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Lack of apoptosis in first trimester decidual artery smooth muscle cells
Abstracts:
R.T.C.
and T.G.W.M.S.
Canada
A.17
1996
Trophoblast-endothelial interaction in placental bed capillaries of normotensive and and venules preeclamptic pregnancies. BPiinenborn, L. Vercruysse,
M. Hanssens & F.A. Van Ass&e. Dept. Obstet. Gynaec.,Univ. of Leuven, Belgium Aim: To evaluate the association between interstitial trophoblast (IT) and capillaries and venules, in normotensive (NT) and preeclamptic (PE) placental bed. Methods: Placental bed biopsies of 9 NT and 7 PE patients were double-immunostained for cytokeratin and CD3 1 (endothelial marker). PerivascularIT-endothelium associationwas evaluated as % of vesselcross-sections showing (1) perivascularIT within 15 p distance of, (2) closely apposed to, and (3) inserted into the endothelium. The findings were further related to the mean tissuedensity of IT within the area. Results: No difference was found between NT and PE, neither in tissue IT density, nor in % of vessel crosssectionswith different degreesof associatedpenvascular IT. IT density was positively correlated with % vessels with close penvascularIT in both groups, but only in PE there was a correlation of IT density with % vessels showing endothelial gaps. Conclusion: Although there was no difference in trophoblast-endothelium association between NT and PE, the observed correlation between IT density and endothelial disruption in PE requires Ilxther study in the light of reported evidenceof endothelial damage in PE.
Lack of Apoptosis in First Trimester Decidual Artery Smooth Muscle Cells C. Craven, L. Zhou, K. Ward, Department of Obstetrics and Gynecology, U. Utah, Salt Lake City, Utah, USA. Objective: A uteroplacental artery has a dilated lumen compared to the spiral artery in the secretory endometrium (SE). This has beenattributed to the destruction of smooth muscle cells @MC) by invasive cytotrophoblast. We hypothesize that the cellular mechanism of SMC loss may be apoptosis. Since vessel change occurs early in pregnancy, we sought to compare the rate of apoptosis in SE arteries to those in first trimester decidua. Methods: In situ evidence of apoptosis was sought in arteries in late SE biopsies [n=5], decidua of elective abortion (EAB) [n=lO], and of spontaneous abortion (SAB) [n=9]. Apoptosis was determined by specific staining of the 3’-OH ends of fragmented DNA, detected by enzyme conjugation of digoxigen to DNA with immunologic detection (TUNEL Assay). The number of vessel cross sections, and the location and number of apoptotic cells was determined for each tissue section. Results: Apoptotic cell nuclei were identified in the stroma of each tissue stained, and positive control slides demonstrated apoptotic nuclei. No apoptotic cells were identified in any arterial cross sections: O/95 SE, O/404 EAB, and O/230 SAB. Conclusion: SMC do not appear to be lost by apoptosis in secretory endometrium or decidua.
Presence of Endovascular Cytotrophoblasts in First Trimester Decidual Spiral Arteries C. Craven and K. Ward, Department of Obstetrics and Gynecology, University of Utah, Salt Lake City, Utah, USA. Objective: Endovascular cytotrophoblasts (EV CTB) are said to induce physiologic change in spiral arteries in pregnancy. These cells may also prevent blood flow to the intervillous space in the first trimester. We sought to determine the presence of EV CTB in spiral arteries in decidua. Methods: Decidual biopsies of first trimester elective abortion tissues [n=171 were stained with antibodies were against cytokeratin (CTK), von Willebrand Factor (vWF), placental lactogen (PL), and a-SMA [DAK0 reagents]. Dilated spiral arteries without fibrinoid change in the walls were called partially transformed vessels (PTV); dilated arteries whose wall contained flbrinoid material and cytotrophoblasts were called totally transformed vessels (‘M’V). Arteries were identified and percentage of occlusion by EV CTB estimated. Results: 42 PTV and 25 TTV were identified. No PTV had EV CTB (0142). 21J25 !M!V (84%) had no EV CTB. 3/25 TTV (12%) had EV CTB occupying ~5% of the lumen, and l/25 (4%) had EV CTB occupying 525% of the lumen. No TTV or PTV had EV CTB totally occluding arterial lumen. Conclusion: EV CTB are infrequently seen in spiral arteries of decidua in the first trimester.
a-Smooth Muscle Actin is Preserved in Arteries Showing Physiologic Change Catherine Craven and K. Ward, Department of Obstetrics and Gynecology, University of Utah, Salt Lake City, Utah, USA. Objective: Spiral arteries undergoing physiologic change become dilated. This dilation has been attributed to the destruction of smooth muscle cells by invasive cytotrophoblasts. We investigated whether arterial change is caused by a loss of vascular a-smooth muscle actin (c&MA). Methods: Hematoxylin and eosin stained slides were selected for arteries demonstrating physiologic change, defined as arterial dilation with fibrinoid material and cytotrophoblasts in the arterial wall. Decidual samples from elective abortion [n=7], and placental bed biopsies [n=71 were stained with antibodies were against cytokeratin (CTK), von Willebrand Factor (vWF), human placental lactogen (HPL), and a-ShL4 [DAK0 reagents]. Results: 25 decidual and 10 myometrial spiral arteries showed physiologic change. All had CTK or HPL positive cells in the wall, and some vWF staining of the luminal lining cells. Each artery had preservation c&MA staining in the arterial wall. Conclusion: Arterial dilation in physiologic change is not due to simple destruction of the smooth muscle cells as aSMA containing cells are present in the wall of totally transformed spiral arteries in the first trimester decidua and at term.
