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Biomedical subjects

U Lang

Publications and source records attributed to U Lang.

At least 37 records · Page 2Linked to original sources
PubMed2000

Cardiovascular responses of perimenopausal women to hormonal replacement therapy.

OBJECTIVE: This study was undertake to test the hypothesis that hormone replacement therapy alters cardiovascular function during the first several months of therapy. STUDY DESIGN: Serial estimates of blood pressure, heart rate, stroke volume, and venous capacitance were obtained before and at 1, 5, 9, and 21 weeks after the beginning of hormone replacement therapy with daily estradiol and intermittent norethindrone. Measurements were performed by means of electrocardiography, automated blood pressure measurement (Dynamap; Critikon Company LLC, Tampa, Fla), echocardiography, and plethysmography. RESULTS: Hormone replacement therapy did not alter heart rate, blood pressure, or venous capacitance. End-diastolic volume and stroke volume were unchanged after 1 week of hormone replacement therapy but rose thereafter. After 5 weeks of hormone replacement end-diastolic volume and stroke volume were increased by 13 +/- 5 mL and 9 +/- 2 mL, respectively, and after 9 weeks the increases totaled 23 +/- 5 mL and 17 +/- 3 mL, respectively. As a result cardiac output rose progressively to a level 1.1 +/- 0.3 L/min (18%) greater than pretreatment values and systemic vascular resistance fell 15%. These changes were associated with a 3-fold increase in serum estradiol levels. CONCLUSION: The studied regimen of hormone replacement therapy produces progressive cardiac remodeling and peripheral vasodilatation during the first 2 months of therapy.

Blood Pressure↗
PubMed2000

Premarin-induced increases in coronary and uterine blood flow in nonpregnant sheep.

OBJECTIVE: Menopause is associated with an increased incidence of cardiovascular disease among women, and estrogen replacement therapy is thought to reduce the risk of coronary artery disease. The mechanism by which this occurs is unclear, but coronary arterial endothelial and vascular smooth muscle cells have been shown to contain estrogen receptors, and their stimulation appears to increase nitric oxide synthesis. One conjugated estrogen preparation (Premarin) is widely used in postmenopausal hormone replacement therapy, but little is known about its effects on cardiovascular hemodynamics. STUDY DESIGN: This study was designed to determine whether Premarin, like 17beta-estradiol, has significant effects on cardiac output and coronary and uterine blood flows at doses used clinically (0.625, 1.25, and 2.5 mg). Nonpregnant oophorectomized sheep were implanted with instruments to measure cardiac output, left coronary (circumflex) artery blood flow, uterine blood flow, heart rate, and systemic arterial blood pressure. After recovery from surgery, the animals received intravenous bolus injections of either 17beta-estradiol (1.0 microg/kg), Premarin (0.625, 1.25, or 2. 5 mg), or vehicle on different days. RESULTS: The 1.0-microg/kg dose of 17beta-estradiol significantly increased coronary blood flow by 15% +/- 2% from baseline (mean +/- SEM). Premarin also increased coronary blood flow significantly at the 1.25- and 2.5-mg dose levels by 12% +/- 3% and 14% +/- 4%, respectively. As expected 17beta-estradiol increased uterine blood flow from a baseline of 15 +/- 3 mL/min to 169 +/- 19 mL/min. Premarin treatment was associated with a significant increase in uterine blood flow, which increased from an average baseline of 14 +/- 4 mL/min to 46 +/- 10 mL/min, 95 +/- 18 mL/min, and 135 +/- 20 mL/min at the three doses tested (0. 625, 1.25, and 2.5 mg, respectively). 17beta-Estradiol also increased cardiac output by 12% +/- 3%. Premarin increased cardiac output 2% +/- 3%, 9% +/- 4%, and 11% +/- 3%, with only the highest dose producing a significant change. 17beta-Estradiol also increased heart rate by 12% +/- 1%, whereas Premarin at doses of 0.625, 1.25, and 2.5 mg increased it by 4% +/- 3%, 7% +/- 4%, and 10% +/- 2%, respectively (increase significant only at the highest dose). Neither 17beta-estradiol nor Premarin altered either stroke volume or systemic arterial pressure. CONCLUSION: Premarin, like 17beta-estradiol, has significant systemic, coronary, and uterine vascular effects. These vascular effects may help to explain in part why these compounds are cardioprotective.

Animals↗
PubMed2000

Role of cell contractions in cAMP-induced cardiomyocyte atrial natriuretic peptide release.

