regulate the host inflammatory response. Activation of adenosine monophosphate–activated protein kinase (AMPK) has been linked to reduced systemic oxidative stress through antioxidant defense pathways, preventing alveolar bone loss. We aimed to investigate if both HO-1 and AMPK would be modulated by the effects elicited by adenosine signaling in human gingival fibroblasts under inflammatory conditions (IL-1b stimulation).