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F Lyall

Publications and source records attributed to F Lyall.

At least 19 recordsLinked to original sources
PubMed2006

Early embryonic demise: no evidence of abnormal spiral artery transformation or trophoblast invasion.

Invasion by extravillous trophoblast of uterine decidua and myometrium and the associated spiral artery 'transformation' are essential for the development of normal pregnancy. Small pilot studies of placental bed and basal plate tissues from miscarriages have suggested that impaired interstitial and endovascular trophoblast invasion may play a role in the pathogenesis of miscarriage. The hypothesis that early miscarriage is associated with reduced extravillous trophoblast invasion and spiral artery transformation was tested in a large series of placental bed biopsies containing decidua and myometrium and at least one spiral artery from early, karyotyped embryonic miscarriages (<or=12 weeks' gestation; n = 50) dated from the last menstrual period and ultrasound scan dated normal pregnancies (n = 78). Frozen sections were immunostained to demonstrate trophoblast (cytokeratin), myometrium and spiral artery medial smooth muscle (desmin), and endothelium (von Willebrand factor). Trophoblast invasion and individual features of spiral artery transformation were assessed histologically in spiral arteries of miscarriages (n = 176) and controls (n = 246) and analysed statistically using a logistic regression model. Trophoblast invasion of uterine tissues and spiral artery transformation did not differ between euploid and aneuploid early miscarriage and also did not differ significantly from normal pregnancy. These findings suggest that failed trophoblast invasion and spiral artery transformation do not have a pivotal role in the pathogenesis of early miscarriage.

Abortion, Spontaneous↗
PubMed2006

Late sporadic miscarriage is associated with abnormalities in spiral artery transformation and trophoblast invasion.

Trophoblast invasion of uterine decidua and myometrium, and spiral artery transformation, are essential for the development of normal pregnancy; this process is impaired in pre-eclampsia, fetal growth restriction, and pre-term labour. The hypothesis that late miscarriage is associated with reduced trophoblast invasion and spiral artery transformation was tested in a large series of placental bed biopsies containing decidua and myometrium from late, karyotyped, embryonic miscarriage (>or=13 weeks' gestation; n = 26; n = 96 spiral arteries) and gestationally matched ultrasound-dated normal pregnancies (n = 74; n = 236 spiral arteries). Cryostat sections were immunostained using an avidin-biotin peroxidase technique for cytokeratin, desmin, and von Willebrand factor to detect trophoblast, myometrium, and vascular smooth muscle and endothelium, respectively. Trophoblast invasion and individual features of spiral artery transformation were assessed and analysed using a logistic regression model. Compared with normal pregnancy, myometrial spiral arteries in late miscarriage showed reduced endovascular (4% vs. 31%, p = 0.001) and intramural trophoblast (76% vs. 88%, p = 0.05), and less extensive fibrinoid change (4% vs. 18%, p = 0.01). In contrast, endovascular trophoblast in decidual spiral arteries was increased (40% vs. 66%, p = 0.04). These findings suggest that, in common with pre-eclampsia, late sporadic miscarriage may be associated with reduced trophoblast invasion and inadequate transformation of myometrial spiral arteries.

Abortion, Spontaneous↗
PubMed2005

Dissolved oxygen concentration in culture medium: assumptions and pitfalls.

Oxygen is a key factor in the regulation of cytotrophoblast differentiation, proliferation and invasion in early pregnancy. Abnormalities in oxygen concentration have also been linked to a number of pregnancy disorders. Cell culture models have been used to study the effect of oxygen on cytotrophoblast behaviour in vitro, however, there is often little or no validation of oxygen levels in these cell culture systems. In this study, dissolved oxygen levels in culture medium maintained in standard culture conditions (18% O(2)) measured 18%. On transfer to a low oxygen environment (2% O(2)), oxygen levels decreased to 6-8% after 4h and reached 2% only after 24h in culture. Culture medium pre-gassed with nitrogen to remove dissolved oxygen quickly absorbed oxygen when exposed to ambient air during dispensing and required further incubation in a 2% oxygen environment before dissolved oxygen levels equilibrated to 2%. Thus, cultured cells placed in a low oxygen environment would be exposed to varying levels of oxygen before the desired level of oxygen exposure is reached. This study highlights the importance of validation of oxygen levels and potential problems associated with in vitro studies on the regulatory effects of oxygen.

