DOCSLIB.ORG

Regulation of Placental Autophagy by the Bcl-2 Family Proteins Myeloid Cell Leukemia Factor 1 (Mcl-1) and Matador/Bcl-2 Related Ovarian Killer (Mtd/Bok)

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Regulation of Placental Autophagy by the Bcl-2 Family Proteins Myeloid Cell Leukemia Factor 1 (Mcl-1) and Matador/Bcl-2 Related Ovarian Killer (Mtd/Bok) Regulation of Placental Autophagy by the Bcl-2 Family Proteins Myeloid Cell Leukemia Factor 1 (Mcl-1) and Matador/Bcl-2 Related Ovarian Killer (Mtd/Bok) by Manpreet Kalkat A thesis submitted in conformity with the requirements for the degree of Master of Science Department of Physiology University of Toronto © Copyright by Manpreet Kalkat, 2010 Regulation of Placental Autophagy by the Bcl-2 Family Proteins Myeloid Cell Leukemia Factor 1 (Mcl-1) and Matador/Bcl-2 Related Ovarian Killer (Mtd/Bok) Manpreet Kalkat Master of Science Department of Physiology University of Toronto 2010 Abstract The process of autophagy is defined as the degradation of cellular cytoplasmic constituents via a lysosomal pathway. Herein I sought to examine the regulation of autophagy in the placental pathologies preeclampsia (PE) and intrauterine growth restriction (IUGR). I hypothesized that the Bcl-2 family proteins Mcl-1L and MtdL regulate placental autophagy and contribute towards dysregulated autophagy in PE. My results demonstrate that Mcl-1L acts to repress autophagy via a Beclin 1 interaction, while MtdL induces autophagy when it interacts with Mcl-1L. My data indicate that while autophagy is elevated in PE, a pathology characterized by oxidative stress, it is decreased in IUGR, a hypoxic pathology. Treatment with sodium nitroprusside to mimic PE caused a decrease in Mcl-1L and an increase in MtdL levels in response to oxidative stress, thereby inducing autophagy. Overall, my data provide insight into the molecular mechanisms contributing to the pathogenesis of preeclampsia. ii Acknowledgments I would like to acknowledge the support my supervisor, Dr. Isabella Caniggia, who has provided me with many valuable lessons that have been instrumental in both my professional and personal growth in this early stage of my scientific career. I would also like to express my gratitude for the guidance, feedback and support provided to me by the members of my student supervisory committee: Dr. Mingyao Liu, Dr. Jim Woodgett and Dr. Stephen Lye. I'd like to extend my heartfelt thanks to all the members of the Caniggia Lab and the other labs of the sixth floor of TCP for their encouragement and moral support throughout the ups and downs of research. In particular, I would like to thank Julia Garcia for her scientific feedback, suggestions and excellent advice. I'd also like to thank Livia Deda, Tharini Sivasubramaniyam, Antonella Racano and Jocelyn Ray for their consistent scientific and emotional support, and importantly, for all the of the laughter and humour they have all brought to the lab every day. Finally, I'd like to thank my family, who have not seen much of me in the last two years (for which I apologize) but without whom I would not have had the luxury to explore my intellectual pursuits. iii Contributions I would like to acknowledge the contributions of the following people in the generation of the data described in this thesis: Julia Garcia, for the generation of the HEK293-GFP and HEK293-GFPMtdL stably transfected cell lines and for the construction of the FlagMtdL, Mcl-1L and RFP-Mcl-1L vectors. Doug Holmyard, for processing of placental tissue and HEK293 stably transfected cell lines for electron microscopy. Mount Sinai Hospital Biobank (Toronto, Canada) and Dr. Tulia Todros (University of Turin, Italy) for supplying human placental tissue for immunoblot analysis and immunofluorescence staining. iv Table of Contents Acknowledgments .......................................................................................................................... iii Table of Contents ............................................................................................................................ v List of Figures ................................................................................................................................. x Chapter 1 ......................................................................................................................................... 1 1 Introduction ................................................................................................................................ 1 1.1 The Placenta ........................................................................................................................ 1 1.1.1 Early Placental Development .................................................................................. 1 1.1.2 Development of the Villous Structure .................................................................... 4 1.1.3 Onset of placental perfusion and oxidative stress ................................................... 8 1.1.4 Preeclampsia ........................................................................................................... 8 1.1.5 Cell Death and Placentation .................................................................................... 9 1.1.6 Intrauterine growth restriction (IUGR) ................................................................. 10 1.2 Autophagy ......................................................................................................................... 11 1.2.1 Autophagic Induction ............................................................................................ 12 1.2.2 Autophagic Nucleation and Expansion ................................................................. 17 1.2.3 Autophagosome Fusion ........................................................................................ 19 1.2.4 Mitophagy ............................................................................................................. 