| Autor: |
Deshpande, D.A., Guedes, A.G.P., Graeff, R., Dogan, S., Subramanian, S., Walseth, T.F., Kannan, M.S. |
| Přispěvatelé: |
Deshpande, D.A., Guedes, A.G.P., Graeff, R., Dogan, S., Subramanian, S., Walseth, T.F., Kannan, M.S., Yeditepe Üniversitesi |
| Jazyk: |
angličtina |
| Rok vydání: |
2018 |
| Popis: |
Asthma is an inflammatory disease in which proinflammatory cytokines have a role in inducing abnormalities of airway smooth muscle function and in the development of airway hyperresponsiveness. Inflammatory cytokines alter calcium (Ca2+) signaling and contractility of airway smooth muscle, which results in nonspecific airway hyperresponsiveness to agonists. In this context, Ca2+ regulatory mechanisms in airway smooth muscle and changes in these regulatory mechanisms encompass a major component of airway hyperresponsiveness. Although dynamic Ca2+ regulation is complex, phospholipase C/inositol tris-phosphate (PLC/IP3) and CD38-cyclic ADP-ribose (CD38/cADPR) are two major pathways mediating agonist-induced Ca2+ regulation in airway smooth muscle. Altered CD38 expression or enhanced cyclic ADP-ribosyl cyclase activity associated with CD38 contributes to human pathologies such as asthma, neoplasia, and neuroimmune diseases. This review is focused on investigations on the role of CD38-cyclic ADP-ribose signaling in airway smooth muscle in the context of transcriptional and posttranscriptional regulation of CD38 expression. The specific roles of transcription factors NF-kB and AP-1 in the transcriptional regulation of CD38 expression and of miRNAs miR-140-3p and miR-708 in the posttranscriptional regulation and the underlying mechanisms of such regulation are discussed. © 2018 Deepak A. Deshpande et al. National Institutes of Health Mathur S. Kannan and Deepak A. Deshpande received support through grants from the National Institutes of Health. |
| Databáze: |
OpenAIRE |
| Externí odkaz: |
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