Beneficial effects of prolactin and laminin on human pancreatic islet-cell cultures

Mol Cell Endocrinol. 2007 Jan 15;263(1-2):120-33. doi: 10.1016/j.mce.2006.09.011. Epub 2006 Nov 1.


The problem of pancreas donor shortage could be addressed through in vitro islet-cell proliferation prior to transplantation into diabetic patients. Therefore, we set out to evaluate the effects of prolactin (rhPRL) and laminin on primary cultures of human pancreatic islets. Our results showed that rhPRL induced an increase in islet-cell number and in cumulative insulin secretion (p<0.01). However, glucose-induced insulin secretion was enhanced only in the presence of both laminin and rhPRL. In addition, we describe, for the first time in human islets, the PRL-induced activation of JAK2, and signal transducer and activator of transcription (STAT) 1, 3 and 5. Our results demonstrate a significant beneficial effect of rhPRL and laminin on human islets and support widely held notion that the closer physiological stimuli and environment of beta cells are mimicked, the better are the results in cell proliferation and secretory function, both essential for successful islet transplantation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Aged
  • Blotting, Western
  • Cell Proliferation / drug effects
  • Cells, Cultured / drug effects
  • Enzyme Activation / drug effects
  • Female
  • Fluorescent Antibody Technique
  • Glucose / pharmacology
  • Humans
  • Immunoprecipitation
  • Insulin / metabolism
  • Insulin Secretion
  • Islets of Langerhans / cytology
  • Islets of Langerhans / drug effects*
  • Islets of Langerhans / metabolism
  • Janus Kinase 2 / metabolism
  • Laminin / pharmacology*
  • Male
  • Middle Aged
  • Prolactin / pharmacology*
  • RNA, Messenger / genetics
  • RNA, Messenger / metabolism
  • Reverse Transcriptase Polymerase Chain Reaction
  • STAT Transcription Factors / metabolism


  • Insulin
  • Laminin
  • RNA, Messenger
  • STAT Transcription Factors
  • Prolactin
  • Janus Kinase 2
  • Glucose