21 1.3 Bcl-2 family members ....................................................................................................... 21 1.3.1 Bcl-2 family regulation of apoptosis ..................................................................... 21 1.3.2 Bcl-2 Proteins and Mitochondrial Morphogenesis ............................................... 25 1.3.3 Bcl-2 proteins and non-apoptotic cell death ......................................................... 25 1.3.4 Bcl-2 family members and autophagy .................................................................. 26 1.3.5 Bcl-2 family proteins and the placenta ................................................................. 27 1.4 Myeloid Cell Leukemia Factor 1 ...................................................................................... 28 v 1.5 Matador/Bcl-2 related ovarian killer (Mtd/Bok) ............................................................... 30 1.6 Human Placenta and Mtd/Mcl-1 ....................................................................................... 32 1.7 Rationale and Hypothesis ................................................................................................. 33 Chapter 2 ....................................................................................................................................... 34 2 Materials and Methods ............................................................................................................. 34 2.1 In Vitro Studies ................................................................................................................. 34 2.1.1 Cell Culture ........................................................................................................... 34 2.1.2 Protein Extraction ................................................................................................. 35 2.1.3 Bradford Protein Assay ......................................................................................... 35 2.1.4 Western Blot Analysis .......................................................................................... 35 2.1.5 Immunoprecipitation studies ................................................................................. 36 2.1.6 Immunofluorescence staining ............................................................................... 37 2.1.7 Electron Microscopy ............................................................................................. 39 2.1.8 Transient Transfection Experiments ..................................................................... 39 2.1.9 SNP Treatment ...................................................................................................... 40 2.1.10 Etoposide Treatment ............................................................................................. 41 2.1.11 Rapamycin Treatment ........................................................................................... 41 2.1.12 Glucose Starvation ................................................................................................ 41 2.1.13 Oxygen Experiments ............................................................................................. 41 2.2 Human Placental Tissue Experiments .............................................................................. 42 2.2.1 Collection and Sampling ....................................................................................... 42 2.2.2 Protein Extraction ................................................................................................. 44 2.2.3 Western Blotting ................................................................................................... 44 2.2.4 Immunofluorescence Staining .............................................................................. 45 2.2.5 Electron Micrographs ............................................................................................ 46 2.3
Load more

Recommended publications
  • Placental Site Nodule (PSN): an Uncommon Diagnosis with a Common Presentation
    ISSN: 2377-9004 Sneha and Ramesh Kumar. Obstet Gynecol Cases Rev 2021, 8:199 DOI: 10.23937/2377-9004/1410199 Volume 8 | Issue 2 Obstetrics and Open Access Gynaecology Cases - Reviews CASE REPORT Placental Site Nodule (PSN): An Uncommon Diagnosis with a Common Presentation 1* 2 Check for Sneha GS and Ramesh Kumar R updates 1Assistant Professor, Department of Obstetrics and Gynaecology, SDM Medical College and Hospital, SDM University, Karnataka, India 2Professor, Department of Obstetrics and Gynaecology, SDM Medical College and Hospital, SDM University, Karnataka, India *Corresponding author: DR. Sneha GS, Assistant Professor, Department of Obstetrics and Gynaecology, SDM Medical College and Hospital, SDM University, 580009, Dharwad, Karnataka, India ferentiated from aggressive lesions of intermediate tro- Abstract phoblast like placental site trophoblastic tumor and epi- Placental site nodule is an uncommon, benign, generally thelioid trophoblastic tumor and from nontrophoblastic asymptomatic lesion of trophoblastic origin, which may of- ten be detected several months to years after the tenancy diseases like squamous cell carcinoma [1,4]. from which it resulted. PSN usually presents as menorrha- gia, intermenstrual bleeding or an abnormal pap smear. Case Report PSN is benign, but it is important to distinguish it from the A 29-yrs-old female patient para 3, living 3, abor- other benign and malignant lesions like decidua, placental polyp, exaggerated placental site and placental site tropho- tion 5, underwent laprotomy and tubectomy 2 yrs back blastic tumor and squamous cell carcinoma. Follow ups of presented with history of irregular menstrual cycles typical PSNs do not show recurrence or malignant potential. with menorrhagia since 6 months preceded by normal PSN is an uncommon condition which should be suspected cycles.
