Prolactin and Angiogenesis: Biological Implications of Microheterogeneity

Abstract

Prolactin (PRL) was discovered in 1928. It is found in all vertebrates including humans. The name ‘prolactin’ is derived from its established role, in female mammals, in mammopoiesis. That raised the first mystery regarding its role in the human male and in non-mammalian vertebrates. More than 300 effects have been produced by injecting PRL into animals of all phylogenic groups. That raised the second mystery i.e. absence of any reliable and relevant bio assay for PRL till today. Following the approaches of Reductionist Biology, prolactin has been purified and characterized from a number of vertebrate groups. That raised the third mystery i.e. extensive microheterogeneity in structure and its doubtful relevance to physiology. The mechanism of action of prolactin has been studied extensively and that gave rise to the fourth mystery as to why it does not follow the second messenger model in signaling pathways, as in the case of other membrane receptor acting hormones like epinephrine or Luteinizing hormone (LH) or FSH etc. Prolactin behaves more like a cytokine and growth factor than like a hormone! In spite of exhibiting multiple physiological effects on a variety of tissues like brain (behavior), gonadal and mammary tissues, accessory sex organs like ventral prostate, immune system of phagocytes and lymphocytes etc, no disease whose origin can be ascribed to mutations in PRL or PRL receptor genes has yet been discovered. That is the fifth mystery. There is no known clinical model of prolactin deficiency. Hyperprolactinemia due to tumors of pituitary lactotrophs is the only known pathological condition. Long term hyperprolactinemia can lead to amenorrhea in women, loss of libido in men and infertility in both.