Circulating TGF-beta1 does not cross the intact blood-brain barrier

J Mol Neurosci. 2003;21(1):43-8. doi: 10.1385/JMN:21:1:43.

Abstract

Transforming growth factor-beta (TGF-beta) from the periphery can cross the disrupted blood-brain barrier (BBB) to exert neuroprotective effects on the brain. Here, we quantify its permeation across the normal mouse BBB. By high-performance liquid chromatography, we show that TGF-beta1 is stable in circulating blood but does not cross the intact BBB after intravenous injection any faster than the vascular marker 99mTc-albumin. This poor rate of influx cannot be explained by rapid efflux out of the brain or lack of lipophilicity as measured by the octanol/buffer partition coefficient, although the hydrogen bonding potential was relatively high, consistent with poor penetration. Thus, the therapeutic potential of TGF-beta1 administered in blood is probably limited to situations in which the BBB has been disrupted.

Publication types

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

MeSH terms

  • Animals
  • Biological Transport / drug effects
  • Blood-Brain Barrier / drug effects*
  • Blood-Brain Barrier / physiology*
  • Hydrogen Bonding / drug effects
  • Injections, Intravenous
  • Male
  • Membrane Lipids / chemistry
  • Metabolic Clearance Rate / drug effects
  • Metabolic Clearance Rate / physiology
  • Mice
  • Technetium Tc 99m Aggregated Albumin / blood
  • Technetium Tc 99m Aggregated Albumin / pharmacokinetics
  • Time Factors
  • Transforming Growth Factor beta / blood*
  • Transforming Growth Factor beta / pharmacokinetics*
  • Transforming Growth Factor beta / therapeutic use
  • Transforming Growth Factor beta1

Substances

  • Membrane Lipids
  • Technetium Tc 99m Aggregated Albumin
  • Tgfb1 protein, mouse
  • Transforming Growth Factor beta
  • Transforming Growth Factor beta1