    [Show full text]
  • Implantation Site Intermediate Trophoblasts in Placenta Cretas
    Modern Pathology (2004) 17, 1483–1490 & 2004 USCAP, Inc All rights reserved 0893-3952/04 $30.00 www.modernpathology.org Implantation site intermediate trophoblasts in placenta cretas Kyu-Rae Kim1, Sun-Young Jun1, Ji-Young Kim2 and Jae Y Ro1 1Department of Pathology, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea and 2Department of Pathology, Cha General Hospital, College of Medicine Pochun Cha University, Seoul, Korea Placenta cretas are defined as abnormal adherences or ingrowths of placental tissue, but their pathogenetic mechanism has not been fully explained. During histologic examination of postpartum uteri, we noticed that the number of implantation site intermediate trophoblasts was increased in the placental bed of placenta cretas. To validate our observation and to address the pathogenetic role of implantation site intermediate trophoblasts in placenta cretas, we examined postpartum uteri with placenta cretas (n ¼ 34) and noncretas (n ¼ 22), obtained from Cesarean or immediate postpartum hysterectomy specimens. Using antibody to CD146, a marker for implantation site intermediate trophoblasts, we found that placenta cretas had significantly thicker layer of implantation site intermediate trophoblasts (230071200 lm) than noncretas (150071200 lm, Po0.025). We also observed that the confluent distribution of cells was more frequent in placenta cretas (97%) than noncretas samples (45%, Po0.001), and that the total number of implantation site intermediate trophoblasts within the superficial myometrium of the placental bed was significantly higher in placenta cretas than noncretas. Using antibodies to Ki-67, Bcl-2 and cleaved caspase-3 to determine the proliferative index and apoptotic rates of implantation site intermediate trophoblasts, we found that they were close to zero in both groups and did not differ significantly.
    [Show full text]
  • From Trophoblast to Human Placenta
    From Trophoblast to Human Placenta (from The Encyclopedia of Reproduction) Harvey J. Kliman, M.D., Ph.D. Yale University School of Medicine I. Introduction II. Formation of the placenta III. Structure and function of the placenta IV. Complications of pregnancy related to trophoblasts and the placenta Glossary amnion the inner layer of the external membranes in direct contact with the amnionic fluid. chorion the outer layer of the external membranes composed of trophoblasts and extracellular matrix in direct contact with the uterus. chorionic plate the connective tissue that separates the amnionic fluid from the maternal blood on the fetal surface of the placenta. chorionic villous the final ramification of the fetal circulation within the placenta. cytotrophoblast a mononuclear cell which is the precursor cell of all other trophoblasts. decidua the transformed endometrium of pregnancy intervillous space the space in between the chorionic villi where the maternal blood circulates within the placenta invasive trophoblast the population of trophoblasts that leave the placenta, infiltrates the endo– and myometrium and penetrates the maternal spiral arteries, transforming them into low capacitance blood channels. Sunday, October 29, 2006 Page 1 of 19 From Trophoblasts to Human Placenta Harvey Kliman junctional trophoblast the specialized trophoblast that keep the placenta and external membranes attached to the uterus. spiral arteries the maternal arteries that travel through the myo– and endometrium which deliver blood to the placenta. syncytiotrophoblast the multinucleated trophoblast that forms the outer layer of the chorionic villi responsible for nutrient exchange and hormone production. I. Introduction The precursor cells of the human placenta—the trophoblasts—first appear four days after fertilization as the outer layer of cells of the blastocyst.
