RESUMEN
Antiphospholipid antibodies (aPL) are autoantibodies that attack phospholipid through anti-beta 2-glycoprotein 1. The actions of aPL are associated with events leading to thrombosis and morbidity in pregnancy. Antiphospholipid syndrome (APS) is diagnosed when a patient is persistently positive for aPL and also has recognised clinical manifestations such as recurrent pregnancy losses, arterial or venous thrombosis and in a catastrophic case, can result in death. Unfortunately, the pathogenesis of APS is still not well established. Recently, microRNA expressed in many types of diseased tissues were claimed to be involved in the pathological progression of diseases and has become a useful biomarker to indicate diseases, including APS. Objective: This systematic review aims to search for research papers that are focussing on microRNA expression profiles in APS. Method: Three search engines (Ebcohost, ProQuest and Ovid) were used to identify papers related to expression of specific microRNA in antiphospholipid syndrome. Results and Discussion: A total of 357 papers were found and screened, out of which only one study fulfilled the requirement. In this particular study blood samples from APS patients were tested. The microRNAs found to be related to APS were miR-19b and miR-20a. No data was found on specific microRNA being expressed in obstetric antiphospholipid syndrome. Analysis on the microRNA target genes revealed that most genes targeted by miR-19b and miR-20a involve in TGF-Beta Signalling and VEGF, hypoxia and angiogenesis pathways. Conclusion: In view of the limited data on the expressions of microRNA in APS we recommend further research into this field. Characterization of microRNA profile in blood as well as in placenta tissue of patients with APS could be useful in identifying microRNAs involved in obstetric APS.
RESUMEN
Objective: The placenta constitutes a physical and immunological barrier against infectious agents. Toll-like receptors (TLRs) are essential components for the induction of innate immunity responses in different human tissues including the placenta. We investigated the expressions of TLR2 and TLR4 in the decidua and amniotic cells in non-infl amed placenta and placenta with infection. Materials and Methods: There were a total 74 placentas (37 with infection and 37 without infection- 25 bacterial, 10 viral and 2 toxoplasma). TLR2 and TLR4 expressions were assessed using immunohistochemical technique. Positive cells were indicated by cytoplasmic staining and the percentage of positive in 100 cells was recorded and graded. The grades were 1+ (75%). Results: We found signifi cantly higher expression of TLR2 in the amniotic cells and decidua cells in infected placentas as compared to non-infl amed placentas among the preterm placenta. A higher number of cases have TLR4 expression in the amnion of preterm infected placenta than in term placenta. This, however, is not statistically signifi cant. Conclusion: Our fi ndings suggest that TLR2 plays a role in the innate immunity in bacterial and viral infection in the placenta, however, their role in protection against toxoplasma may be limited. This study further supports the observations that TLR2 expression was higher in placenta with infection which strengthened the role of TLR2 in the protection of preterm placenta against infection.