Absorption↗
PubMed2005

Priming and remodelling of human placental bed spiral arteries during pregnancy--a review.

It is now well known that in order to establish human hemochorial placentation and to provide a progressive increase in blood supply to the growing fetus, the uterine spiral arteries must undergo considerable alterations. This physiological modification is thought to be brought about by the interaction of invasive cytotrophoblast with the spiral artery vessel wall. Despite intensive research our understanding of the mechanisms that control human trophoblast invasion in normal, let alone abnormal pregnancy, are still poorly understood. This is partly due to difficulties in obtaining "true" placental bed biopsies and most investigators have relied on in vitro models of trophoblast invasion. Clearly interpretation of such studies must be tempered with a degree of caution. This review outlines why the placental bed is important, how we can sample and study it, what morphology actually occurs in the placental bed spiral arteries during pregnancy and then briefly summarise the findings on the placental bed in pre-eclampsia.

Arteries↗
PubMed2002

Transforming growth factor beta expression in human placenta and placental bed during early pregnancy.

Normal human pregnancy depends on physiological transformation of spiral arteries. Pre-eclampsia and fetal growth restriction are associated with impaired trophoblast invasion and spiral artery transformation. Recent data obtained from studies on placenta suggest that temporal changes in expression of TGF-beta3 play a key role in trophoblast invasion and that over-expression of TGF-beta3 in pre-eclampsia is responsible for inadequate trophoblast invasion. There are, however, no studies of specific TGF-betas in the placental bed throughout pregnancy although this is where the invasive trophoblast and spiral arteries are located. In this study we have used immunohistochemistry, Western blot analysis, ELISA and RT-PCR to examine the expression of TGF-beta1, TGF-beta2 and TGF-beta3 in placental bed biopsies and placentas from 7--19 weeks' gestation. The results show that TGF-beta1, 2 and 3 are expressed in the placenta throughout this time but the striking temporal changes in TGF-beta3 expression previously reported were not observed. Extravillous trophoblast within the placental bed expressed TGF-beta2 but not TGF-beta1 or TGF-beta3 while extracellular TGF-beta1 and cytoplasmic TGF-beta2 were detected in decidua. These data suggest that TGF-beta1 and TGF-beta2 but not TGF-beta3 may play a role in trophoblast invasion.

Adult↗
PubMed2001

Transforming growth factor-beta expression in human placenta and placental bed in third trimester normal pregnancy, preeclampsia, and fetal growth restriction.

Normal human pregnancy depends on physiological transformation of spiral arteries by invasive trophoblasts. Preeclampsia (PE) and fetal growth restriction (FGR) are associated with impaired trophoblast invasion and spiral artery transformation. Recent studies have suggested that transforming growth factor (TGF)-beta3 is overexpressed in the placenta of PE patients and that this may be responsible for failed trophoblast invasion. There are, however, no studies on TGF-betas in the placenta in FGR or in the placental bed in PE or FGR. In this study we have used immunohistochemistry, Western blot analysis, and enzyme-linked immunosorbent assay to examine the expression of TGF-beta1, TGF-beta2, and TGF-beta3 in placenta and placental bed of pregnancies complicated by PE and FGR and matched control pregnancies. The results show that TGF-beta1, -beta2, and -beta3 are not expressed in villous trophoblasts but are present within the placenta. TGF-beta1, -beta2, and, to a much lesser extent, TGF-beta3 were present within the placental bed but only TGF-beta2 was present in extravillous trophoblast. No changes in expression of either isoform were found in placenta or placental bed in PE or FGR compared with normal pregnancy. These data are not consistent with overexpression of TGF-beta3 being responsible for failed trophoblast invasion in PE. Our findings suggest that the TGF-betas do not have a pathophysiological role in either PE or FGR.

Adult↗
PubMed2001

Human trophoblast invasion and spiral artery transformation: the role of PECAM-1 in normal pregnancy, preeclampsia, and fetal growth restriction.