    [Show full text]
  • Gestational Trophoblastic Disease: a Histopatholgical Romp Through
    Problematic Pathologies of Neoplastic Placentation Matthew Cesari, MD, CM, FRCPC Gynecologic Pathologist, Sunnybrook Health Sciences Centre Assistant Professor, University of Toronto March 13, 2016 OBJECTIVES • To describe key concepts in placentation; • To relate these concepts to the classification of non-molar gestational trophoblastic disease; • To develop an approach to the diagnosis of non-molar gestational trophoblastic disease. Basic Concepts in Placentation Fertilization Robboy, 2nd Ed. Basic Concepts in Placentation IMPLANTATION (DAYS 6-11) Fertilization Robboy, 2nd Ed. Basic Concepts in Placentation IMPLANTATION (DAYS 6-11) and NIDATION Fertilization Robboy, 2nd Ed. Cytotrophoblast (trophoblastic stem cell) Proliferation of pre-villous trophoblast: Syncytiotrophoblast (Villous) Intermediate (terminally differentiated) trophoblast Basic Concepts in Placentation IMPLANTATION NIDATION (pre-villous trophoblast) Fertilization MESENCHYMAL VILLOUS FORMATION Courtesy: Dr. K. Grondin Basic Concepts in Placentation FERTILIZATION IMPLANTATION NIDATION (pre-villous trophoblast) MESENCHYMAL VILLOUS FORMATION PRIMARY VILLI CHORION FRONDOSOM CHORION LAEVE (“placental disk”) (“membranes”) IMPLANTATION OXYGENATION (“anchoring”) Basic Concepts in Placentation FERTILIZATION IMPLANTATION NIDATION (pre-villous trophoblast) MESENCHYMAL VILLOUS FORMATION PRIMARY VILLI P L Chorion A frondosum C E Primary villi N Chorion T laeve A VIT Implantation-type intermediate C Villous Intermediate trophoblast Trophoblast Chorionic-type S Intermediate trophoblast
    [Show full text]
  • The Role of Polarity Protein Angiomotin (AMOT) in the Human Placenta
    The Role of Polarity Protein Angiomotin (AMOT) in the Human Placenta by Abby Patricia Farrell A thesis submitted in conformity with the requirements for the degree of Master of Science Institute of Medical Science University of Toronto © Copyright by Abby Farrell 2018 The Role of Polarity Protein Angiomotin (AMOT) in the Human Placenta Abby Patricia Farrell Master of Science Institute of Medical Science University of Toronto 2018 Abstract Angiomotin (AMOT) is a scaffolding protein involved in cell polarity regulation, cell migration and early embryo lineage differentiation, yet its biological significance in the human placenta remains unknown. I hypothesized that AMOT controls trophoblast cell polarity and migration, and is further regulated by transforming growth factor beta (TGF) signalling and upstream oxygen tension. AMOT localization to extravillous trophoblast (EVT) cells, corroborated by AMOT 80 overexpression increasing JEG3 cell migration rate, supports a role for AMOT in EVT migration. TGF1/3 treatment decreased AMOT protein levels and redistributed AMOT from the tight- junction to cytoplasmic F-actin in JEG3 cells. TGF1/3 also prompted a novel association between AMOT 80 and Partitioning Defective Protein-6. Similarly, low oxygen exposure negatively regulated AMOT levels and localization. Furthermore, Jumonji C Domain Containing Protein-6 (JMJD6), an oxygen sensor, was discovered to positively regulate AMOT via lysyl hydroxylation. Finally, AMOT levels were found markedly reduced in preeclampsia, a disease characterized by aberrant TGF signalling and chronic hypoxia. In conclusion, this study reveals AMOT is a mediator of TGF and oxygen signalling to regulate trophoblast migration in the human placenta. ii Table of Contents Table of Contents ........................................................................................................................
