During the lactation process, women produce vast quantities of milk
for their babies - up to nearly a liter per day. To do this breasts
change dramatically during pregnancy, developing the tissue so that
cells can make lots of milk. But when weaning finishes, the breasts need
to be remodeled so that they can return to a non-pregnant form.
The human body can usually cope with the limited amount of detritus
created from normal cellular lifecycles through the deployment of immune
cells to remove the material. But just how it manages to eradicate the
large amounts of dead or redundant mammary cells, and left over milk,
following breastfeeding without triggering inflammation due to the
quantities of immune cells which would be needed, was not fully known.
‘Milk-producing cells are, in effect, cannibalized by other cells following the period of breastfeeding, revealed a new study.’
Soon after lactation, many of the milk-making cells are killed off,
in a process called 'apoptosis'. It had been thought that they were then
removed through phagocytosis - flushing away the redundant cells by
A ground-breaking study into the changes that occur in a woman's breast,
from growing into one that provides milk for a new-born, and then back
to its normal state, has discovered that milk-producing cells are, in
effect, cannibalized by other cells following the period of
breastfeeding. However Nasreen Akhtar, the scientist who carried out this study and
who is now a Fellow at the University of Sheffield, and her supervisor
Charles Streuli, Professor of Cell Biology at The University of
Manchester, were intrigued why there was no significant inflammation,
pain and tissue damage associated with phagocytosis on such a big scale.
Dr Akhtar said, "Immune-cell phagocytosis might be extremely painful
and damaging. So we thought something else must be standing in for the
immune cells. What we didn't expect to find was a molecular switch that
turned milk-secreting cells into cannibalistic cell eaters. We
discovered that these cells were now able to eat or otherwise remove
vast quantities of redundant milk-producing cells."
It turned out that a protein called Rac1 is central for the cellular
switch. Dr Akhtar found that Rac1 is vital for milk production as well
as for the tissue remodelling that occurs after lactation. Moreover,
Rac1 also triggers the 'part-time' phagocytic activity that is carried
out by the breast epithelial cells. Indeed, Rac1 was needed for clearing
post-lactating dead cells and residual milk, helping to reshape the
breast back to non-pregnancy.
The study, reported in the journal Developmental Cell
, was one of
the first to look at how the breast remodels back to its 'normal' state
after babies have stopped suckling, revealing a central requirement for
the Rac1 signalling protein.
There may also be a role for Rac1 in breast cancer. "Although we
cannot be certain at this point, Rac1 may be crucial for breast cancer
development. We are studying this process, as it could provide new
opportunities for treating the disease," Professor Streuli said.
"And in the future, there may be completely new ways to treat breast
cancer - if normal breast cells can eat their slightly altered
neighbors, could we find a way to get healthy cells to consume and
destroy all the cancer cells?"
The research was reported in a publication 'Rac1 controls both the
secretory function of mammary glands and its remodeling for successive
gestations' in the journal Developmental Cell
; the paper can be found here.