R.T.C.
and T.G.W.M.S.
Canada
A.17
1996
Trophoblast-endothelial interaction in placental bed capillaries of normotensive and and venules preeclamptic pregnancies. BPiinenborn, L. Vercruysse,
M. Hanssens & F.A. Van Ass&e. Dept. Obstet. Gynaec.,Univ. of Leuven, Belgium Aim: To evaluate the association between interstitial trophoblast (IT) and capillaries and venules, in normotensive (NT) and preeclamptic (PE) placental bed. Methods: Placental bed biopsies of 9 NT and 7 PE patients were double-immunostained for cytokeratin and CD3 1 (endothelial marker). PerivascularIT-endothelium associationwas evaluated as % of vesselcross-sections showing (1) perivascularIT within 15 p distance of, (2) closely apposed to, and (3) inserted into the endothelium. The findings were further related to the mean tissuedensity of IT within the area. Results: No difference was found between NT and PE, neither in tissue IT density, nor in % of vessel crosssectionswith different degreesof associatedpenvascular IT. IT density was positively correlated with % vessels with close penvascularIT in both groups, but only in PE there was a correlation of IT density with % vessels showing endothelial gaps. Conclusion: Although there was no difference in trophoblast-endothelium association between NT and PE, the observed correlation between IT density and endothelial disruption in PE requires Ilxther study in the light of reported evidenceof endothelial damage in PE.
Lack of Apoptosis in First Trimester Decidual Artery Smooth Muscle Cells C. Craven, L. Zhou, K. Ward, Department of Obstetrics and Gynecology, U. Utah, Salt Lake City, Utah, USA. Objective: A uteroplacental artery has a dilated lumen compared to the spiral artery in the secretory endometrium (SE). This has beenattributed to the destruction of smooth muscle cells @MC) by invasive cytotrophoblast. We hypothesize that the cellular mechanism of SMC loss may be apoptosis. Since vessel change occurs early in pregnancy, we sought to compare the rate of apoptosis in SE arteries to those in first trimester decidua. Methods: In situ evidence of apoptosis was sought in arteries in late SE biopsies [n=5], decidua of elective abortion (EAB) [n=lO], and of spontaneous abortion (SAB) [n=9]. Apoptosis was determined by specific staining of the 3’-OH ends of fragmented DNA, detected by enzyme conjugation of digoxigen to DNA with immunologic detection (TUNEL Assay). The number of vessel cross sections, and the location and number of apoptotic cells was determined for each tissue section. Results: Apoptotic cell nuclei were identified in the stroma of each tissue stained, and positive control slides demonstrated apoptotic nuclei. No apoptotic cells were identified in any arterial cross sections: O/95 SE, O/404 EAB, and O/230 SAB. Conclusion: SMC do not appear to be lost by apoptosis in secretory endometrium or decidua.
Presence of Endovascular Cytotrophoblasts in First Trimester Decidual Spiral Arteries C. Craven and K. Ward, Department of Obstetrics and Gynecology, University of Utah, Salt Lake City, Utah, USA. Objective: Endovascular cytotrophoblasts (EV CTB) are said to induce physiologic change in spiral arteries in pregnancy. These cells may also prevent blood flow to the intervillous space in the first trimester. We sought to determine the presence of EV CTB in spiral arteries in decidua. Methods: Decidual biopsies of first trimester elective abortion tissues [n=171 were stained with antibodies were against cytokeratin (CTK), von Willebrand Factor (vWF), placental lactogen (PL), and a-SMA [DAK0 reagents]. Dilated spiral arteries without fibrinoid change in the walls were called partially transformed vessels (PTV); dilated arteries whose wall contained flbrinoid material and cytotrophoblasts were called totally transformed vessels (‘M’V). Arteries were identified and percentage of occlusion by EV CTB estimated. Results: 42 PTV and 25 TTV were identified. No PTV had EV CTB (0142). 21J25 !M!V (84%) had no EV CTB. 3/25 TTV (12%) had EV CTB occupying ~5% of the lumen, and l/25 (4%) had EV CTB occupying 525% of the lumen. No TTV or PTV had EV CTB totally occluding arterial lumen. Conclusion: EV CTB are infrequently seen in spiral arteries of decidua in the first trimester.
a-Smooth Muscle Actin is Preserved in Arteries Showing Physiologic Change Catherine Craven and K. Ward, Department of Obstetrics and Gynecology, University of Utah, Salt Lake City, Utah, USA. Objective: Spiral arteries undergoing physiologic change become dilated. This dilation has been attributed to the destruction of smooth muscle cells by invasive cytotrophoblasts. We investigated whether arterial change is caused by a loss of vascular a-smooth muscle actin (c&MA). Methods: Hematoxylin and eosin stained slides were selected for arteries demonstrating physiologic change, defined as arterial dilation with fibrinoid material and cytotrophoblasts in the arterial wall. Decidual samples from elective abortion [n=7], and placental bed biopsies [n=71 were stained with antibodies were against cytokeratin (CTK), von Willebrand Factor (vWF), human placental lactogen (HPL), and a-ShL4 [DAK0 reagents]. Results: 25 decidual and 10 myometrial spiral arteries showed physiologic change. All had CTK or HPL positive cells in the wall, and some vWF staining of the luminal lining cells. Each artery had preservation c&MA staining in the arterial wall. Conclusion: Arterial dilation in physiologic change is not due to simple destruction of the smooth muscle cells as aSMA containing cells are present in the wall of totally transformed spiral arteries in the first trimester decidua and at term.