    [Show full text]
  • Placental Pathology
    PLACENTAL PATHOLOGY Michael K Fritsch MD, PhD This set of lectures is designed to review the gross and histologic criteria used in the diagnosis of common placental pathology. I have included some clinical correlation but have not discussed pathogenesis in detail. At the end of these notes are templates we use at Northwestern University for signing out placentas. I would like to acknowledge Dr. Linda Ernst (Head of the Perinatal Service at Northwestern) for her outstanding knowledge, collegiality and organizational skills and who established the high-quality perinatal service at NU before I arrived. In addition, I am indebted to Dr. Don Singer, who mentored me through innumerable difficult perinatal and placental cases while I was an Assistant Professor at the University of Wisconsin-Madison. NORMAL HISTOLOGY REVIEW: 1) Membranes: The amnion lines the amniotic sac containing the fetus. The amnion consists of a single layer of cuboidal epithelium, its basement membrane, and a collagen layer. The chorion lies deep to the amnion and consists of a sparsely cellular collagen layer. The chorion rests on a layer of intermediate trophoblast cells (clear to eosinophilic cytoplasm). Amnion, chorion, and intermediate trophoblast cells are fetal in origin. Deep to the intermediate trophoblast layer is the decidual layer (maternal in origin). This layer contains decidualized maternal cells, vessels, fibrin, and often some degree of hemorrhage. 2) Umbilical cord: The outer surface of the umbilical cord is covered by a single layer of cuboidal amniotic epithelium. There is often focal squamous metaplasia. Normally, 3 vessels (2 arteries and 1 vein) are embedded in a myxoid paucicellular matrix (Wharton's jelly).
    [Show full text]
  • Exaggerated Placental Site Tumour
    International Journal of Reproduction, Contraception, Obstetrics and Gynecology Jayakrishnan N et al. Int J Reprod Contracept Obstet Gynecol. 2016 Jul;5(7):2425-2427 www.ijrcog.org pISSN 2320-1770 | eISSN 2320-1789 DOI: http://dx.doi.org/10.18203/2320-1770.ijrcog20162140 Case Report A placental dilemma: exaggerated placental site tumour Niranjana Jayakrishnan*, Krishnapillai Jayakrishnan Department of Obstetrics and Gynaecology, KJK hospital, Shawallace Lane, Nalanchira ,Trivandrum, Kerala, India Received: 25 April 2016 Revised: 08 June 2016 Accepted: 09 June 2016 *Correspondence: Dr. Niranjana Jayakrishnan, E-mail: [email protected] Copyright: © the author(s), publisher and licensee Medip Academy. This is an open-access article distributed under the terms of the Creative Commons Attribution Non-Commercial License, which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. ABSTRACT Exaggerated placental site is defined as a non-neoplastic lesion characterized with infiltration of extravilleous intermediate trophoblasts into the myometrium and the walls of blood vessels of the normal placental implantation area. They are commonly seen following spontaneous or elective abortions and present rarely as a cause of third stage bleeding or post-partum hemorrhage. A case of an exaggerated placental site is presented in this article. It is aimed to review the current information about this rare condition. We encountered a case of exaggerated placental site (EPS) reaction following evacuation of a missed abortion in a 34 year old lady. She presented to us, with bleeding per vaginum, not responding to medical management. Hysteroscopy was done and a fleshy mass noted in the posterior wall was resected and sent for examination.
    [Show full text]
  • Exaggerated Placental Site Reaction: Case Report of a Rare Benign Trophoblastic Lesion
    International Journal of Reproduction, Contraception, Obstetrics and Gynecology Shetty A et al. Int J Reprod Contracept Obstet Gynecol. 2015 Oct;4(5):1647-1649 www.ijrcog.org pISSN 2320-1770 | eISSN 2320-1789 DOI: http://dx.doi.org/10.18203/2320-1770.ijrcog20150771 Case Report Exaggerated placental site reaction: case report of a rare benign trophoblastic lesion Archana Shetty, Aparna Narasimha*, Jyalakshmi V. J. Department of Pathology, Sapthagiri Institute of Medical Sciences and Research Centre, Bangalore, India Received: 17 August 2015 Accepted: 03 September 2015 *Correspondence: Dr. Aparna Narasimha, E-mail: [email protected] Copyright: © the author(s), publisher and licensee Medip Academy. This is an open-access article distributed under the terms of the Creative Commons Attribution Non-Commercial License, which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. ABSTRACT Exaggerated placental site is a rare benign non-neoplastic trophoblastic lesion in which the intermediate trophoblastic cells extensively infiltrate into the endometrium and the underlying myometrium. The importance of this lesion lies in that the cells of this lesion display an identical morphological and immunophenotypic profile to the intermediate trophoblastic cells found placental site trophoblastic tumour, which are closely related neoplastic lesions Also differentials for this lesion are placental site nodule, choriocarcinoma and epithelioid trophoblastic tumour all of which have varied lines of treatment and interventions. We present a rare case of an exaggerated placental site reaction in a lady, who was in her first trimester of pregnancy and presented with signs of a septic abortion. Keywords: Exaggerated placental site, intermediate trophoblast, Myometrium, Placental site nodule, Ki- 67 INTRODUCTION a heart rate of 110 beats per minute.
