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HORMONES AND SIGNALING

PACAP and gastrin regulate the histidine decarboxylase promoter via distinct mechanisms

¹Gastrointestinal Sciences, University of Manchester, Hope Hospital, Salford, M6 8HD United Kingdom; ²Division of Digestive Diseases and Nutrition, University of Massachusetts Memorial Medical Center, Worcester 01605; and ³Gastrointestinal Unit, Massachusetts General Hospital, Boston, Massachusetts 02114

Submitted 9 May 2002 ; accepted in final form 3 June 2003

The enterochromaffin-like (ECL) cell controls gastric acid secretion via histamine, generated by L-histidine decarboxylase (HDC). HDC expression is regulated by gastrin. However, gastrin is not alone in controlling ECL cell function. For example, the neural peptide pituitary adenylate cyclase-activating polypeptide (PACAP) also increases ECL cell proliferation. To investigate a potential role of PACAP in regulating HDC expression, we generated a series of HDC promoter-luciferase reporter constructs and transiently transfected them into PC12 cells (stably expressing the gastrin-CCK-2 receptor). We found that PACAP regulates HDC promoter activity. This is temporally biphasic, involving both adenyl cyclase and phospholipase C-dependent pathways. Deletional analysis, block mutation, and EMSA demonstrated a PACAP-response element at -177 to -170, wholly necessary for the effects of PACAP and discrete from known gastrin-responsive elements. Discrete neural and endocrine pathways regulate ECL cells through different patterns of postreceptor signaling and promoter activation, which may be appropriate to their functions in vivo.

histamine

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