During early human pregnancy extravillous cytotrophoblasts invade the uterus and spiral arteries transforming them into large vessels of low resistance. Failure of trophoblast invasion and spiral artery transformation occurs in preeclampsia and fetal growth restriction (FGR); these processes are not well understood. Recent studies have suggested that cytotrophoblasts that invade spiral arteries mimic the endothelial cells they replace and express PECAM-1. It was also reported that in preeclampsia, cytotrophoblasts fail to express PECAM-1 and that failure to express endothelial cell adhesion molecules may account for failed trophoblast invasion. Despite the possible importance of adhesion molecules in trophoblast invasion, no study has systematically investigated the expression of PECAM-1 in the placental bed throughout the period of invasion, particularly in the myometrial segments where the key failure occurs. There are no studies on PECAM-1 expression in the placental bed in FGR. We have examined the expression of PECAM-1 in placental bed biopsies and placentas from 8 to 19 weeks of gestation and in the placenta and placental bed in the third trimester in cases of preeclampsia, FGR, and control pregnancies. PECAM-1 was expressed on endothelium of vessels in the placenta and placental bed but not by villous or extravillous trophoblasts in normal or pathological samples. These findings do not support a role for PECAM-1 in normal invasion or in the pathophysiology of preeclampsia or FGR.

Adult↗
PubMed2001

Heme oxygenase expression in human placenta and placental bed: reduced expression of placenta endothelial HO-2 in preeclampsia and fetal growth restriction.

In this study we tested the hypothesis that expression of heme oxygenases HO-1 and HO-2, which are responsible for the production of carbon monoxide, are reduced in the placenta and placental bed of pregnancies complicated by preeclampsia (PE) and fetal growth restriction (FGR) compared with control third-trimester pregnancies. Placental protein expression was determined by Western blotting (n=10 in each group) and immunohistochemistry (controls n=18, PE n=19, FGR n=10). Extravillous trophoblast expression was determined by immunohistochemistry of placental bed biopsy samples (controls n=17, PE n=19, FGR n=10). Western blot analysis of placental homogenates showed no overall differences in HO-2 among groups. However, immunohistochemical analysis showed a reduction in HO-2 expression in endothelial cells in both abnormal groups (PE P<0.01; FGR P<0.0005 vs. control group) but no differences in villous trophoblast staining. HO-1 was undetectable by Western blotting in control and abnormal pregnancies and immunoreactivity was very low, suggesting that there is little HO-1 in the placenta. Within the placental bed, HO-2 but not HO-1 was detected on all populations of extravillous trophoblast, but expression of HO-2 or HO-1 did not change in PE or FGR. The reduced expression of HO-2 on endothelial cells in PE and FGR may be responsible for reduced placental blood flow in these conditions. The data do not show changes in HO in the placental bed in PE or FGR.

Adult↗
PubMed2000

Hemeoxygenase expression in human placenta and placental bed implies a role in regulation of trophoblast invasion and placental function.

The purpose of this study was to examine the expression of hemeoxygenases HO-1 and HO-2, which are responsible for the production of carbon monoxide (CO), in the human placenta and placental bed and to determine the role of inhibitors of HO on placental perfusion pressure. We hypothesized that HO is expressed within the placenta and that invading cytotrophoblast cells (CTB) express HO isoforms. The expression of HO-1 and HO-2 was studied on placenta and placental bed biopsies, obtained using a transcervical sampling technique, from normal human pregnancies between 8 and 19 wk gestation and at term. In the placenta, HO-2 immunostaining was prominent in syncytiotrophoblast in the first trimester and reduced toward term (P<0.0005). HO-2 endothelial immunostaining was weak in the first trimester, but increased by term (P<0.0005). Within the placental bed, HO-2 was expressed by CTB in cell columns, the cytotrophoblast shell, and cell islands. Both intravascular CTB and interstitial CTB expressed HO-2. HO-1 immunostaining was low in the placenta but intense on the CTB within the placental bed. A striking feature was the absence of HO-1 from the proximal layers of cell columns, with strong expression on the more distal CTB layers of the cell columns. In placental perfusion studies, a significant dose-dependent increase in perfusion pressure was observed in the presence of zinc protoporphyrin, an inhibitor of HO. These results suggest a role for CO in placental function, trophoblast invasion, and spiral artery transformation. Hemeoxygenase expression in human placenta and placental bed implies a role in regulation of trophoblast invasion and placental function.

Blotting, Western↗
PubMed1999

Hemoxygenase and nitric oxide synthase do not maintain human uterine quiescence during pregnancy.

