Introduction – The maternal condition preeclampsia currently has an incidence of 3-5%1 and affects both neonates and mothers globally as the most common cause of mortality2. Preeclampsia can be identified beginning at 20 weeks gestation by hypertension, protein present in urine, and, most concerning, damage to additional organs1. Inhibition of spiral artery reformation in preeclampsia limits the amount oxygen the placenta receives, as well as its maturation, thus leading to “oxidative stress”3. While delivery of the baby is important3, research on preeclampsia has illuminated inflammation and apoptosis prevention4-6 and the health of both the mother and infant in relation to discovered microparticles7. Methods – Human umbilical vein endothelial cells were gathered to determine the presence of SIRT1 when faced with IL-6 and serum from a preeclamptic patient through Western blot4. The endothelial cell’s rate of apoptosis was also examined with annexin V-FITC/PI4. Cells of trophoblasts (with and without oxygen) were combined with mononuclear cells to determine the amount of IL-6 and TNF-alpha produced, as well as the amount of trophoblast division5. Centrifugation of collected blood from preeclamptic women was analyzed with an ELISA and flow cytometry before and after birth6. Flow cytometry was also used in conjunction with fluorescence to examine microparticles, while Doppler provided information about the umbilical and middle cerebral arteries7. Results – SIRT1 in excess decreased the amount of HSP70 and HMGB1 (which typically signal stress and inflammation), along with the rate of apoptosis of the endothelial cells4. Environments without oxygen exacerbated inflammation by illustrating increased IL-6 and TNF-alpha after 1 and 2 days of examination5. Decreased vascularization occurred when sEnd and sFlt1 were increased, and the significant increases seen in preeclamptic women were present before the birth and after for 2 days6. CD105+ and CD31+/42- before the birth were greater and significant, and increased CD31+/42- was also significant after the birth at one week6. Prevalent microparticles from the endothelium were detailed in more numerous deaths and decreased birth weights of neonates, along with severe preeclampsia7. Preeclamptic women demonstrated, by Doppler, resistance and pulsatility that were increased significantly in the umbilical and middle cerebral arteries7. Conclusions – Both the baby and mother can be affected by microparticles7, and microparticles from trophoblasts may promote increased inflammation when there is little oxygen5. Apoptosis is linked to entities such as CD31+/42-6, but minimization of inflammation and apoptosis may be possible with SIRT14.
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- Escudero C, Herlitz K, Troncoso F et al. Role of Extracellular Vesicles and microRNAs on Dysfunctional Angiogenesis during Preeclamptic Pregnancies. Frontiers in Physiology. 2016;7. doi:10.3389/fphys.2016.00098.
- Kell D, Kenny L. A Dormant Microbial Component in the Development of Preeclampsia.Frontiers in Medicine. 2016;3. doi:10.3389/fmed.2016.00060.
- Yin, Y, Feng Y, Zhao H, et. al. SIRT1 inhibits releases of HMGB1 and HSP70 from human umbilical vein endothelial cells caused by IL-6 and the serum from a preeclampsia patient and protects the cells from death.Biomedicine & Pharmacotherapy. 2017;88:449-458. doi:10.1016/j.biopha.2017.01.087.
- Lee S, Romero R, Lee Y, Park I, Park C, Yoon B. Systemic inflammatory stimulation by microparticles derived from hypoxic trophoblast as a model for inflammatory response in preeclampsia.American Journal of Obstetrics and Gynecology. 2012;207(4):337.e1-337.e8. doi:10.1016/j.ajog.2012.06.047.
- Petrozella L, Mahendroo M, Timmons B, Roberts S, McIntire D, Alexander J. Endothelial microparticles and the antiangiogenic state in preeclampsia and the postpartum period. American Journal of Obstetrics and Gynecology. 2012;207(2):140.e20-140.e26. doi:10.1016/j.ajog.2012.06.011.
- Salem M, Kamal S, El Sherbiny W, Abdel Aal A. Flow cytometric assessment of endothelial and platelet microparticles in preeclampsia and their relation to disease severity and Doppler parameters. Hematology. 2014;20(3):154-159. doi:10.1179/1607845414y.0000000178.