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Welcome to The Visible Embryo, a comprehensive educational resource on human development from conception to birth.

The Visible Embryo provides visual references for changes in fetal development throughout pregnancy and can be navigated via fetal development or maternal changes.

The National Institutes of Child Health and Human Development awarded Phase I and Phase II Small Business Innovative Research Grants to develop The Visible Embryo. Initally designed to evaluate the internet as a teaching tool for first year medical students, The Visible Embryo is linked to over 600 educational institutions and is viewed by more than one million visitors each month.

Today, The Visible Embryo is linked to over 600 educational institutions and is viewed by more than 1 million visitors each month. The field of early embryology has grown to include the identification of the stem cell as not only critical to organogenesis in the embryo, but equally critical to organ function and repair in the adult human. The identification and understanding of genetic malfunction, inflammatory responses, and the progression in chronic disease, begins with a grounding in primary cellular and systemic functions manifested in the study of the early embryo.

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Pregnancy Timeline by SemestersFetal liver is producing blood cellsHead may position into pelvisBrain convolutions beginFull TermWhite fat begins to be madeWhite fat begins to be madeHead may position into pelvisImmune system beginningImmune system beginningPeriod of rapid brain growthBrain convolutions beginLungs begin to produce surfactantSensory brain waves begin to activateSensory brain waves begin to activateInner Ear Bones HardenBone marrow starts making blood cellsBone marrow starts making blood cellsBrown fat surrounds lymphatic systemFetal sexual organs visibleFinger and toe prints appearFinger and toe prints appearHeartbeat can be detectedHeartbeat can be detectedBasic Brain Structure in PlaceThe Appearance of SomitesFirst Detectable Brain WavesA Four Chambered HeartBeginning Cerebral HemispheresFemale Reproductive SystemEnd of Embryonic PeriodEnd of Embryonic PeriodFirst Thin Layer of Skin AppearsThird TrimesterSecond TrimesterFirst TrimesterFertilizationDevelopmental Timeline
CLICK ON weeks 0 - 40 and follow along every 2 weeks of fetal development
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Home | Pregnancy Timeline | News Alerts |News Archive Nov 28, 2013

 

In mice, when c-Met signaling stopped, fetal growth slowed, the liver
did not develop fully and it produced fewer blood cells, and the fetus died.

Image Credit: Mikkola lab/University of California Los Angeles







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What causes pregnancy complications

Researchers at the University of California Los Angeles, have identified a specific type of cell and a related cell communication pathway key to the successful growth of a healthy placenta. The findings could greatly bolster our knowledge about the potential causes of complications during pregnancy.

Specifically, the findings could help scientists clarify the particular order in which progenitor cells grow in the placenta, which would allow researchers to track fetal development and identify complications. Progenitor cells are cells that develop into other cells and that initiate growth of the placenta.

The study was led by Dr. Hanna Mikkola, associate professor of molecular, cell, and developmental biology, at UCLA's Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research, and Dr. Masaya Ueno, a UCLA postdoctoral fellow. It is published online by the scientific journal Developmental Cell on Nov. 25 and will appear later in the journal's print edition.


The placenta is the organ that forms inside the uterus during pregnancy and enables oxygen and nutrients to reach the fetus, but little is understood about the biological mechanisms and cellular processes responsible for this interface.


Studying mouse models, Mikkola and her colleagues tracked individual cells in the placenta to determine which cells and which cell communication routes, or signaling pathways, were responsible for the healthy development of the placenta.


The UCLA team was the first to identify the cells that form the placenta: Epcamhi labyrinth trophoblast progenitors, or LaTP cells, can become the various cells necessary to form a specific tissue, in this case the placenta.

Mikkola and her colleagues also found a signaling pathway that consists of hepatocyte growth factor and its receptor, c-Met. The researchers found that this signaling pathway was required for the placenta to keep making LaTP cells.


Production of LaTP cells, in turn, continues the production of the different cells needed to maintain the growth and health of the placenta while the fetus is growing. Placental health enables healthy transmission of oxygen and nutrients through the exchange of blood between the fetus and the mother.


