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EDITORIAL
Splenic
Remodeling
of Red
By William
I
N THIS
weight
ISSUE
red cell
spleen.”
They
spectrin
and
moval
of this
material
of
tional,
the
that
reticulocyte
proteins
and
aggregate,
along
complex
span
of
splenic
with
following
cell.
splenectomy,
The
spleen
serves
the
different
but
not
humans.
red
cells.
It does,
this
spleen
cell
show
re-
surface
or
nonfunc-
membrane
red
large
through-
cells
protein
yet
is not
complex
another
animals.
of
of
includes
protein-lipid
normal
in different
The
however,
red
of
of
aggregate
is absent
Thus
is written
and spleens.
a third
of his red cells; when
he awakens
rapid
blood
stream.
The human
spleen
for
normal
to the
presence
an
remodeling”
spleen
survival
functions
in
the
the
attached
the
not be especially
harmful
to the cell.”
the intricate
relation
between
red cells
erythropoietic,
of
“When
Since
contain
“surface
much
remains
the
describe
a “high
molecular
is normally
removed
by the
membranes
that
reticulocytes.
protein
life
creased
propose
other
Surfaces
H. Crosby
OF BLOOD,
Lux and John’
membrane
protein
complex
that
maturing
the
out
Cell
chapter
In the
a sleeping
dog
ability
to sequester
of
mouse
can
the
it is
sequester
the spleen
injects
them
back
does
not provide
this sort of
some
demust
into the
reservoir
youngest
of
the circulating
red cells. Blood
squeezed
from normal
spleens
has a reticulocyte
count
twice that ofblood
in the open
circulation.2
When
the spleen
is removed
from
a patient
with
hereditary
hemolytic
anemia
of a sort
not cured
postsplenectomy
the
cells
unchanged.3
remains
conclude
parts
It
that
or
young
through
is known,
changes
in
reticulocyte
the
red
presence
in
of these
splenectomy
the
be doubled,
of
move
red
cells.
slowly
Removal
of
mean
although
target
volume,
the
cells
while
their
their
mature
from
on
blood
the
area
to
certain
normal
dogs
smear.
erythrocytes
surface
red
counter-
accomplishes
spleen
the
of
it is tempting
than
of
that
turnover
observations,
of the splenic
circulation.
somehow
the spleen
indicates
a normal
these
more
appearance
“leptocytes”
have
may
basis
courses
that
immature
results
the
cells
stagnant
furthermore,
these
humans
count
On
The
formed
remains
after
larger
than
normal.4
During
total
maturation
surface
Mature
cells
versus
3 for
function
the
there
carry
normal
erythrocytes,
is also
a modification
a heavier
reticulocytes.5
of
From
of
area
the
orientation
Division
of
negative
Because
of
the
in
charge
the
fatty
Hematology-Oncology.
addition
of
the
with
an
erythrocytes’
acids
Scripps
at
to
the
quality
of
isoelectric
Clinic
surface,
and
Research
of
surface.
point
electrostatic
the
decrease
the
of
charge
the
pattern
Foundation,
I,
is
a
as well
La
Jolla.
Calif
Invited
editorial
Supported
Address
Clinic
©
Blood,
and
1977
submitted
by ERDA
for
reprint
Research
by Grune
June
Contract
requests:
Foundation.
& Stratton,
Vol. 50, No. 4 (October),
16. 1977;
E(04-3)899
William
1977
and
June
NASA
H. Crosby.
10666
Inc.
accepted
ISSN
N.
Torrey
M.D..
Pines
20,
1977.
Contract
NAS
Division
Road.
9-14341.
of Hematology-Oncology.
La Jolla,
Calif
Scripps
92037.
0006-4971.
643
From www.bloodjournal.org by guest on January 21, 2015. For personal use only.
644
WILLIAM
as the total
This surface
amount
charge,
mechanical
of fatty acids on the reticulocyte
repelling
all cells of like charge,
injury
during
millions
of
collisions
surface
protects
that
occur
must
the
stance?
passage
extended
Several
from
cracks
between
sinus
wall.
bodies
the
It
are
not;
they
amputates
that
its
reduced
sion.
Jolly
that
pass
cell
portion
portion.
the
off of bits
ments
may
cytes
represent
have
through
along
the
the
cell
not be a mechanism
hand,
the pinched-off
bits
John.
Yet
culating
has
been
of normal
fragments
another
means
erythrocytes
“culling”
cells that
hereditary
function
splenectomy.
The
now
others
persist
do
not,
the
one
aspect
weight
“dust”
seen
that
cell
constituent
circulating
remains,
the
or
although
disposal
as beads
attached
tional
membrane
diluted
some
portion
Is the protein
to the inner
layer
of the
constituent
of erythroblasts
after
red
This
cells8’9
and
may
may
be reof Lux
and
among
cirin the spleen.
and
remove
viable
erythrocytes’#{176}
surviving
longer
that
cells
cells
erythro-
schistocytes.
phenomena
red cells
by
splenic
surface.
On the other
areas
of red cell sur-
provokes
possess
the
blood
smears
of the spleen.
the spleen
remodels
of defective
the
in mitosis,
the
divides
in two.
These
tiny frag-
of red
recognize
deformity
If some
inclu-
are Howellorganisms.7
remodeling.