Incubation of spontaneously beating ventricular cardiomyocytes from neonatal rats with prostaglandin E(2) (0.1 microM) or forskolin (0.1 microM) simultaneously increased the rate of cellular contraction and atrial natriuretic peptide (ANP) secretion. Both responses were maximal within 10-20 min of application and were accompanied by three- to fourfold increases in cAMP formation. By contrast, a higher regimen of forskolin (10 microM) promoted a 20- to 30-fold increase in basal cAMP production, which was accompanied by the abolition of contractile activity and ANP release. Low regimens of forskolin (0.1 microM) doubled the occurrence of cytosolic Ca(2+) transients associated with monolayer contraction, whereas higher regimens of forskolin (10 microM) completely suppressed Ca(2+) transients. Moreover, in quiescent cultures that were pretreated with ryanodine, tetrodotoxin, nifedipine, or butanedione monoxime, prostaglandin E(2) (0.1 microM) and forskolin (0.1 microM) failed to elicit significant ANP secretion, suggesting that cAMP-elevating agents promote ANP secretion to a great extent via an increase in cellular contraction frequency in ventricular cardiomyocytes.

Animals↗
PubMed2000

Effects of chronic reduction in uterine blood flow on fetal and placental growth in the sheep.

Pregnancy is associated with a significant increase in uteroplacental blood flow (UBF), which is responsible for delivering adequate nutrients and oxygen for fetal and placental growth. The present study was designed to determine the effects of vascular insufficiency on fetal and placental growth. Thirty-nine late-term pregnant ewes were instrumented to investigate the effects of chronic UBF reduction. Animals were split into three groups based on uterine blood flow, and all animals were killed on gestational day 138. UBF, which began at 851 +/- 74 ml/min (n = 39), increased in controls (C) to 1,409 +/- 98 ml/min (day 138 of gestation) and in the moderately restricted (R(M)) group to 986 +/- 69 ml/min. In the severely restricted (R(S)) group, UBF was only 779 +/- 79 ml/min on gestational day 138. This reduction in UBF significantly affected fetal body weight with R(M) fetuses weighing 3,685 +/- 178 g and R(S) fetuses weighing 2,920 +/- 164 g compared with C fetal weights of 4,318 +/- 208 g. Fetal brain weight was not affected, whereas ponderal index was significantly reduced in R(M) (2.94 +/- 0.09) and R(S) fetuses (2.49 +/- 0.08) compared with the value of the C fetuses (3.31 +/- 0.08). Placental weight was also significantly reduced in the R(M) group, being 302 +/- 24 g, whereas the R(S) group placenta weighed 274 +/- 61 g compared with the C values of 414 +/- 57 g. Fetal heart, liver, lung, and thymus were all significantly smaller in the R(S) group. Thus the present study shows a clear relationship between the level of UBF and both fetal and placental size. Furthermore, the observation that fetal brain weight was not affected, whereas fetal body weight was significantly reduced suggests that this experimental preparation may provide a useful model in which to study asymmetric fetal growth restriction.

Animals↗
PubMed2000

[Heart-kidney-adrenal triangle interactions].

The heart-kidney-adrenal theme at the 42(nd) Journées Internationales d'Endocrinologie Clinique - Henri-Pierre Klotz held in Paris in April 1999 was chosen for at least two reasons. First, cardiovascular signs and symptoms are part of the most important and frequent endocrinopathies whose course is often characterized by cardiovascular complications. Secondly, the treatment of hypertension, heart failure and vascular nephropathies, as well as the prevention of atherosclerosis, call for homonal treatment or therapeutic intervention with agents acting upon endocrine systems that regulate cardiac, renal and vascular functions. The endocrinology specialist should therefore have full knowledge of the latest progress in the fields of the physiological and pathophysiological function of these systems, of the cellular mode of action of the hormones targeting the vardiovascular system, their genesis in classical endocrine organs, and also their local formation and action in tissues. Finally, it is important to be aware of the new therapeutic approaches opened by these recent developments.

Adrenal Glands↗
PubMed1999

Contamination of human milk in Middle Hesse, Germany--a cross-sectional study on the changing levels of chlorinated pesticides, PCB congeners and recent levels of nitro musks.