In mice, when c-Met signaling stopped, fetal growth slowed, the liver did not develop fully and it produced fewer blood cells, and the fetus died.


"Identifying this novel c-Met–dependent multipotent labyrinth trophoblast progenitor is a landmark that may help us understand pregnancy complications that are caused by defective placental exchange, such as fetal growth restriction," Mikkola added.

Abstract Highlights
• Epcamhi cells are multipotent labyrinth trophoblast progenitor (LaTP) cells• c-Met signaling sustains proliferation of LaTP in midgestation placenta• c-Met regulates terminal differentiation and polarization of syncytiotrophoblasts• Loss of c-Met in trophoblasts compromises fetal growth and development

Summary
The placenta provides the interface for gas and nutrient exchange between the mother and the fetus. Despite its critical function in sustaining pregnancy, the stem/progenitor cell hierarchy and molecular mechanisms responsible for the development of the placental exchange interface are poorly understood. We identified an Epcamhi labyrinth trophoblast progenitor (LaTP) in mouse placenta that at a clonal level generates all labyrinth trophoblast subtypes, syncytiotrophoblasts I and II, and sinusoidal trophoblast giant cells. Moreover, we discovered that hepatocyte growth factor/c-Met signaling is required for sustaining proliferation of LaTP during midgestation. Loss of trophoblast c-Met also disrupted terminal differentiation and polarization of syncytiotrophoblasts, leading to intrauterine fetal growth restriction, fetal liver hypocellularity, and demise. Identification of this c-Met-dependent multipotent LaTP provides a landmark in the poorly defined placental stem/progenitor cell hierarchy and may help us understand pregnancy complications caused by a defective placental exchange.

Masaya Ueno1, Lydia K. Lee1, Akanksha Chhabra1, Yeon Joo Kim1, Rajkumar Sasidharan1, Ben Van Handel1, Ying Wang5, Masakazu Kamata6, Paniz Kamran3, 7, Konstantina-Ioanna Sereti3, 7, Reza Ardehali3, 7, Meisheng Jiang5 and Hanna K.A. Mikkola1, 2, 3, 4, Go To Corresponding Author,

1 Department of Molecular, Cell and Developmental Biology, University of California, Los Angeles, Los Angeles, CA 90095, USA
2 Department of Microbiology, Immunology and Molecular Genetics, University of California, Los Angeles, Los Angeles, CA 90095, USA
3 Eli and Edythe Broad Center for Regenerative Medicine and Stem Cell Research, University of California, Los Angeles, Los Angeles, CA 90095, USA
4 Jonsson Comprehensive Cancer Center, University of California, Los Angeles, Los Angeles, CA 90095, USA
5 Molecular and Medical Pharmacology, School of Medicine, University of California, Los Angeles, Los Angeles, CA 90095, USA
6 Department of Hematology and Oncology, University of California, Los Angeles, Los Angeles, CA 90095, USA
7 Department of Cardiology, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA 90095, USA

Mikkola's research was supported by the National Institutes of Health, the Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research at UCLA, the Japan Society for the Promotion of Science, the American Association of Obstetricians and Gynecologists, the California Institute of Regenerative Medicine, the Jonsson Comprehensive Cancer Center at UCLA, and the Ruth L. Kirschstein National Research Service Award.

The Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research at UCLA was launched in 2005 with a UCLA commitment of $20 million over five years. A $20 million gift from the Eli and Edythe Broad Foundation in 2007 resulted in the renaming of the center. With more than 200 members, the Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research is committed to a multi-disciplinary, integrated collaboration of scientific, academic and medical disciplines for the purpose of understanding adult and human embryonic stem cells. The center supports innovation, excellence and the highest ethical standards focused on stem cell research with the intent of facilitating basic scientific inquiry directed towards future clinical applications to treat disease. The center is a collaboration of the David Geffen School of Medicine, UCLA's Jonsson Comprehensive Cancer Center, the Henry Samueli School of Engineering and Applied Science and the UCLA College of Letters and Science.