The nitric oxide (NO)-cGMP pathway has been proposed as a mechanism for relaxation of myometrium during pregnancy and as a modulator of labor. Carbon monoxide (CO), produced by hemeoxygenases (HO-1 and HO-2), also activates soluble guanylate cyclase to increase cGMP. A recent study reported a large increase in HO-1 and HO-2 proteins during pregnancy, suggesting that the HO-CO pathway may be important in the maintenance of uterine quiescence during pregnancy. In this study we used Western blotting, reverse transcription-polymerase chain reaction, and immunohistochemistry to determine HO-1 and HO-2 expression in nonpregnant, pregnant, and laboring myometrium. Immunolocalization of HO was also compared with endothelial and inducible nitric oxide synthases (eNOS and iNOS). In contrast to HO-1 protein, which was not detected in myometrium, HO-2 protein and mRNA were constitutively expressed, although there were no differences in expression between the groups. eNOS was expressed in endothelial cells but not in myometrial smooth muscle. iNOS protein was not detected in myometrium. These data do not support an up-regulation of HO-1 and HO-2 during pregnancy and are not consistent with a role for NO or a major role for CO in human myometrial quiescence. Our results are also in keeping with HO-2 being an noninducible protein.

Blotting, Western↗
PubMed1999

Human trophoblast invasion and spiral artery transformation: the role of nitric oxide.

During early human pregnancy extravillous cytotrophoblasts invade the uterus and also migrate up the spiral arteries, transforming them into large vessels of low resistance. Failure of transformation has been described in pre-eclampsia, fetal growth restriction, and miscarriage. Recent evidence suggests that some maternal vessels undergo structural changes without interaction with cytotrophoblasts. The possibility arises that local vasoactive mediators such as nitric oxide result in spiral artery dilatation before their invasion. In support of this, a recent histological study in the guinea pig suggested that cytotrophoblasts expressed nitric oxide synthase (NOS) as they surrounded vessels. This study tested the hypothesis that invading cytotrophoblasts express NOS and therefore have the potential to induce vasodilatation by releasing nitric oxide. The expression of NOS on extravillous cytotrophoblasts was studied in placental bed biopsies, obtained, using a transcervical sampling technique, from normal human pregnancies between 8 to 19 weeks of gestation and in the third trimester. Whereas eNOS was expressed by syncytiotrophoblast, neither eNOS or iNOS was expressed by extravillous cytotrophoblasts at any time during invasion. The mechanisms controlling spiral artery transformation are pivotal to understanding normal and abnormal placentation. These results suggest that trophoblast-derived nitric oxide is unlikely to contribute to spiral artery dilatation.

Arteries↗
PubMed1999

The differential expression of myometrial connexin-43, cyclooxygenase-1 and -2, and Gs alpha proteins in the upper and lower segments of the human uterus during pregnancy and labor.

There is evidence from many studies indicating that a number of specific quiescent and contractile associated proteins are temporally regulated in the myometrium during pregnancy. In this present investigation we provide data that strongly suggest that myometrial connexin-43, cyclooxygenase-1 and -2 (COX-1 and -2), and Gs alpha proteins are also spatially expressed within the human uterus during pregnancy and labor. Using paired lower and upper segment myometrial samples taken from individual women at term and during spontaneous labor, we have measured the expression of these proteins by immunoblotting with specific antibodies. We report that the myometrial gap junction connexin-43 protein is expressed at much greater levels in the upper uterine compared to the lower uterine segment and that this difference is even more pronounced during the course of labor. Conversely, myometrial COX-1 and -2 proteins appear to be expressed at much greater levels in the lower compared to the upper uterine segment. Moreover, the level of expression of both proteins is unaffected by the onset of parturition. In contrast, myometrial Gs alpha protein appears to be uniformly expressed in both lower and upper segments and is similarly down-regulated during parturition, as previously reported. The differential expression of COX-1 and -2 and connexin-43 in the uterus may allow cervical ripening before and dilatation during labor and facilitate effective propagation of contractions from fundus to cervix, which may be further facilitated by the down-regulation of Gs alpha at the onset of parturition.

Adult↗
PubMed1998

Small low-density lipoproteins and vascular cell adhesion molecule-1 are increased in association with hyperlipidemia in preeclampsia.

