The significance of PlGF in the progression of the ovarian hyperstimulation syndrome in patient undergoing an in vitro fertilization procedure
DOI:
https://doi.org/10.28969/IJEIR.v12.i1.r6.22Keywords:
Angiogenesis, Soluble Fms-like tyrosine kinase (sFlt-1), Placental growth factorAbstract
Background: Placenta growth factor is, VEGF family member, a Pleiotropic Factor affects a variety of cell types and regulates various biological responses. PlGF is similar in structure and function to VEGF, and it amplifies VEGF's angiogenic actions. Ovulation stimulation during cycles of in vitro fertilization (IVF) for the mangment of infertility results in ovarian hyperstimulation syndrome (OHSS), an iatrogenic side effect. Considering potential roles of PlGF and its receptor (sflt-1) in angiogenesis, the association of these factors with OHSS among study women during controlled ovarian stimulation have evaluated in the present study.
Methods: comparative cross sectional study including of 60 women who go through controlled ovarian stimulation. On oocyte retrieval day, their serum and follicular fluid were taken. The concentrations of PlGF and sFlt-1 were assessed using ELISA.
Results: Eighteen patients presented with ovarian hyperstimulation syndrome (OHSS) and 42 patients were no OHSS. There was significantly higher serum PIGF in women with OHSS patients as compared to women with no OHSS, 141.4 ± 11.8 versus 91.9 ± 5.4 respectively (p<0.001). Furthermore Follicular fluid PlGF there was significantly higher in women with OHSS patients as compared to women with no OHSS, 163.4 ± 7.2 versus 91.1 ± 5.5 respectively (p<0.001).additionally Follicular fluids PlGF/sFlt ratio significantly higher in women with OHSS patients as compared to women with no OHSS, 0.034 ± 0.01 versus 0.026 ± 0.01 respectively (p<0.001). On the contrary there was significantly lower serum and follicular fluid sFlt in ovarian hyper-stimulated patients
Conclusions: These statistics show that serum and FF PlGF and PlGF to sFlt ratio higher in women with ovarian hyperstimulation syndrome (OHSS) patients as compared to women with no OHSS. So the PlGF may be played an important a role in angiogenesis dysregulation.
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Albonici, L., Giganti, M.G., Modesti, A., Manzari, V. and Bei, R. (2019). Multifaceted Role of the Placental Growth Factor (PlGF) in the Antitumor Immune Response and Cancer Progression. International Journal of Molecular Sciences, 20(12), p.2970. doi:10.3390/ijms20122970.
Bender, H.R., Trau, H.A. and Duffy, D.M. (2018). Placental Growth Factor Is Required for Ovulation, Luteinization, and Angiogenesis in Primate Ovulatory Follicles. Endocrinology, [online] 159(2), pp.710–722. doi:10.1210/en.2017-00739.
Ceci, C., Atzori, M.G., Lacal, P.M. and Graziani, G. (2020). Role of VEGFs/VEGFR-1 Signaling and Its Inhibition in Modulating Tumor Invasion: Experimental Evidence in Different Metastatic Cancer Models. International Journal of Molecular Sciences, [online] 21(4). doi:10.3390/ijms21041388.
Ceci, C., Atzori, M.G., Lacal, P.M. and Graziani, G. (2020). Role of VEGFs/VEGFR-1 Signaling and Its Inhibition in Modulating Tumor Invasion: Experimental Evidence in Different Metastatic Cancer Models. International Journal of Molecular Sciences, [online] 21(4). doi:10.3390/ijms21041388.
Corbett, S., Shmorgun, D., Claman, P., Cheung, A., Sierra, S., Carranza-Mamane, B., Case, A., Dwyer, C., Graham, J., Havelock, J., Healey, S., Hemmings, R., Liu, K., Motan, T., Murdock, W., Smithson, D., Vause, T., Wong, B. and Gysler, M. (2014). The Prevention of Ovarian Hyperstimulation Syndrome. Journal of Obstetrics and Gynaecology Canada, [online] 36(11), pp.1024–1033. doi:10.1016/S1701-2163(15)30417-5.
De Falco, S. (2012). The discovery of placenta growth factor and its biological activity. Experimental and Molecular Medicine, 44(1), p.1. doi:10.3858/emm.2012.44.1.025.
Fainaru, O., Amsalem, H., Bentov, Y., Esfandiari, N. and Casper, R.F. (2010). CD56brightCD16− natural killer cells accumulate in the ovarian follicular fluid of patients undergoing in vitro fertilization. Fertility and Sterility, 94(5), pp.1918–1921. doi:10.1016/j.fertnstert.2009.12.067.
Freitas-Andrade, M., Carmeliet, P., Charlebois, C., Stanimirovic, D.B. and Moreno, M.J. (2012). PlGF knockout delays brain vessel growth and maturation upon systemic hypoxic challenge. Journal of Cerebral Blood Flow and Metabolism: Official Journal of the International Society of Cerebral Blood Flow and Metabolism, [online] 32(4), pp.663–675. doi:10.1038/jcbfm.2011.167.