    [Show full text]
  • Pregnancy, Abortion, and Ectopic Pregnancy
    3 Pregnancy, Abortion, and Ectopic Pregnancy Endometrial Glands and Stroma in pathologic states such as abnormal bleeding or Pregnancy . 35 chronic endometritis. Early Gestational Endometrium (1 to 3 An abortion before the 16th week of preg- Weeks Postfertilization) . 35 nancy is the usual source of endometrial tissue Endometrium in Later Pregnancy (4 or specimens that show apparent gestational More Weeks Postfertilization) . 37 changes. The different types of abortions are Arias-Stella Reaction . 39 defined as follows.“Spontaneous abortions” are Other Glandular Changes in unexpected and unplanned interruptions of Pregnancy . 41 pregnancy that present with bleeding and Trophoblast and Villi . 43 passage of tissue. Approximately 15% to 20% Trophoblastic Cells . 44 Immunohistochemistry of Trophoblastic of early pregnancies end in a spontaneous abor- 1–4 Cells . 46 tion. In addition, many other early pregnan- Placental Implantation Site . 48 cies spontaneously abort before pregnancy is Exaggerated Placental Implantation recognized by the woman and are occult.5;6 Most Site . 53 spontaneous abortions occur before 12 weeks of Placental Site Nodules . 54 pregnancy, and at least half of these are attrib- Chorionic Villi and Villous Trophoblast utable to a genetic (karyotypic) anomaly. An in the First Trimester . 57 “incomplete abortion” is a spontaneous abor- Hydropic Change and Other tion in which the conceptus and decidua are Pathologic Changes in Abortions . 58 incompletely passed, thus requiring curettage. Chorionic Villi and Villous Trophoblast A “missed abortion” refers to an abortion with After the First Trimester . 59 Placental Polyps . 61 retained products of conception but no abnor- Placenta Accreta . 62 mal bleeding for 5 to 8 weeks after death of the Endometrium Associated with Ectopic embryo or fetus.
    [Show full text]
  • Trophoblastic Vasculogenic Mimicry in Gestational Choriocarcinoma
    Modern Pathology (2011) 24, 646–652 646 & 2011 USCAP, Inc. All rights reserved 0893-3952/11 $32.00 Trophoblastic vasculogenic mimicry in gestational choriocarcinoma Ie-Ming Shih Departments of Pathology, Oncology and Gynecology and Obstetrics, Johns Hopkins Medical Institutions, Baltimore, MD, USA Angiogenesis is a characteristic feature of solid tumors, which depend on the newly formed vasculature to prevent hypoxia and to sustain uncontrolled tumor cell proliferation. In this study, we investigated the blood supply system in 10 gestational choriocarcinomas on the basis of histopathological and immunohistochemical features. In all examined cases, morphological analysis demonstrated that blood channels within the center of choriocarcinomas were surrounded by neoplastic trophoblastic cells rather than by endothelial cells. Similarly, there was a lack of CD31 and CD34-positive endothelial cells within choriocarcinomas. In the periphery of choriocarcinomas, tumor cells invaded uterine stroma-derived blood vessels where trophoblastic cells replaced endothelial cells, forming anastomoses between endothelium-lined blood vessels and trophoblast- lined pseudovascular channels. Masson’s trichrome staining revealed minimal amounts of connective tissue within choriocarcinomas. In contrast, CD31 and CD34-positive blood vessels were present in other types of gestational trophoblastic neoplasms including 8 placental site trophoblastic tumors and 12 epithelioid trophoblastic tumors. These findings provide cogent evidence that choriocarcinoma represents
    [Show full text]
  • A Tumor-Like Trophoblastic Lesion (Placental Site Nodule)
