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FAM3A is a recently identified mitochondrial protein that stimulatespancreatic-duodenal homeobox 1 (PDX1) and insulin expressions by promoting ATPrelease in islet β cells. In this study, the role of intracellular ATPin FAM3A-induced PDX1 expression in pancreatic β cells was furtherexamined. Acute FAM3A inhibition using siRNA transfection in mouse pancreaticislets significantly reduced PDX1 expression, impaired insulin secretion, andcaused glucose intolerance in normal mice. In vitro, FAM3A overexpressionelevated both intracellular and extracellular ATP contents and promoted PDX1expression and insulin secretion. FAM3A-induced increase in cellular calcium(Ca2+) levels, PDX1 expression, and insulin secretion,while these were significantly repressed by inhibitors of P2 receptors or theL-type Ca2+ channels. FAM3A-induced PDX1 expression wasabolished by a calmodulin inhibitor. Likewise, FAM3A-induced β-cellproliferation was also inhibited by a P2 receptor inhibitor and an L-typeCa2+ channels inhibitor. Both intracellular andextracellular ATP contributed to FAM3A-induced PDX1 expression, insulinsecretion, and proliferation of pancreatic β cells.

Intracellular ATP Signaling Contributes to FAM3A-Induced PDX1 Upregulation in Pancreatic Beta Cells