Effect of microcystin-LR on human placental villous trophoblast differentiationin vitro

2014 ◽  
Vol 31 (4) ◽  
pp. 427-439 ◽  
Author(s):  
Gordon C. Douglas ◽  
Twanda L. Thirkill ◽  
Priyadarsini Kumar ◽  
Minerva Loi ◽  
Elizabeth D. Hilborn
Keyword(s):  
Villous Trophoblast ◽  
Differentiationin Vitro

scholarly journals Gestational trophoblastic neoplasia: Retrospective analysis of clinical profile, treatment pattern and outcome

2016 ◽  
Author(s):  
Paramjeet Kaur ◽  
Ashok K. Chauhan ◽  
Anil Khurana ◽  
Yashpal Verma ◽  
Nupur Bansal
Keyword(s):  
High Risk ◽  
Risk Group ◽  
Hydatidiform Mole ◽  
Single Agent ◽  
High Risk Group ◽  
Treatment Pattern ◽  
Gestational Trophoblastic Neoplasia ◽  
Trophoblastic Tumor ◽  
Villous Trophoblast ◽  
Invasive Mole

Background: Gestational trophoblastic disease is a spectrum of cellular proliferation arising from the placental villous trophoblast. Gestational triphoblastic neoplasia (GTN) is a collective term for GTD that invade locally or metastasize. GTD includes hydatidiform mole (complete and partial) and GTN include invasive mole, choricocarcinoma, placental site trophoblastic tumor and epitheliod trophoblastic tumor. Aim: To evaluate clinicopathological profile, treatment pattern and clinical outcome in patients with gestational trophoblastic neoplasia (GTN). Materials and Methods: Twelve cases of gestational trophoblastic neoplasia treated between 2012 to November 2015 in deptt of Radiotherapy – II, PGIMS, Rohtak were evaluated in this retrospective study. Data was analyzed on the basis of age, histopathology, stage, type of treatment received and treatment related toxicities. Disease free survival was estimated. Results: Out of 12 women 7 (58 %) had hydatidiform mole, 4 (33%) invasive mole and 01 (8%) had choriocarcinoma. All the cases were given chemotherapy. Two patients had low risk disease. Among high risk group seven patients had score of less than 7 and five patients had risk score of 7 or higher. Five patients were given single agent methotrexate, seven patients received multidrug regimens. All patients are on regular follow up. One patient (high risk group) expired as she did not receive treatment. Conclusion: GTN are rare and proliferative disorders with proper diagnosis and treatment most of the cases are amenable to treatment with favorable outcome.

Massive Perivillous Fibrin Deposition and Chronic Histiocytic Intervillositis a Complication of SARS-CoV-2 Infection

2021 ◽  
pp. 109352662110207
Author(s):  
T Marton ◽  
B Hargitai ◽  
K Hunter ◽  
M Pugh ◽  
P Murray
Keyword(s):  
Placental Insufficiency ◽  
Intrauterine Death ◽  
Fibrin Deposition ◽  
Fetal Demise ◽  
Trophoblastic Cells ◽  
Stage Disease ◽  
Villous Trophoblast ◽  
Fetal Movements ◽  
Active Viral Replication ◽  
End Stage

An emerging complication of COVID-19 (SARS-CoV-2) infection is reported. A 23-year-old patient presented with high temperature and reduced fetal movements at 25 + 5/40 weeks of gestation. RT-PCR proved maternal COVID-19 infection. Ultrasound examination confirmed intrauterine death. Placenta histology showed necrosis of the villous trophoblast, associated with Chronic Histiocytic Intervillositis (CHI) and Massive Perivillous Fibrin Deposition (MPFD) with up to 90% - of the intervillous spaces being involved. Immunohistochemistry showed CD68 positive histiocytes in the intervillous spaces and the villous trophoblast was positive for the COVID-19 spike protein. RNA scope signal was indicative of the presence of the viral genome and active viral replication in the villous trophoblastic cells, respectively. MPFD is a gradually developing end-stage disease with various etiology, including autoimmune and alloimmune maternal response to antigens expressed at the feto-maternal interface and frequently accompanies chronic alloimmune villitis or histiocytic intervillositis. Covid-19 infection is associated with similar pattern of histological changes of the placenta leading to placental insufficiency and fetal death. This case report supports maternal- fetal vertical transmission of SARS-CoV-2 virus leading to placental insufficiency and fetal demise. MPFD and CHI appear to be the typical placental histology for SARS-CoV-2 virus infection associated fetal demise.

