Journal articles: 'Cellule Fetali'

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Bozzato, Gianni. "Quando inizia ad esistere l’individuo umano?" Medicina e Morale 48, no. 1 (February 28, 1999): 77–93. http://dx.doi.org/10.4081/mem.1999.811.

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Nel saggio sono posti in rilievo i seguenti principali aspetti di ordine biologico che contrastano con le argomentazioni sostenute da N. M. Ford nel suo libro When did I begin? 1) Nel cosiddetto pre-embrione, le cellule non sono totipotenti. (Ossia, non sono in grado di esprimere la totipotenza residua nucleare e cioè produrre altrettanti pre-embrioni. Nel presente articolo l’analisi della questione riguardante la totipotenza del pre-embrione, delle sue cellule o del loro nucleo viene soltanto appena accennata). La possibilità che il pre-embrione (individuo originario) dia origine a più gemelli monozigoti c. d. “identici” non è la conseguenza della totipotenza delle cellule, ma del loro distacco fisico dal pre-embrione, oppure della loro semplice “separazione/isolamento” dal suo schema di organizzazione dell’espressione genica del DNA (schema di OEG-DNA). 2) Le cellule del pre-embrione, inoltre, sono “identiche e indiscernibili” soltanto dal punto di vista genetico (genotipico), ma non da quello biologico (fenotipico). Anche dal punto di vista biologico (v. schema di OEG-DNA) il pre-embrione non è un semplice aggregato di cellule individuali, ma è una unità integrata e cioè un sistema individuale di cellule che possiede già una sua identità biologica, dunque ontologica. 3) Durante lo sviluppo, le cosiddette fasi (o stadi) e le forme anatomiche dell’embrione sono sempre precedute e prodotte da forme temporali (schemi di processi biochimici). Pertanto, sempre dal punto di vista dell’identità biologica (e ontologica), lo zigote (o il pre-embrione), anche nel caso di successiva gemellazione, è già un individuo umano in sviluppo (in atto) molto tempo prima che “appaia” - all’osservatore - un indizio “visibile” della sua forma anatomica individuale; dunque, ancor prima della “comparsa” della stria primitiva. 4) Proprio per il fatto che l’identità biologica dell’individuo umano non corrisponde alla sua identità genetica (ovvero il genotipo non è il fenotipo), i gemelli c. d. “identici” non sono mai veramente identici tra loro; essi sono sempre diversi fin dall’inizio del loro sviluppo, il quale avviene per biforcazione (una rottura di simmetria) dello schema di OEG-DNA dell’individuo pre-embrione originario. Lo studio della conformazione delle loro membrane fetali ci consente, infatti, di dedurre e di affermare che essi sono già in formazione (in atto) molto tempo prima della comparsa della stria primitiva e, in quanto biologicamente diversi, che sono già distinti; dunque, potenzialmente discernibili.

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Jordan, Jeanne A., Dale Huff, and Julie A. DeLoia. "Placental Cellular Immune Response in Women Infected with Human Parvovirus B19 during Pregnancy." Clinical Diagnostic Laboratory Immunology 8, no. 2 (March 1, 2001): 288–92. http://dx.doi.org/10.1128/cdli.8.2.288-292.2001.

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ABSTRACT Human parvovirus B19 can cause congenital infection with variable morbidity and mortality in the fetus and neonate. Although much information exists on the B19-specific antibody response in pregnant women, little information is available describing the cell-mediated immune (CMI) response at the maternal-fetal interface. The focus of this study was to characterize the CMI response within placentas from women who seroconverted to B19 during their pregnancies and compare it to controls. Immunohistochemical techniques were used to identify the various immune cells and the inflammatory cytokine present within placental tissue sections. Group 1 consisted of placentas from 25 women whose pregnancies were complicated by B19 infection; 6 women with good outcome (near-term or term delivery), and 19 with poor outcome (spontaneous abortion, nonimmune hydrops fetalis, or fetal death). Group 2 consisted of placentas from 20 women whose pregnancies were complicated with nonimmune hydrops fetalis of known, noninfectious etiology. Group 3 consisted of placentas from eight women whose pregnancies ended in either term delivery or elective abortion. The results of the study revealed a statistically significant increase in the number of CD3-positive T cells present within placentas from group 1 compared to group 2 or 3 (13.3 versus 2 and 1, respectively) (P < 0.001). In addition, the inflammatory cytokine interleukin 2 was detected in every placenta within group 1 but was absent from all placentas evaluated from groups 2 and 3. Together, these findings demonstrate evidence for an inflammation-mediated cellular immune response within placentas from women whose pregnancies are complicated with B19 infection.

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Jeanty, Cerine, S. Christopher Derderian, and Tippi C. MacKenzie. "Maternal–fetal cellular trafficking." Current Opinion in Pediatrics 26, no. 3 (June 2014): 377–82. http://dx.doi.org/10.1097/mop.0000000000000087.

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Fjeldstad, Heidi ES, Guro M. Johnsen, and Anne Cathrine Staff. "Fetal microchimerism and implications for maternal health." Obstetric Medicine 13, no. 3 (December 6, 2019): 112–19. http://dx.doi.org/10.1177/1753495x19884484.

