Abstract:
Understanding how oocyte morphogens regulate folliculogenesis and how their
actions and interactions are integrated into the overall processes in physiology
and pathophysiology of reproductive systems of mammals is an existing challenge.
Growth of an oocyte in mammal starts with an avascular structure called a
‘primordial follicle’ and subsequent to ovulation this avascular structure transforms
into a heavily vascular corpus luteum. This primordial follicle activation is a
complex process and it is not yet completely understood. Vascular endothelial
growth factor (VEGF) is well-known for its ability to regulate angiogenesis from the
existing blood vessels. Studies on VEGF play a pivotal role in understanding the
primordial follicle activation and progression of their growth. The objective of the
current study was to determine the effect of VEGF165a and VEGF165b on porcine
primordial follicle development invitro. VEGF165a is known to be a pro-angiogenic
factor where VEGF165b is anti-angiogenic. The tissue samples were treated with
VEGF165a and VEGF165b with 0ng/ml, 0.1, 1.0, 10.0 ng/ml and the day 0 (Negative
control) sample was fixed in 10% neutral buffered formalin instantly. The
preliminary data were obtained from short-term (72 hours) in vitro culture of
porcine ovarian cortical stripes and tissues were incubated under 5% CO2 with the
humidified atmospheric conditions at 37.50C. Out of three different dose regimes in
VEGF165a treated tissues, 0.1ng/ml resulted in the highest viable follicle count
(92.6%) while 1.0ng/ml and 10ng/ml had shown 65.3% and 24.8% viable follicle
count, respectively. The highest VEGF165a concentration recorded the highest follicle
degeneration. Among the VEGF165b treated tissues, 0.1ng/ml, 1.0ng/ml and
10.0ng/ml have shown 65.3%, 43.7%, 17.3% follicle viability respectively. As
VEGF165b is an anti-angiogenic factor, it contributed to the increase follicular
degeneration in all treatments. It showed a pattern of follicle degeneration where
higher concentrations had accelerated the follicle degeneration. In conclusion it was
evident that the lowest VEGF165a concentration (0.1ng/ml) improved the follicular
viability, where 1 and 10ng/ml VEGF165a increased the follicular degeneration. Also
VEGF165b has a negative effect on follicular viability in-vitro. In animal’s body both
VEGF165a and VEGF165b coexist while showing equilibrium. It needs to be further
investigated to find the ideal concentrations of VEGF165a and VEGF165b that promote
cell viability in vitro