Human milk samples from women in Middle Hesse, Germany were chemically analyzed for contamination levels of alpha-, beta- and gamma-HCH, HCB, p,p'-DDE and p,p'-DDT as well as the PCB-congeners no. 28, 31, 49, 52, 101, 118, 138, 153, 156, 170 and 180. Changes in concentrations of these compounds in human milk over an extended time period were studied by comparing samples from 1984/85, 1990/91 and 1995. In addition, concentrations of the nitro-aromatic compounds musk xylene and musk ketone were determined in the 1995 samples. The study showed statistically highly significant (p<0.001) reductions in levels of beta- and gamma-HCH, HCB, p,p'-DDE and p,p'-DDT, in human milk from 1995 compared to samples from 1984/85. A weakly significant reduction (p<0.05) of alpha-HCH was also observed. For low-chlorinated PCB congeners, on the other hand, a highly significant increase of PCB no. 28 was detected and concentrations of congeners no. 31, 49 and 52 remained unchanged. Concentrations of the high-chlorinated congeners no. 101, 138, 153 and 180 dropped (highly significant). A highly significant reduction of PCB no. 118 and 156 occurred between 1990/91 and 1995, but a highly significant increase was found for no. 170. Lower levels of hydrocarbon contamination of human milk samples from 1995 than were found in samples from 1984/85 and 1990/91 can be seen to result partially from voluntary reductions, but primarily reflect restrictive environmental legislation in the Federal Republic of Germany. Mean concentrations of musk xylene and musk ketone in samples from 1995 were 41 microg/kg and 10 microg/kg milk fat, respectively.

Adult↗
PubMed1999

Epidermal cyst of the clitoris: a rare cause of clitorimegaly.

Epidermal cysts are slowly growing, intradermal or subcutaneous tumors with a wall composed of true epidermis. They occur most commonly on the face, scalp, neck, and trunk. We report the unusual case of a 16-year-old girl with an epidermal cyst of the clitoris. The tumor was removed by local excision.

Adolescent↗
PubMed1998

Autocrine regulation of endothelial exocytosis: von Willebrand factor release is induced by prostacyclin in cultured endothelial cells.

Vascular endothelial cells respond to external stimuli by altering the secretion of several bioactive molecules, including von Willebrand factor (vWf), prostacyclin (PGI2) and nitric oxide (NO). The release of all three molecules is regulated by a rise in cytosolic calcium ([Ca2+]i). In the present study we investigated whether cAMP-dependent signaling provides differential regulation of these effector systems by modulating the effect of [Ca2+]i in cultured human endothelial cells. The stable PGI2 analog iloprost, like other cAMP-raising agents (forskolin and adenosine), caused an acute dose-dependent increase in vWf release and potentiated the secretory response to thrombin. In contrast, iloprost, forskolin and adenosine failed to induce PGI2 release and inhibit thrombin-induced release. Our findings indicate cAMP-raising agents have opposite effects on [Ca2+]i-mediated vWf secretion and PGI2 release. PGI2 may potentiate vWf release and inhibit its own release in an autocrine manner.

Adenosine↗
PubMed1998

MAP kinase mediates epidermal growth factor- and phorbol ester-induced prostacyclin formation in cardiomyocytes.

We studied the role of protein kinase C (PKC) and mitogen-activated protein kinase (MAPK) in epidermal growth factor (EGF)-induced prostacyclin (PGI2) production in cultured, spontaneously-beating neonatal ventricular rat cardiomyocytes. To this purpose, the effect of EGF on cardiomyocyte MAPK phosphorylation, MAPK activity and PGI2-production were investigated, and compared to those induced by the PKC activator 4 beta phorbol 12-myristate 13-acetate (PMA). Both EGF (0.1 microM) and PMA (0.1 microM) induced the rapid and reversible phosphorylation of 42 KDa-MAPK in ventricular cardiomyocytes, responses that were accompanied by transient increases in MAPK activity (190-230% of control values within 5 min), and two- to three-fold increases in PGI2 formation. The tyrosine kinase inhibitors lavendustin (1 microM) and genistein (10 microM) strongly inhibited EGF-induced MAPK activation and PGI2-formation, but had no effect on PMA-stimulated responses. Experiments with the PKC inhibitor CGP 41251 (1 microM) or with PKC-downregulated cells demonstrated that in contrast to the PMA-stimulated responses, EGF-induced MAPK activation and PGI2-production were PKC-independent processes. Investigating the role of MAPK in EGF- and in PMA-promoted PGI2-formation, we found that the MAPK-inhibitor 6-thioguanine (500 microM), as well as the MAPK-kinase-inhibitor PD98059 (50 microM) abolished both EGF- and PMA-stimulated PGI2-production in cardiomyocytes. Our results indicate that MAPK-activation is at the basis of both growth factor receptor and PKC-dependent eicosanoid-formation in ventricular cardiomyocytes, where EGF-induced prostaglandin-production takes place via a PKC-independent pathway.