The pregnancy disorder preeclampsia is characterized by endothelial cell dysfunction that may be promoted by abnormal increases in circulating lipids, particularly triglycerides and free fatty acids. Serum triglyceride concentration is a major regulatory determinant of low-density lipoprotein (LDL) size and density distribution. Smaller, denser LDL particles have several intrinsic properties capable of inducing endothelial dysfunction. The present nested, case-control study of gestationally matched preeclamptic and normal pregnant women tested the hypothesis that hypertriglyceridemia in preeclampsia is accompanied by decreases in LDL peak particle diameter (predominant LDL size). Plasma LDL peak particle diameter was determined by nondenaturing 2% to 16% polyacrylamide gel electrophoresis. Correlations of LDL diameter with the concentration of serum triglycerides, free fatty acids, total cholesterol, LDL-cholesterol, and apolipoprotein B (apo B) were determined. In the same individuals, we measured serum concentrations of a marker of vascular dysfunction previously reported to be increased in preeclampsia, soluble vascular cell adhesion molecule-1 (VCAM-1), and examined the association of VCAM-1 with LDL diameter and serum lipids. LDL peak particle diameter was decreased in preeclampsia relative to normal pregnancy (P < .01). The LDL-cholesterol:apo B ratio, which frequently decreases with decreasing LDL diameter, was also decreased (P < .04). Triglyceride concentrations were increased in preeclampsia (P < .0002), and there was a significant inverse relationship between LDL peak particle diameter and triglycerides (r = -.55, P < .02). Serum soluble VCAM-1 concentrations were markedly increased in preeclampsia (P < .0003). Apo B (P < .004), free fatty acids (P < .01), total cholesterol (P < .01), and LDL-cholesterol (P < .02) were also increased. VCAM-1 correlated with apo B (r = .50, P < .03) and LDL-cholesterol (r = .50, P < .03), but showed no relationship with the LDL diameter, LDL-cholesterol:apo B ratio, or other lipids. We conclude that the predominance of smaller, denser LDL, a potential contributor to endothelial cell dysfunction, is a feature of preeclampsia. However, the serum VCAM-1 level, one indicator of endothelial involvement, may be influenced more by quantitative lipoprotein changes (serum apo B or LDL-cholesterol) than by LDL particle size.

Case-Control Studies↗
PubMed1998

Gene expression of nitric oxide synthase in cultured human term placental trophoblast during in vitro differentiation.

The human placental syncytiotrophoblast is derived from differentiating cytotrophoblasts and is in contact with maternal blood. This endothelial function positions the trophoblast to regulate maternal-fetal exchange and to influence circulatory dynamics through paracrine interactions in the placenta. Two isoforms of nitric oxide synthase (NOS) are expressed in placenta, and northern analysis, reverse transcription-polymerase chain reaction (RT-PCR), and immunocytochemistry were used to correlate expression of the type II, inducible NOS (iNOS) and the type III, endothelial NOS (eNOS) with state of differentiation in cultured trophoblast from term placentae. It was also tested whether cytokines known to induce NOS in other cell systems would induce iNOS in human trophoblast. The mRNA for eNOS was detected by RT-PCR, but not by Northern analysis, in cultures grown for 24 h when cytotrophoblasts were dominant. In contrast, eNOS mRNA was abundant in cultures grown for 72 h when syncytiotrophoblast was present. Immunocytochemical staining for eNOS protein showed specific fluorescence in a few cells in cultures at 24 h, but the vast majority of cells expressed eNOS at 72 h. The iNOS isoform was expressed neither basally in any trophoblast culture nor was this isoform induced in cultures exposed to interleukin-1, tumour necrosis factor-alpha, interferon-gamma and lipopolysaccharide. The in vitro pattern of trophoblast eNOS expression models the in vivo pattern of eNOS expression described for villous trophoblast. The results suggest that eNOS plays a role in human trophoblast differentiation and function.

Base Sequence↗
PubMed1998

Increased nitrotyrosine in the diabetic placenta: evidence for oxidative stress.

