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Isoform‐specific regulation of transforming growth factor‐β mRNA expression in macrophages in response to adrenoceptor stimulation

Transforming growth factor‐beta (TGF‐β) is a multifunctional cytokine responsible for both immune regulation and tissue repair. Although TGF‐β consists of TGF‐β1, ‐β2, and ‐β3 in mammals, isoform‐selective transcriptional regulation is less well documented in myeloid linage cells such as macrophages. In the present study, the effect of the stress‐related catecholamine adrenaline on the expression of TGF‐β isoforms in RAW264.7 macrophages and murine bone marrow‐derived macrophages was examined. Treatment with adrenaline markedly increased the mRNA expression of TGF‐β3 but not of TGF‐β1 and ‐β2. Agonist and antagonist studies indicated that adrenaline‐induced TGF‐β3 mRNA expression is mediated via β2‐adrenoceptor. Protein kinase A (PKA) inhibitor H89 was found to block an increase in adrenoceptor‐mediated TGF‐β3 mRNA expression. The membrane‐permeable cAMP analog 8‐Br‐cAMP increased the mRNA expression of TGF‐β3 but not of TGF‐β1 and ‐β2. Thus, the β2‐adrenoceptor‐mediated cAMP‐PKA pathway appears to enhance TGF‐β3 mRNA expression in macrophages. Adrenoceptor‐mediated TGF‐β3 expression by macrophages may influence immune regulation and tissue repair in conditions of stress, during which the sympathetic‐nervous system releases catecholamines.