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Results: 5

1.
Figure 4

Figure 4. Serum TNF-α positively correlates to AT1-AA bioactivity. From: Autoantibody-mediated angiotensin receptor activation contributes to preeclampsia through TNF-alpha signaling.

A positive correlation between the level of AT1-AA bioactivity and serum TNF-α level was identified in preeclamptic women. Spearman’s rank correlation was used to determine an r-value (r=0.85, n=20, P<0.001).

Roxanna A. Irani, et al. Hypertension. ;55(5):1246-1253.
2.
Figure 2

Figure 2. TNF-α blockade reduces AT1-AA-induced preeclamptic-like features. From: Autoantibody-mediated angiotensin receptor activation contributes to preeclampsia through TNF-alpha signaling.

The key features of PE, hypertension (A) and proteinuria (B) present in the PE-IgG-injected pregnant mice were reduced by co-injection with a TNF-α blocker. In addition, sFlt-1 (C) and sEng (D) were also reduced with the co-injection of the autoantibody and the TNF-α blocker. n=9 for each variable. *P<0.05 versus NT-IgG. **P<0.05 versus PE-IgG.

Roxanna A. Irani, et al. Hypertension. ;55(5):1246-1253.
3.
Figure 1

Figure 1. TNF-α is increased in AT1-AA-injected pregnant mice. From: Autoantibody-mediated angiotensin receptor activation contributes to preeclampsia through TNF-alpha signaling.

Serum TNF-α was elevated in PE-IgG injected pregnant mice but not in NT-IgG injected pregnant mice. Co-injection of losartan or 7-aa resulted in decreased serum TNF-α levels in PE-IgG injected pregnant mice. Non-pregnant animals injected with similarly purified human IgG fractions (white bars) did not demonstrate increased cytokine levels. n=9 for each variable. *P<0.05 versus NT-IgG. **P<0.05 versus PE-IgG.

Roxanna A. Irani, et al. Hypertension. ;55(5):1246-1253.
4.
Figure 3

Figure 3. Autoantibody-induced placental damage can be prevented by TNF-α neutralization. From: Autoantibody-mediated angiotensin receptor activation contributes to preeclampsia through TNF-alpha signaling.

Placentas assessed by H&E staining (Panel A, 40X) indicate that PE-IgG injected mice had damaged placentas: calcifications (thin arrow) and fibrotic areas (thick arrow). Their labyrinth zones appear heterogeneous and have abnormal pools of blood (inset box). Placental apoptosis was assessed by TUNEL staining (Panel B, 10X, scale bar=1 mm). PE-IgG injected mice had increased apoptosis in their labyrinth zones as compared to NT-IgG injected animals. Quantification of the TUNEL assay (C) indicates a reduction in the TUNEL-positive cells in mice co-injected with PE-IgG and a TNF-α blocker as compared to the PE-IgG injected animals. n=18 placentas per variable, from 9 different mice in each group. Green; TUNEL-positive cells. Blue; DAPI-positive nuclei. Mice injected with NT-IgG or the anti-TNF-α antibody alone had unremarkable placentas. *P<0.05 versus NT-IgG. **P<0.05 versus PE-IgG.

Roxanna A. Irani, et al. Hypertension. ;55(5):1246-1253.
5.
Figure 5

Figure 5. TNF-α blockade prevents AT1 receptor-mediated damage in human placental villous explants. From: Autoantibody-mediated angiotensin receptor activation contributes to preeclampsia through TNF-alpha signaling.

Culturing human villous explants with PE-IgG resulted in TNF-α secretion (A). Co-culturing the explants with PE-IgG and losartan (5μM) or 7-aa (1μM) reduced the cytokine level. Apoptosis was increased in explants incubated with AT1-AA and was partially diminished by blocking TNF-α activity as demonstrated by a TUNEL assay (B). Green; TUNEL-positive cells. Blue; DAPI-positive nuclei. 10X. Quantification of TUNEL staining (C) indicates that co-incubation with PE-IgG and an anti-TNF-α agent (5μg/ml) reduces the amount of apoptosis. Secretion of sFlt-1 (D) and sEng (E) were reduced by co-incubation of the autoantibody with an anti-TNF-α antibody. Six different placentas were collected, and from each, n=4 for every variable, total n=24 per variable. *P<0.05 versus NT-IgG. **P<0.05 versus PE-IgG.

Roxanna A. Irani, et al. Hypertension. ;55(5):1246-1253.

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