scholarly journals Protease Inhibitor Anti-HIV, Lopinavir, Impairs Placental Endocrine Function

2021 ◽  
Vol 22 (2) ◽  
pp. 683
Author(s):  
Camille Fraichard ◽  
Fidéline Bonnet-Serrano ◽  
Christelle Laguillier-Morizot ◽  
Marylise Hebert-Schuster ◽  
René Lai-Kuen ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Metastatic Lymph Node ◽  
Endocrine Function ◽  
Maternal Circulation ◽  
Hormone Production ◽  
Mitofusin 2 ◽  
Villous Trophoblast ◽  
Activating Transcription Factor ◽  
Upr Pathway

Protease Inhibitors (PI e.g., ritonavir (RTV) and lopinavir (LPV)) used to treat pregnant mothers infected by HIV induce prematurity and endocrine dysfunctions. The maintenance of pregnancy relies on placental hormone production (human Chorionic Gonadotrophin (hCG) and progesterone (P4)). Those functions are ensured by the villous trophoblast and are mainly regulated by the Unfolded Protein Response (UPR) pathway and mitochondria. We investigated, in vitro, if PI impair hCG and P4 production and the potential intracellular mechanisms involved. Term villous cytotrophoblast (VCT) were cultured with or without RTV or LPV from 6 to 48 h. VCT differentiation into syncytiotrophoblast (ST) was followed measuring hCG and P4 secretion. We evaluated the expression of P4 synthesis partners (Metastatic Lymph Node 64 (MLN64), cholesterol side-chain cleavage (P450SCC), Hydroxy-delta-5-Steroid Dehydrogenase and 3 Beta-and steroid delta-isomerase 1 (HSD3B1)), of mitochondrial pro-fusion factors (Mitofusin 2 (Mfn2), Optic Atrophy 1 (OPA1)) and of UPR factors (Glucose-Regulated Protein 78 (GRP78), Activating Transcription Factor 4 (ATF4), Activating Transcription Factor 6 (ATF6), spliced X-box Binding Protein 1 (sXBP1)). RTV had no significant effect on hCG and P4 secretion, whereas lopinavir significantly decreased both secretions. LPV also decreased P450SCC and HSD3B1 expression, whereas it increased Mfn2, GRP78 and sXBP1 expression in ST. RTV has no effect on the endocrine placenta. LPV impairs both villous trophoblast differentiation and P4 production. It is likely to act via mitochondrial fusion and UPR pathway activation. These trophoblastic alterations may end in decreased P4 levels in maternal circulation, inducing prematurity.

scholarly journals Effect of retinoids on the morphology of epidermal differentiationin vitro

1983 ◽  
Vol 14 (3) ◽  
pp. 253-254
Author(s):  
Raya Brown ◽  
Robert H. Gray ◽  
I.A. Bernstein
Keyword(s):  
Differentiationin Vitro

scholarly journals IMMUNOFLUORESCENT EXAMINATION OF THE HUMAN CHORIONIC VILLUS FOR BLOOD GROUP A AND B SUBSTANCE

1965 ◽  
Vol 121 (6) ◽  
pp. 1039-1050 ◽  
Author(s):  
H. A. Thiede ◽  
J. W. Choate ◽  
H. H. Gardner ◽  
H. Santay
Keyword(s):  
Blood Group ◽  
Chorionic Villus ◽  
Chorionic Villi ◽  
Specific Fluorescence ◽  
Blood Group A ◽  
Villous Trophoblast ◽  
Group Substance ◽  
If Technique ◽  
Group A ◽  
B Blood Group

