Introduction
The term thrombopoietin (TPO) was first penned in 1958 to describe the primary regulator
of platelet production. Multiple efforts to purify the hormone were unsuccessful throughout
the 1970s and 1980s because the protein was scarce and starting materials for purification
biochemically complex. Even purification of thrombocytopenic plasma, which is the
richest source of TPO, was unsuccessful.1,2 However, the cloning of the proto-oncogene c-mpl
3 opened an alternative route to the identification of TPO. Detailed study of the c-mpl gene revealed that it encoded an orphan hematopoietic cytokine receptor. Its tissue
distribution and experiments designed to eliminate its expression suggested that c-mpl encoded the TPO receptor.4,5 In 1994, using three distinct strategies, five separate groups either purified protein
or cloned cDNA for TPO.6 This review will focus on the physiology of TPO production and function, concentrating
on recent findings that help to explain platelet homeostasis and how our understanding
of TPO can translate into better patient care for thrombocytopenic patients.