Analysis of Variance↗
PubMed1998

Invasion of cytotrophoblastic JEG-3 cells is stimulated by hCG in vitro.

Trophoblast invasion into the uterine wall is controlled by many factors. Previously, a human chorionic gonadotropin (hCG) receptor has been found to be expressed on invasive trophoblast as well as on choriocarcinoma cells implying a possible role for the hormone in trophoblast invasion. Therefore, this study examined the role of hCG in the invasion of trophoblastic (JEG-3) cells. Increasing hCG concentrations were applied in a trophoblast invasion model, JEG-3, through matrigel-coated filters. The proliferation was quantified by WST-1 cleavage assay. Cell migration was studied by examining the number of cells that had passed the uncoated porous (8-microm pore size) filters. After staining, filters were examined microscopically for cells on the underside of the membrane. A quantitative protease assay was also performed. Flow cytometric analysis of alpha5 and alpha6 integrin subunits, which are essential for interactions between cells and extracellular matrix, was performed. hCG increased significantly (P<0.01) the in vitro invasion of trophoblastic JEG-3 cells in a dose-dependent manner. Migration was also increased by hCG (P<0.01). However, cell proliferation remained unchanged. The second messenger analogue dibutyryl cAMP (db cAMP) and the cAMP elevating factor (forskolin) mimicked the effects of hCG by stimulating a dose-dependent increase of trophoblastic cell UEG-3) invasion. The collagenolytic activity of trophoblastic cells (EG-3) was increased by hCG stimulation. No changes were shown in the expression of alpha5 and alpha6 integrin subunits on JEG-3 cells. In vitro hCG is a regulatory factor of invasion and migration in trophoblastic JEG-3 cells, whereas proliferation is not influenced. The endogenous production of hCG by the trophoblast in vivo implies an autocrine control of invasion processes by hCG.

Bucladesine↗
PubMed1998

Invasion of cytotrophoblastic (JEG-3) cells is up-regulated by interleukin-15 in vitro.

PROBLEM: Trophoblast invasion into the uterus is controlled by many factors. Some cytokines (interleukin [IL]-1, IL-6, and IL-10) have been shown previously to play an important role in placentation. The human placenta is an important source of IL-15, although the cellular source of IL-15 in the placenta has not yet been specified. IL-15 influences cell adhesion and migration by redistributing adhesion molecules in lymphocytes and has been shown to have effects on endothelial cells and in some human tumors. METHOD OF STUDY: To study the role of IL-15 in trophoblast invasion, we investigated the effect of IL-15 (concentrations, 1-10 ng/ml) in a trophoblast invasion model (JEG-3 with matrigel-coated filters). Cell invasion was assessed using matrigel-coated filters and was expressed as the quotient of invading cells in comparison with the number of cells that had passed the control membrane. Cell migration was studied by examining the number of cells that had passed the filters without matrigel. Cell proliferation was quantified by a tetrazolium salt WST-1 cleavage assay. Matrix metalloproteinase (MMP)-1, MMP-2, and MMP-9 activities were measured by specific enzyme assays. RESULTS: IL-15 significantly (P < 0.05) increased the in vitro invasion of cytotrophoblastic (JEG-3) cells in a dose-dependent manner. There was a fourfold increase in the invasion at a concentration of 10 ng/ml of IL-15. Migration also was increased by a factor of 2.3 (P < 0.05). Cell proliferation, however, remained unchanged. The collagenolytic activity of cytotrophoblastic (JEG-3) cells was increased by IL-15 stimulation. A significant increase in MMP-1 concentration occurred after the incubation of JEG-3 cells with IL-15. No changes appeared in MMP-2, MMP-9, and tissue inhibitor of metalloproteinase-1 concentrations. CONCLUSIONS: Trophoblast invasion and migration, but not proliferation, are enhanced by IL-15. Our results suggest a role for IL-15 in the modulation of MMP-1 secretion by JEG-3 cells. Furthermore, we speculate, that IL-15 might be related to the changes of cell adhesion molecule phenotype during the process of invasion.

Cell Division↗
PubMed1998

[Expression of cell adhesion molecules in the extravillous trophoblast in placentas of preterm pregnancies and in placentas at term].

