Introduction Maternal thyroid dysfunction is associated with complications of malplacentation including miscarriages and pre-eclampsia. We hypothesise that thyroid hormones (TH) play an important role within human decidua in regulating placentation.

Methods Deciduas from human pregnancy were obtained from 1st (8–11 weeks) and 2nd trimester (12–20 weeks) surgical terminations of pregnancy. Primary cultures of total decidual cells (TDC), and immunomagnetic bead isolated populations of stromal-enriched (CD10+ve) and stromal-depleted (CD10-ve) cells, uterine natural killer cells (uNKs; CD56+ve) and macrophages (CD14+ve) were treated with T3 (0.10,100 nM). Assessments were made of cell viability (MTT assay), cytokine and angiogenic growth factor secretion (immunomediated assay) and the effects of decidual cell-conditioned media on extravillous trophoblast (EVT) invasion through Matrigel®.

Results Immunohistochemistry showed the expression of TH transporters (MCT8, MCT10) and receptors (TRa1, TRb1) required for TH-responsiveness in uNKs and macrophages from early gestation. The viability of TDC and cell isolates were unaffected by T3. In 1st trimester, T3 reduced IL-10 secretion by TDC and CD10-ve cells (p < 0.01), and reduced GM-CSF, IL-10, IL-1b, IL-6, MCP-1 by macrophages (p < 0.01). In 2nd trimester, T3 increased IL-10 by TDC (p < 0.01) and reduced IL-10 by uNKs (p < 0.001). T3 increased VEGF secretion by 1st trimester uNKs (p < 0.05), and angiopoietin-2 by 2nd trimester TDC and uNKs (p < 0.05). Conditioned media from T3-treated TDC and macrophages did not alter EVT invasion compared to untreated controls.

Conclusion TH regulate decidual cytokine and angiogenic growth factor secretion in a cell-specific and gestation-dependent manner. The summation of TH effects upon the secretome do not affect EVT invasion.