OBJECTIVE: To evaluate the presence of nitrotyrosine (NT) residues in placental villous tissue of diabetic pregnancies as an index of vascular damage linked to oxidative stress. RESEARCH DESIGN AND METHODS: Villous tissue was collected and flash frozen after delivery from 10 class C and D IDDM patients (37.9+/-3.2 weeks) and 10 normotensive pregnant individuals (37.5+/-3.8 weeks). Serial sections of tissue were immunostained with specific antibodies to NT, endothelial nitric oxide synthase (eNOS), inducible nitric oxide synthase (iNOS), and manganese superoxide dismutase (MnSOD). Sections were scored for intensity of immunostaining (0-3) by three observers blinded to the identity of tissue. RESULTS: All tissues demonstrated immunostaining for eNOS in both syncytiotrophoblast and stem villous vascular endothelium with no apparent differences between groups. Immunostaining for iNOS was seen in the villous stroma, but again was not different between the two groups. Significantly more intense NT staining was apparent in vascular endothelium and villous stroma (both P < 0.02) of diabetic placentas. The endothelium of large villous vessels of diabetic tissues also showed more intense immunostaining for MnSOD (P < 0.01). CONCLUSIONS: In these diabetic pregnancies, we were unable to show increased eNOS, unlike previous findings in preeclamptic pregnancies. The presence of NT may indicate vascular damage in the diabetic placenta due to peroxynitrite action formed from increased synthesis/interaction of nitric oxide and superoxide. The apparently paradoxical increase in MnSOD expression may be an adaptive response to increased superoxide generation.

Biomarkers↗
PubMed1997

Circulating cell adhesion molecule concentrations in diabetic women during pregnancy.

OBJECTIVE: To determine whether circulating concentrations of defined cell adhesion molecules, which are thought to reflect endothelial expression, are increased in insulin-dependent diabetic women during pregnancy. METHODS: Pregnant diabetic women demonstrating good glycemic control and without major complications before pregnancy were studied at 8-12 (n = 15), 18 (n = 15), 28 (n = 16), 32 (n = 16), and 36 (n = 16) weeks' gestation. A subgroup of ten diabetic women was sampled longitudinally through all five gestational ages. The diabetic women were compared with healthy nondiabetic women sampled cross sectionally at 12 (n = 20), 28 (n = 19), and 36 (n = 19) weeks' gestation. Nonpregnant diabetic (n = 22) and nonpregnant nondiabetic women (n = 28) also were studied. Plasma concentrations of the cell adhesion molecules E-selectin, intercellular adhesion molecule-1 (ICAM-1), and vascular endothelial cell adhesion molecule-1 (VCAM-1) were measured by enzyme-linked immunosorbent assay. RESULTS: Significantly higher median (range) concentrations of E-selectin (63.0 [20.2-107.0] ng/mL) and ICAM-1 (281.5 [171.6-778.4] ng/mL) but not VCAM-1 (459.7 [301.0-909.7] ng/mL) were found in nonpregnant diabetic women compared with nonpregnant nondiabetic women (43.5 [18.1-93.2], 243.6 [174.4-329.2], and 476.0 [253.8-929.4] ng/mL, respectively). During pregnancy these significant differences between diabetic and control groups were lost. The median (range) concentration of E-selectin (50.0 [21.2-96.3] ng/mL) was significantly lower in pregnant compared with nonpregnant diabetic women. The plasma concentrations of E-selectin and ICAM-1 did not change significantly with gestation in either diabetic or nondiabetic pregnant groups. Vascular endothelial cell adhesion molecule-1 concentration changed significantly with gestation in the diabetic pregnant group only. CONCLUSION: Circulating concentrations of defined vascular cell adhesion molecules are not increased abnormally in diabetic women with good glycemic control during otherwise uncomplicated pregnancy.

Adult↗
PubMed1997

Inducible (type II) nitric oxide synthase in human placental villous tissue of normotensive, pre-eclamptic and intrauterine growth-restricted pregnancies.

We have utilized two distinct monospecific antibodies against the type II (macrophage or inducible) nitric oxide synthase (NOS) isoform to localize the distribution of the enzyme within the human placenta in tissues from normotensive pregnancies and those complicated by pre-eclampsia and/or intrauterine growth restriction. Both antibodies immunolocalize to cells in the villous stroma on frozen sections of villous tissue. Colocalization studies with anti-CD14 or anti-CD45 antibodies that recognize cells of leucocyte or monocyte/macrophage lineage indicate that Hofbauer cells are expressing type II NOS. This is in contrast to expression of type III (endothelial) NOS which is seen in syncytiotrophoblast and in villous vascular endothelium. In some, but not all, normotensive and pathologic placental tissue, some type II NOS immunostaining could be seen in syncytiotrophoblast and vascular endothelium; however, no differences could be discerned between groups of tissues. Expression of type II NOS by Hofbauer cells may indicate they are involved in surveillance against maternal immune insult or maternal pathogens whereby they secrete nitric oxide to exert a cytostatic/cytotoxic effect.

Female↗