Thus
protein
aggregate
spleen
blood.
all involve
be mentioned
that
metabolic
attrition.
in diseases
sinus
simply
channels,
within
tiny
Heinz
body-damaged
of abnormal
cells
in postsplenectomy
culling
function
above
whereby
It must
through
as
the
situa-
the
the
in plasma
smears
postsplenectomy
destruction
of entire
presence
of acanthocytes”
provides
evidence
for the
The processes
described
a mechanical
occur
found
on
of surface
membrane
deficient.
examples
flaw
reticulocytes
and even
also
this
venous
thus
affect
other
organelles,
described
way
are
the
the
remodeling
of the red cell
may contain
abnormal
requires
red
in
In
within
erythrocyte
surrounding
may
form
Inclusion
interstices.
along
sub-
during
through
that
deformable.
membrane
cell
be
of explaining
involves
the
are in some
spherocytes
tight
km
The
stickiof the
lose
cells
easily
escapes
cytoplasm
of red
may
face to be got rid of as
moved
the high
molecular
endothelial
itself
completely
inclusion.
The
of
may
reticulocytes
of the cytoplasm’s
participation
and then,
at its narrow
waist,
often
one of them
is quite
tiny.
or they
pinching-offphenomenon
the
amount
cell
do
175
unsticky.
relative
tangles
lose inclusion
bodies
sinuses,
squeezing
are
finds
the
liberated
small
of red
sedimented,
cells
ultimately
containing
The
by
of the
red
Examples
of inclusions
that
bodies,
iron-laden
mitochondria,
Pinching
can
but
how
Red cells
the splenic
processes
cannot
red
spleen,
known.
into
squeeze,
cords.
In a process
reminiscent
red cell becomes
a figure-eight
The fragments
are unequal;
The
in the
are
cords
cytoplasmic
is a tight
tion, the migrating
lumen
except
for
surface
sojourn
mechanisms
the splenic
CROSBY
be different.6
red cell from
traveled
in a 4-mo
life span.
The
mature
red cell is extremely
reticulocyte,
with its softer
surface
charge,
is less so. Does
this
ness drag upon
the reticulocyte
as it bumps
its way across
the
splenic
filter?
During
their
H.
the spleen
flaw
and
normal
of
cells.
normal
red
or portions
of red cell remodeling
aggregate
of Lux and
red cell membrane,
and reticulocytes?
the
and
after
cell
surfaces
of red
might
John
The
people
cells.
occur
present
or is it a funcIf it is in beads,
From www.bloodjournal.org by guest on January 21, 2015. For personal use only.
SPLENIC
then
REMODELING
OF
mechanical
for the
inclusion
RBC
SURFACES
removal
ameboid
body.
645
is feasible.
Smoothly
movement
of young
If this were the case,
distributed
(essential,
of the aggregate
must somehow
require
the mysterious
circulation
of the spleen.
Whatever
the splenic
mechanism
for its removal,
discovered
Lux
phenomenon
and
John
does
not
may
result
remains
in the
necessarily
present
in
a few
entire
offending
as
of
the
they
red
cells
any
to
cells,
remove
the
the
harmful.
protein
to
red
be
existence
it is
would
learned
or
cells
Its
demise
aggregate
remodeled
of
finding
it. If, however,
premature
remains
newly
complex
This
possesses
their
It
protein
it is not
that
micro-
fascinating,
weight
that
cell
disease.
permitting
the
of the
postsplenectomy.
suggest,
circulating
ambknce
molecular
population
of
hemolytic
portions,
high
cell
destruction
in discernible
destroys
the
red
mean,
splenic
in only
result
is that
perhaps,
red cells),
it could
not be pinched
off as an
the metabolic
removal
or disaggregation
not
if the
if it
spleen
removes
only
to survive.
REFERENCES
1. Lux
SE,
John
characterization
cell
Isolation
of a high
membrane
mally
KM:
protein
removed
and
molecular
weight
complex
by the
spleen.
which
Blood
6.
partial
red
is
nor-
7.
Nathan
Engli
Med
of
red
8.
Berendes
cytes
in
M:
the
14:558-563,
erythrocytes
the
Hereditary
anemia.
Blood
Crosby
WH:
and
leptocytes
261-274,
5.
of
reticulo-
spleen.
The
9.
nonspherocytic
5:233-253,
1950
pathogenesis
(target
of
cells).
spheroBlood
7:
1952
Ponder
mobility
served
175-182,
of
with
red
Ponder
cells
improved
1955
RI,
to
from
with
RV:
and
their
apparatus.
after
Electrophoretic
ghosts
i
Exp
as
ob-
Biol
32:
JG:
and
HM:
Dean
N Engl
in
the
Assoc
Am
Miwa
S,
from
kinase
(PK)
37:25-31,
in
1974
red
cells
phenacetin
1:173-183,
Acanthocytes
279:947,
ex-
spleen
bodies
after
Haematol
J Med
the
Jpn
Heinz
splenectomy
11.
tomy.
of
within
I,
pyruvate
Haematol
BrJ
N
of mitochondrial
reticulocytes
ministration.
cell.
relationship
Ishihara
erythrocyte
Selwyn
red
Trans
mechanism
Acta
red
1966
N,
patients
the
The
destruction.
trusion
human
occurring
Matsumoto
deficiency.
in
L:
79:426-438,
F: The
in
1958
1969
Weiss
cell
lipids
Rubbish
fragmentation
Uchino
10.
E,
of
4:344-349,
DG:
Weed
cell
spleen
Blood
Studies
281:558-559,
Physicians
WH:
hemolytic
cytes
proportion
1959
3. Crosby
4.
The
JI:
Br J Haematol
50:625-641,
1977
2.
Munn
cells.
after
1968
ad1955
splenec-
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1977 50: 643-645
Splenic remodeling of red cell surfaces [editorial]
WH Crosby
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