Namavar Jahromi, B., Parsanezhad, M.E., Shomali, Z., Bakhshai, P., Alborzi, M., Moin Vaziri, N. and Anvar, Z. (2018). Ovarian Hyperstimulation Syndrome: A Narrative Review of Its Pathophysiology, Risk Factors, Prevention, Classification, and Management. Iranian Journal of Medical Sciences, [online] 43(3), pp.248–260. Available at: https://pubmed.ncbi.nlm.nih.gov/29892142/.
Naredi, N., Talwar, P. and Sandeep, K. (2014). VEGF antagonist for the prevention of ovarian hyperstimulation syndrome: Current status. Medical Journal Armed Forces India, 70(1), pp.58–63. doi:10.1016/j.mjafi.2012.03.005.
Nejabati, H.R., Mota, A., Farzadi, L., Ghojazadeh, M., Fattahi, A., Hamdi, K. and Nouri, M. (2017). Follicular fluid PlGF/sFlt-1 ratio and soluble receptor for advanced glycation end-products correlate with ovarian sensitivity index in women undergoing A.R.T. Journal of Endocrinological Investigation, [online] 40(2), pp.207–215. doi:10.1007/s40618-016-0550-5.
Nelson, S.M. (2017). Prevention and management of ovarian hyperstimulation syndrome. Thrombosis Research, 151, pp.S61–S64. doi:10.1016/s0049-3848(17)30070-1.
Pan, P., Fu, H., Zhang, L., Huang, H., Luo, F., Wu, W., Guo, Y. and Liu, X. (2010). Angiotensin II upregulates the expression of placental growth factor in human vascular endothelial cells and smooth muscle cells. BMC Cell Biology, 11(1), p.36. doi:10.1186/1471-2121-11-36.
Pfeifer, S., Butts, S., Dumesic, D., Fossum, G., Gracia, C., La Barbera, A., Mersereau, J., Odem, R., Paulson, R., Penzias, A., Pisarska, M., Rebar, R., Reindollar, R., Rosen, M., Sandlow, J., Vernon, M. and Widra, E. (2016). Prevention and treatment of moderate and severe ovarian hyperstimulation syndrome: a guideline. Fertility and Sterility, 106(7), pp.1634–1647. doi:10.1016/j.fertnstert.2016.08.048.
Pietrowski, D., Szabo, L., Sator, M., Just, A. and Egarter, C. (2011). Ovarian hyperstimulation syndrome is correlated with a reduction of soluble VEGF receptor protein level and a higher amount of VEGF-A. Human Reproduction, 27(1), pp.196–199. doi:10.1093/humrep/der349.
Radomska-Leśniewska, D.M., Białoszewska, A. and Kamiński, P. (2021). Angiogenic Properties of NK Cells in Cancer and Other Angiogenesis-Dependent Diseases. Cells, 10(7), p.1621. doi:10.3390/cells10071621.
Soares, S.R., Gomez, R., Simon, C., Garcia-Velasco, J.A. and Pellicer, A. (2008). Targeting the vascular endothelial growth factor system to prevent ovarian hyperstimulation syndrome. Human Reproduction Update, 14(4), pp.321–333. doi:10.1093/humupd/dmn008.
Sun, B., Ma, Y., Li, L., Hu, L., Wang, F., Zhang, Y., Dai, S. and Sun, Y. (2021). Factors Associated with Ovarian Hyperstimulation Syndrome (OHSS) Severity in Women With Polycystic Ovary Syndrome Undergoing IVF/ICSI. Frontiers in Endocrinology, [online] 11, p.615957. doi:10.3389/fendo.2020.615957.
Sur, D. and Chakravorty, R. (2016). Association of Coronary Heart Disease Risk and Lipid Profile in Indian Women With Polycystic Ovarian Syndrome. Journal of Clinical Gynecology and Obstetrics, [online] 5(1), pp.23–26. doi:10.14740/jcgo.v5i1.375.
Tal, R., Seifer, D.B., Grazi, R.V. and Malter, H.E. (2014). Follicular fluid placental growth factor is increased in polycystic ovarian syndrome: correlation with ovarian stimulation. Reproductive Biology and Endocrinology, 12(1), p.82. doi:10.1186/1477-7827-12-82.
Wang, L., Qi, H., Baker, P.N., Zhen, Q., Zeng, Q., Shi, R., Tong, C. and Ge, Q. (2017). Altered Circulating Inflammatory Cytokines Are Associated with Anovulatory Polycystic Ovary Syndrome (PCOS) Women Resistant to Clomiphene Citrate Treatment. Medical Science Monitor: International Medical Journal of Experimental and Clinical Research, [online] 23, pp.1083–1089. doi:10.12659/msm.901194.
Wise, L.M., Stuart, G.S., Real, N.C., Fleming, S.B. and Mercer, A.A. (2018). VEGF Receptor-2 Activation Mediated by VEGF-E Limits Scar Tissue Formation Following Cutaneous Injury. Advances in Wound Care, [online] 7(8), pp.283–297. doi:10.1089/wound.2016.0721.

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