Invasion of the human trophoblast is regulated by cell adhesion molecules (CAM) such as integrins and members of the immunoglobulin superfamily, which also play an important role in a number of immunological reactions. Abnormal trophoblast invasion of the uterus and its arterial system has been related to preterm delivery. We examined the differences of CAM expression in the extravillous trophoblast of preterm (n = 18) and term pregnancies (n = 21). Placenta and decidua frozen sections were examined by double-staining immunohistochemistry using antibodies against the immunoglobulin superfamily (ICAM-1, ICAM-2, ICAM-3, VCAM-1), integrins (alpha 2 beta 1, alpha 3 beta 1, alpha 4 beta 1, alpha 5 beta 1, alpha 6 beta 1) and cytokeratin. The percentage of immunopositive extravillous trophoblast cells and the intensity of immunoreactivity for the mentioned CAM antibodies was assessed. The expression of alpha 3 beta 1, alpha 5 beta 1 and VCAM-1 (p < 0.05) in the extravillous trophoblast of preterm placentas was lower than in normal placentas, whereas the expression of alpha 6 beta 1 in the extravillous trophoblast of preterm placentas was higher than at term (p < 0.05). No differences were observed for alpha 2 beta 1, alpha 4 beta 1, ICAM-1, ICAM-2 and ICAM-3. Our results show that there is a different expression of cell adhesion molecules in the extravillous trophoblast of placentas in preterm delivery. These differences in CAM might be associated with abnormal immunological and cell-cell interactions between mother and developing fetus and thus cause preterm labor and delivery.

Antibodies, Monoclonal↗
PubMed1998

[Which contraceptive methods are recommended for young women with type 1 diabetes mellitus? A survey among practitioners in Germany].

AIM: The aim of this study was to find out which recommendations German gynecologists gave to young patients with type 1 diabetes mellitus in respect to contraception. In addition, it was asked to what extent German gynecologists/obstetricians had experience regarding counselling of young women with type 1 diabetes. SUBJECTS AND METHODS: A structured questionnaire containing questions about attitudes, health care beliefs and contraception in young women with type 1 diabetes was developed. 804 attendees of the Giessen Gynecological Seminar which was held in January 1997 were asked to participate in the study. RESULTS: Only 142 (17.7%) of the questionnaires were returned. There was no consensus in respect to contraception in young women with diabetes. 61% of the respondents referred to the micropill (< 0.3 mg estrogen) as the preferred contraceptive method for young women with diabetes. Condoms were regarded as second line contraceptive devices in this age and patient group. There was only very limited experience in regard to counselling and treating adolescents/young women with type 1 diabetes. CONCLUSION: Among the German gynecologists questioned there was no consensus in respect to contraception in young women with diabetes. Most importantly, there was only very limited individual experience in regard to counselling and treating adolescents/young women with type 1 diabetes among the doctors who participated in the study.

Adolescent↗
PubMed1997

[Pathophysiology of left ventricular hypertrophy in arterial hypertension].

The role of left ventricular hypertrophy as an independent risk factor for subsequent cardio-vascular events is well established, therefore the authors, in this brief review, describe the endocrine function of the heart and the role played by various factors, including hormones, in the development of cardiac remodeling during the course of hypertension. They then outline the present state of our knowledge concerning transmembrane signaling in the cardiomyocyte in response to an activation of specific receptors for vasoactive hormones of the renin-angiotensin II-aldosterone system.

Aldosterone↗
PubMed1997

Maternal plasma fibronectin: a predictor of preterm delivery.

OBJECTIVE: Current opinion holds that there are several distinct groups among patients with preterm labour: one of them is characterized by bacterial infection, another one by the presence of placental vascular abnormalities with endothelial damage. The aim of this study was to investigate plasma fibronectin, a suspected biochemical marker of endothelial damage, as an indicator for pregnancies with a high risk of preterm delivery. METHODS: Plasma fibronectin levels were measured in patients with preterm labour (n = 80) and in healthy pregnant women with uncomplicated (control) pregnancies (n = 64) between the 22nd and 36th week of gestation. Furthermore, the plasma concentrations of fibronectin in 15 newborns at term and ten babies born preterm were measured to study the relationship between preterm delivery and plasma fibronectin concentration in newborns. Fibronectin was measured by nephelometry. RESULTS: The mean concentration of fibronectin in patients with preterm labour was 0.44 g/l (S.D., 0.15) vs. 0.25 g/l (S.D., 0.12) in uncomplicated control pregnancies matched for gestational age. In control patients who actually delivered at term, fibronectin values were found to be lower than in control patients who underwent preterm delivery (0.25 g/l; S.D., 0.05; vs. 0.46 g/l; S.D., 0.15; P < 0.05). Particularly high values were detected in patients with preterm labour delivering before 32 weeks of gestation (0.60 g/l; S.D., 0.16). There was no significant difference between fibronectin concentrations in the umbilical arterial and venous blood of premature infants and mature infants. Leucocyte concentration, bacteriological smear and cervical dilatation did not correlate with fibronectin concentrations in patients with preterm delivery or controls. CONCLUSION: We conclude that the higher plasma concentrations of fibronectin in women with preterm labour may be a biochemical marker and a predictor of preterm delivery.

