Transforming growth factor-beta (TGF-beta 1) inhibits pancreatic acinar cell growth

Am J Physiol. 1992 Feb;262(2 Pt 1):G364-8. doi: 10.1152/ajpgi.1992.262.2.G364.


Effects of transforming growth factor (TGF)-beta 1 on mouse pancreatic acinar cell growth and rapid intracellular responses to cholecystokinin (CCK) were examined in vitro. TGF-beta 1 inhibited [3H]thymidine incorporation stimulated by either the CCK analogue caerulein, epidermal growth factor, or insulin. TGF-beta 1 inhibition of growth stimulated by a maximal dose of caerulein (1 nM) was dose dependent with one-half maximal effects occurring at approximately 5 pM and maximal inhibition seen with 30 pM. In contrast to its effects on CCK-stimulated [3H]thymidine incorporation, TGF-beta 1 had no effect on CCK-stimulated increases in amylase release or intracellular Ca2+ concentration. To determine whether TGF-beta 1 might be an autocrine growth regulator, pancreatic mRNA was probed for the presence of TGF-beta 1 transcripts. TGF-beta 1 mRNA was not detected in whole pancreas but was detectable with increasing abundance over time in primary cultures of pancreatic acinar cells. The appearance of the TGF-beta 1 mRNA corresponded to the period of rapid cellular proliferation in vitro. These results suggest that TGF-beta 1 may be an autocrine growth inhibitor in the pancreas and that the inhibitory effects of TGF-beta 1 on pancreatic acinar cell growth occur at sites distal to those involved in stimulus-secretion coupling.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Cell Division
  • Cholecystokinin / pharmacology
  • Pancreas / cytology*
  • Pancreas / drug effects
  • RNA, Messenger / metabolism
  • Time Factors
  • Transforming Growth Factor beta / genetics
  • Transforming Growth Factor beta / pharmacology*


  • RNA, Messenger
  • Transforming Growth Factor beta
  • Cholecystokinin