cartilage.
We
report
the
biological
effect
of
the
platelet
lysate
(PL),
a
PRP
derivative,
on
primary
human
articular
chondrocytes
(HAC)
cultured
under
both
physiological
and
inflammatory
condition.
Added
to
the
culture
medium,
PL
induced
a
strong
mitogenic
response
in
the
chondrocytes.
The
in
vitro
expanded
cell
population
maintained
a
chondrogenic
re-‐differentiation
potential
as
revealed
by
micromass
culture
in
vitro
as
well
as
in
vivo
as
demonstrated
by
ectopic
cartilage
formation
in
nude
mice.
Furthermore,
in
chondrocytes
cultured
in
the
presence
of
the
pro-‐inflammatory
cytokine
IL-‐1α,
the
PL
induced
a
drastic
enhancement
of
the
synthesis
of
the
cytokines
IL-‐6
and
IL-‐8
and
of
NGAL,
a
lipocalin
expressed
in
cells
of
the
chondrogenic
lineage.
These
events
were
controlled
by
the
p38
MAP
kinase
and
NF-‐κΒ
pathways.
The
pro-‐inflammatory
effect
of
the
PL
was
a
transient
phenomenon.
In
fact,
after
an
initial
up
regulation,
we
observed
a
significant
reduction
of
the
NF-‐κΒ
activity
together
with
the
repression
of
the
inflammatory
enzyme
ciclooxygenase-‐2
(COX-‐2).
Moreover,
the
medium
of
chondrocytes
cultured
in
the
contemporary
presence
of
PL
and
IL-‐1α,
showed
a
significant
enhancement
of
the
chemoattractant
activity
versus
untreated
chondrocytes.
On
the
whole,
our
findings
support
the
concept
that
the
platelet
products
have
a
direct
beneficial
effect
on
articular
chondrocytes
and
at
the
same
time
could
drive
in
sequence
a
trans