Adolescent↗
PubMed1997

Estrogen-induced increases in coronary blood flow are antagonized by inhibitors of nitric oxide synthesis.

OBJECTIVE: Estrogen receptors have been found in coronary arterial endothelial and vascular smooth muscle cells. Therefore the present study was designed to determine if estradiol-17 beta can increase coronary blood flow and if so whether the changes are mediated by nitric oxide. STUDY DESIGN: Five oophorectomized non-pregnant sheep were chronically instrumented to measure blood pressure, heart rate, cardiac output, left circumflex coronary blood flow and central venous pressure. Animals received estradiol-17 beta (1.0 micrograms/kg) and cardiovascular responses were followed for 135 min. RESULTS: Estradiol-17 beta (1.0 micrograms/kg) increased left circumflex (coronary) blood flow 28 +/- 3%, cardiac output 15 +/- 1% and heart rate by 13 +/- 3%. Coronary vascular resistance decreased 23 +/- 5%, systemic vascular resistance decreased by 12 +/- 2% while blood pressure did not change significantly. Administration of the nitric oxide synthetase inhibitor L-nitroarginine methylester (L-NAME), had no effect on basal coronary blood flow but completely reversed estradiol-17 beta induced increases in coronary blood flow. CONCLUSION: These results demonstrate that estrogen increases coronary blood flow in the non-pregnant sheep and that L-NAME, an inhibitor of nitric oxide, is able to reverse the estrogen induced flow changes.

Animals↗
PubMed1997

Expression of cell adhesion molecules in the extravillous trophoblast is altered in IUGR.

PROBLEM: The invasion of trophoblast cells into the uterine wall and its arterial system is essential for the normal development of pregnancy. Cell adhesion molecules (CAM), such as the immunoglobulin superfamily and integrins, play a crucial role in a number of immunological reactions and in the invasion of the human trophoblast. Intrauterine growth restriction (IUGR) has been associated with abnormal trophoblast invasion. Therefore, the expression of CAM in the extravillous trophoblast of pregnancies complicated by IUGR might be different from normal pregnancies. METHOD OF STUDY: Normal (n = 21) and IUGR (n = 19) placentas were collected and stored at -70 degrees C. Immunohistochemistry (avidin-biotin complex peroxidase-doublestaining) of frozen tissue sections was performed using antibodies specific for the immunoglobulin superfamily vascular adhesion molecule-1 (VCAM-1; CD 106), intercellular adhesion molecule (ICAM-1) (CD 54), ICAM-2 (CD 102), ICAM-3 (CD 50), the integrins alpha 2 beta 1, alpha 3 beta 1, alpha 4 beta 1, alpha 5 beta 1, alpha 6 beta 1 and cytokeratin. The percentage of immunopositive extravillous trophoblast cells (EVT) and the intensity of the immunoreactivity for the various CAM and integrin antibodies was assessed. RESULTS: In IUGR placentas, there was less expression of VCAM-1 (CD 106), alpha 2 beta 1, alpha 3 beta 1, and alpha 5 beta 1 (P < 0.05) in the extravillous trophoblast than in normal pregnancies. Finally we observed for the first time that ICAM-3 was expressed on EVT and that its expression was markedly up-regulated in the EVT or IUGR placentas. No differences were found for ICAM-1 (CD 54), ICAM-2 (CD 102), alpha 4 beta 1 and alpha 6 beta 1. CONCLUSION: Our data show that there are significant differences in the expression of cell adhesion molecules of the extravillous trophoblast from IUGR and normal pregnancies. These differences might reflect changes in the immunological reactions and cell-cell interactions between mother and the developing fetus which could interfere with fetal growth.

Antigens, CD↗