The chorionic villi of term placentas were examined for A and B blood group substance using the IF technique with heterologous and homologous antisera. No specific fluorescence was found in either the villous trophoblast or vessels of the chorionic villi. The implications of these findings in relation to the question of trophoblastic antigenicity are discussed.

scholarly journals Mechanism of LIN28B in Trophoblastic Villous Cells of Unexplained Recurrent Abortion

2021 ◽  
Author(s):  
QiaoYao Huang ◽  
YanRu Niu ◽  
LiJun Song ◽  
JinZhi Huang ◽  
Chenxi Wang ◽  
...  
Keyword(s):  
Negative Control ◽  
Cellular Level ◽  
Cellular Migration ◽  
Migration And Invasion ◽  
Invasion And Migration ◽  
Akt Phosphorylation ◽  
Real Time Quantitative Pcr ◽  
Villous Trophoblast

Abstract Background: LIN28B plays an important role in early embryonic development, but its role in villous trophoblast implantation and differentiation remains unknown. To verify the role of LIN28B in trophoblastic villous tissue and cells from women with URSA(unexplained recurrent spontaneous abortion)and artificial termination of pregnancy (negative control, NC). Methods:The Lin28b gene and its protein expression level were detected with real-time quantitative PCR, Western immunoblotting analysis, and immunocytochemistry. The gene was also overexpressed in chorionic villous cell lines (HTR-8/SVneo and BeWo) to examine its effect on trophoblast function.Results: The expression of LIN28B mRNA and protein of URSA villi was lower than that in the NC group. At the cellular level, overexpression of LIN28B enhanced cellular migration, and invasion, and inhibited apoptosis. LIN28B may inhibit apoptosis by promoting Akt phosphorylation and by inhibiting Bad phosphorylation and Bcl-2 expression. In addition, LIN28B inhibited cell fusion and reduced cellular syncytia. Conclusions: LIN28B can inhibit cell proliferation, invasion and migration in vitro, and promote apoptosis and fusion. The low expression of LIN28B in URSA villous trophoblast cells may be one of the causes of abortion. The role of LIN28B in villous trophoblasts needs further study.

scholarly journals Does LIN28B gene dysregulation make women more likely to abort?

2021 ◽  
Author(s):  
QiaoYao Huang ◽  
YanRu Niu ◽  
LiJun Song ◽  
JinZhi Huang ◽  
Chenxi Wang ◽  
...  
Keyword(s):  
Negative Control ◽  
Cellular Level ◽  
Cellular Migration ◽  
Migration And Invasion ◽  
Invasion And Migration ◽  
Akt Phosphorylation ◽  
Real Time Quantitative Pcr ◽  
Villous Trophoblast

Background: LIN28B plays an important role in early embryonic development, but its role in villous trophoblast implantation and differentiation remains unknown. To verify the role of LIN28B in trophoblastic villous tissue and cells from women with URSA(unexplained recurrent spontaneous abortion)and artificial termination of pregnancy (negative control, NC). Methods:The Lin28b gene and its protein expression level were detected with real-time quantitative PCR, Western immunoblotting analysis, and immunocytochemistry. The gene was also overexpressed in chorionic villous cell lines (HTR-8/SVneo and BeWo) to examine its effect on trophoblast function. Results: The expression of LIN28B mRNA and protein of URSA villi was lower than that in the NC group. At the cellular level, overexpression of LIN28B enhanced cellular migration, and invasion, and inhibited apoptosis. LIN28B may inhibit apoptosis by promoting Akt phosphorylation and by inhibiting Bad phosphorylation and Bcl-2 expression. In addition, LIN28B inhibited cell fusion and reduced cellular syncytia. Conclusions: LIN28B can inhibit cell invasion and migration in vitro, and promote apoptosis and fusion. The low expression of LIN28B in URSA villous trophoblast cells may be one of the causes of abortion. The role of LIN28B in villous trophoblasts needs further study.

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