Re: Pinocytosis is stimulated by positive ions

why?? why not negative ions??
how does the cell know what ions it need??


Hi Paul,

When one simplifies science in order to explain issues to people outside 
one's restricted field  (i.e. the rest of the world), one has to take 
shortcuts. Pinocytosis (the act of engulfing extracellular liquid + 
content through endocytosis) is observed in many cell types and is 
regulated in different ways, depending on where it is happening. I suspect 
that the authors of your school book did not want to complicate things by 
giving specific examples. There are several cell types however that do 
pick up calcium from their environment by pinocytosis, such as liver cells 
(2) and capillary endothelium (1). The process can be controlled in other 
ways too, but all endocytosis share the common mechanism of forming so-
called clathrin-coated vesicles to generate the engulfed bubbles of plasma 
membrane: this process is controlled, in part, by calcium. So my answer to 
your first question is that nature has favoured the use of some cations 
for signalling; single negative ions (such as chloride) are much less 
used. Fernando and co-workers concluded that pinocytosis was responsible 
for about 10-15% of the total calcium intake: ions are "usually" imported 
by other means, namely specific carrier proteins or calcium channels.
As for your second question, the answer is feedback. There are processes 
in the cell which demand the compound in question and if the concentration 
goes down, they will stop working properly. This can trigger the 
mechanisms for import (or production, when applicable) of the compound.

I hope you are satisfied with the answers. If not, you can always rephrase 
and re-post them.
Take care,

Erik M. von Stedingk


(1) Williams SK, Wagner RC Microvasc Res 1981 Mar;21(2):175-82. Regulation 
of micropinocytosis in capillary endothelium by multivalent cations.
(2) Fernando KC, Barritt GJ. Mol Cell Biochem. 1996 Sep 6;162(1):23-9. 
Pinocytosis in 2,5-di-tert-butylhydroquinone-stimulated hepatocytes and 
evaluation of its role in Ca2+ inflow.