Immunohistochemical Study of VEGF in Placenta of Hypertensive Mothers

  • Sharath Kumar H K Department of Pathology, Mysore Medical College and Research Institute
  • Chaitra N Department of Pathology, Mysore Medical College and Research Institute
  • Nataraju G Department of Pathology, Mysore Medical College and Research Institute
  • Bharathi M Department of Pathology, Mysore Medical College and Research Institute
DOI: https://doi.org/10.21276/apalm.2834
Keywords: Hypertensive placenta, Immunohistochemistry, Syncytiotrophoblasts, VEGF

Abstract

Background: Pregnancy is most commonly complicated by Hypertensive disorders. In India, the incidence of gestational hypertension varies from 0.5-1.8%. VEGF is a prime regulator of angiogenesis and overall maintenance of endothelial cell health. This study aims to determine the role of VEGF in placentae of Hypertensive and Normotensive pregnancies by assessing its immunohistochemical expression in Syncytiotrophoblasts.   Methods: The study was conducted in the Department of Pathology in our institute. This is a case-control study which included 50 placentae. Out of which,25 were from Normal mothers and 25 placentae from Hypertensive mothers. Immunohistochemistry for VEGF was performed on tissue section using commercially available monoclonal antibodies. The results were interpreted by evaluating Positivity and Intensity of Immunostaining.   Result: Out of 25 Hypertensive placentae, 22 showed Positivity for VEGF immunostaining. Out of 25 Normotensive placentae, 23 showed Negative results for syncytiotrophoblastic staining of VEGF. The difference in VEGF expression in syncytiotrophoblast of hypertensive and normotensive placentae was statistically significant.   Conclusion: Hypoxia acts as a potent stimulus for induction of VEGF mRNA in an attempt to normalize fetal blood flow and thus VEGF is increased. This results in the notable increase in immunohistochemical expression of VEGF in the syncytiotrophoblasts of hypertensive placenta.

References

1. Azliana AF, Zainul-Rashid MR, Chandramaya SF, Farouk WI, Nurwardah A, Wong YP, et al. Vascular endothelial growth factor expression in placenta of hypertensive disorder in pregnancy. Indian J Pathol Microbiol 2017; 60:515-20.
2. Thobbi VA, Anwar A. A study of maternal morbidity and mortality due to Pre eclampsia and eclampsia. Al Ameen J Med Sci 2017;10(3):174-179.
3. Dutta DC. Textbook of obstetrics. 7th edition. New Delhi: Jaypee Brothers Medical Publishers;2013.
4. Klagsbrun M, D’Amore PA. Vascular Endothelial Growth Factor and its Receptors. Cytokine & Growth Factor Reviews 1996; 7(3):259-270.
5. Redman WC, Sargent LL. Latest Advances in Understanding Preeclampsia. Science 2005; 308:1592-1594
6. Baergen RN. Manual of Benirschke and Kaufmann’s Pathology of the Human Placenta. New York: Springer;2005.
7. Yelumalai S, Muniandy S, Zawiah Omar S, Qvist R. Pregnancy‑induced hypertension and preeclampsia: Levels of angiogenic factors in Malaysian women. J Clin Biochem Nutr 2010; 47:191‑7.
8. Kurtoglu E, Altunkaynak BZ, Aydin I, Ozdemir AZ, Altun G, Kokcu A, Kaplan S. Role of vascular endothelial growth factor and placental growth factor expression on placenta structure in pre-eclamptic pregnancy. J Obstet Gynaecol Res 2015; 41(10):1533-1540.
9. Sgambati E, Marini M, Thyrion GDZ, Parretti E, Mello G, Orlando C et al., VEGF expression in the placenta from pregnancies complicated by hypertensive disorders. Br J Obstet Gynaecol 2004; 111:564-570

10. Walker JJ. Pre‑eclampsia. Lancet 2000; 356:1260‑5.
11. Maynard S, Epstein FH, Karumanchi SA. Preeclampsia and angiogenic imbalance. Annu Rev Med 2008; 59:61‑78.
12. Maynard SE, Min JY, Merchan J, Lim KH, Li J, Mondal S, et al. Excess placental soluble fms‑like tyrosine kinase 1 (sFlt1) may contribute to endothelial dysfunction, hypertension, and proteinuria in preeclampsia. J Clin Invest 2003; 111:649‑58.
Published
2020-09-25
Issue
Vol 7 No 9 (2020)
Section
Original Article

Authors who publish with this journal agree to the following terms:

  1. Authors retain copyright and grant the journal right of first publication with the work simultaneously licensed under a Creative Commons Attribution License that allows others to share the work with an acknowledgement of the work's authorship and initial publication in this journal.
  2. Authors are able to enter into separate, additional contractual arrangements for the non-exclusive distribution of the journal's published version of the work (e.g., post it to an institutional repository or publish it in a book), with an acknowledgement of its initial publication in this journal.
  3. Authors are permitted and encouraged to post their work online (e.g., in institutional repositories or on their website) prior to and during the submission process, as it can lead to productive exchanges, as well as earlier and greater citation of published work (See The Effect of Open Access at http://opcit.eprints.org/oacitation-biblio.html).