Abstract:
Vascular endothelial growth factor (VEGF) is well known for its ability to regulate
angiogenesis where it has been reported of playing a crucial role in metastasis of
tumors. Stem cell factor (SCF) plays a crucial role in cell viability. Growth of a
mammalian oocyte starts with an avascular structure called primordial follicle’ and
after the ovulation this avascular structure transforms into a heavily vascular
corpus luteum. Primordial follicle activation has been regulated by many intrinsic
and extrinsic factors of animals many of which have not been studied completely. It
has been observed that the VEGF and its isomers have regulatory effects on the
formation of the vascular bed in developing follicles and it supports the activation
of the dormant follicles. The objective of the current study was to determine the
effect of anti-angiogenic VEGF165b and SCF on porcine primordial follicle
development in vitro. VEGF165b is known to be an anti-angiogenic factor where SCF
is well known for its ability to enhance cell migration, proliferation and cell survival.
The tissue samples were treated with VEGF165b with 0ng/ml, 0.1, 1.0, 10.0 ng/ml and
day 0 (Negative control) samples were fixed instantly in 10% neutral buffered
formalin and each treatment had 6 replicates. Separate three trials were conducted
in order to observe the rest of the effects in each treatment. All the treatments were
supplemented with 10ng/ml of SCF to stabilize the cell survival. All the treated
tissues were subjected to 72hrs of incubation under 5% CO2 with the humidified
atmospheric conditions at 37.50C and followed by a histological assay to obtain the
preliminary data. Out of three different dose regimes in VEGF165b treated tissues,
0.1ng/ml has shown 65.15% of follicle viability. It was numerically the highest
recorded viable follicle count whereas 1.0ng/ml and 10.0ng/ml treatments
reported 39.61% and 20.20% follicle viability respectively. Although, 0.1ng/ml
VEGF165b showed the highest viable follicle count, it was lower than the viability
showed in previous study with 0.1ng/ml VEGF165a (92.6%). It was proposed under
natural conditions these VEGF isomers and SCF were in an equilibrium which
regulated the angiogenesis and anti-angiogenesis. In conclusion it was evident that
VEGF165b did not support the follicle viability alone, even with the presence of SCF
that stabilized the cell viability. Further studies are necessary for understanding the
exact role of VEGF165b and SCF combination effect on cellular viability which may
bring new insights into cancer therapy