    Cumhuriyet Tıp Dergisi Cumhuriyet Tıp Derg 2012; 34: 210-214 Cumhuriyet Medical Journal Cumhuriyet Med J 2012; 34: 210-214 Case report-Olgu sunumu http://dx.doi.org/10.7197/1305-0028.889 A tumor-like trophoblastic lesion (placental site nodule) Tümör benzeri bir trofoblastik lezyon (plasental site nodül) Nilsen Yıldırım Erdoğan*, Mustafa Kara Department of Pathology (Assist. Prof. N. Y. Erdoğan, MD), Department of Obstetrics and Gynecology (Assist. Prof. M. Kara, MD), Bozok University School of Medicine, TR-66200 Yozgat Abstract Placental site nodule, developing from intermediate trophoblasts, is a rare benign lesion. Although it is a benign lesion, it is histopathological differential diagnosis from placental site trophoblastic tumor and epithelioid trophoblastic tumor which are aggressive lesions of the intermediate trophoblasts, and non-trophoblastic neoplasms such as squamous cell carcinoma, is important due to its histological appearance. In our report, placental site nodule diagnosed in 33-year-old, female patient who was suffering from intermittant menometrorrhagia and had a diagnostic curettage is presented. Keywords: Placental site nodule, intermediate trophoblasts, abnormal uterine bleeding Özet Plasental bölge nodülü intermediate trofoblastlardan gelişen nadir görülen benign bir lezyondur. Benign bir lezyon olmasına rağmen histolojik görünümü nedeniyle intermediate trofoblastların agresif lezyonları olan plasental bölge neoplastik tümörü ve epiteloid trofoblastik tümör ile skuamoz hücreli karsinom gibi trofoblastik olmayan neoplazilerden histopatolojik ayrımı önemlidir.Bu makalede intermitan menometroraji şikayeti ile başvurup tanısal küretaj yapılan ve plasental bölge nodülü tanısı alan 33 yaşında bir bayan hasta sunulmuştur. Anahtar sözcükler: Plasental bölge nodülü, intermediate trofoblastlar, anormal uterin kanama Geliş tarihi/Received: May 18, 2011; Kabul tarihi/Accepted: January 01, 2012 *Corresponding author: Dr.
    [Show full text]
  • The Actions of Fibroblast Growth Factors During Peri- Implantation Conceptus Development in Cattle
    THE ACTIONS OF FIBROBLAST GROWTH FACTORS DURING PERI- IMPLANTATION CONCEPTUS DEVELOPMENT IN CATTLE By QIEN YANG A DISSERTATION PRESENTED TO THE GRADUATE SCHOOL OF THE UNIVERSITY OF FLORIDA IN PARTIAL FULFILLMENT OF THE REQUIREMENTS FOR THE DEGREE OF DOCTOR OF PHILOSOPHY UNIVERSITY OF FLORIDA 2010 1 © 2010 Qien Yang 2 To my parents, sister and wife 3 ACKNOWLEDGMENTS This dissertation would not have been possible without the expert guidance of my advisor Dr. Alan Ealy. I remember how great I felt when he accepted me as a PhD student in this lab even I knew nothing about molecular regulation of Interferon tau. He always has great patience, encourages me to try different ideas when there is a chance of failure, he always cares about his students and does his best to help us succeed. His guidance has been an invaluable experience and will be greatly appreciated throughout my scientific career. I still feel great to be his student and work in this fun lab. I would like to express my deep appreciation to all my committee members for their willingness to serve on the committee. Dr. Sally Johnson has been my second advisor and treated me as her own student. Her invaluable input and direction throughout my graduate career set the standard for me. Dr. Peter Hansen has allowed me to use his lab and learn embryo techniques; one chapter of this dissertation would not have been finished without the IVF system in his lab. Dr. Naohiro Terada’s expertise in embryonic stem cell biology has been an excellent source for me in the last 4 and half years.
    [Show full text]