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This review paper outlines the definition, pathophysiology, and potential maternal health consequences of cellular fetal microchimerism, the maternal acquisition of intact cells of fetal origin during pregnancy. Increased rates and amounts of cellular fetal microchimerism are associated with several placental syndromes, including preeclampsia and fetal growth restriction. The discovery of cellular fetal microchimerism and methods of detection are briefly outlined, and we present the mechanisms hypothesized to govern pregnancy-related and long-term maternal health effects of cellular fetal microchimerism. Specifically, we discuss the potential implications of cellular fetal microchimerism in wound healing, autoimmunity, cancer, and possibly cardiovascular disease. Cellular fetal microchimerism represents a novel area of research on maternal and transgenerational health and disease, providing exciting opportunities for developing new disease biomarkers and precision medicine with targeted prophylaxis against long-term maternal disease.

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Gammill, Hilary S., Tessa M. Aydelotte, Katherine A. Guthrie, Evangelyn C. Nkwopara, and J. Lee Nelson. "Cellular Fetal Microchimerism in Preeclampsia." Hypertension 62, no. 6 (December 2013): 1062–67. http://dx.doi.org/10.1161/hypertensionaha.113.01486.

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Saadai, Payam, Tzong-Hae Lee, Geoanna Bautista, Kelly D. Gonzales, Amar Nijagal, Michael P. Busch, Chong Jai Kim, et al. "Alterations in maternal-fetal cellular trafficking after fetal surgery." Journal of Pediatric Surgery 47, no. 6 (June 2012): 1089–94. http://dx.doi.org/10.1016/j.jpedsurg.2012.03.012.

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Hart, Bethany, Elizabeth Morgan, and Emilyn U. Alejandro. "Nutrient sensor signaling pathways and cellular stress in fetal growth restriction." Journal of Molecular Endocrinology 62, no. 2 (February 2019): R155—R165. http://dx.doi.org/10.1530/jme-18-0059.

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Fetal growth restriction is one of the most common obstetrical complications resulting in significant perinatal morbidity and mortality. The most frequent etiology of human singleton fetal growth restriction is placental insufficiency, which occurs secondary to reduced utero-placental perfusion, abnormal placentation, impaired trophoblast invasion and spiral artery remodeling, resulting in altered nutrient and oxygen transport. Two nutrient-sensing proteins involved in placental development and glucose and amino acid transport are mechanistic target of rapamycin (mTOR) and O-linked N-acetylglucosamine transferase (OGT), which are both regulated by availability of oxygen. Impairment in either of these pathways is associated with fetal growth restriction and accompanied by cellular stress in the forms of hypoxia, oxidative and endoplasmic reticulum (ER) stress, metabolic dysfunction and nutrient starvation in the placenta. Recent evidence has emerged regarding the potential impact of nutrient sensors on fetal stress response, which occurs in a sexual dysmorphic manner, indicating a potential element of genetic gender susceptibility to fetal growth restriction. In this mini review, we focus on the known role of mTOR and OGT in placental development, nutrient regulation and response to cellular stress in human fetal growth restriction with supporting evidence from rodent models.

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Korchynska, N. S., О. М. Slobodian, and V. O. Kostyuk. "FETAL ANATOMY OF THE MAXILLARY CELLULAR PROCESS." Clinical anatomy and operative surgery 18, no. 1 (January 23, 2019): 62–66. http://dx.doi.org/10.24061/1727-0847.18.1.2019.10.

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Nijagal, Amar, and Tippi C. MacKenzie. "Clinical implications of maternal-fetal cellular trafficking." Seminars in Pediatric Surgery 22, no. 1 (February 2013): 62–65. http://dx.doi.org/10.1053/j.sempedsurg.2012.10.011.

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Olney, John. "Fetal alcohol syndrome at the cellular level." Addiction Biology 9, no. 2 (June 2004): 137–49. http://dx.doi.org/10.1080/13556210410001717006.

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Park, Hee Jin, Hee Young Cho, and Dong Hyun Cha. "The Amniotic Fluid Cell-Free Transcriptome Provides Novel Information about Fetal Development and Placental Cellular Dynamics." International Journal of Molecular Sciences 22, no. 5 (March 5, 2021): 2612. http://dx.doi.org/10.3390/ijms22052612.

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The amniotic fluid (AF) is a complex biofluid that reflects fetal well-being during development. AF con be divided into two fractions, the supernatant and amniocytes. The supernatant contains cell-free components, including placenta-derived microparticles, protein, cell-free fetal DNA, and cell-free fetal RNA from the fetus. Cell-free mRNA (cfRNA) analysis holds a special position among high-throughput analyses, such as transcriptomics, proteomics, and metabolomics, owing to its ease of profiling. The AF cell-free transcriptome differs from the amniocyte transcriptome and alters with the progression of pregnancy and is often associated with the development of various organ systems including the fetal lung, skin, brain, pancreas, adrenal gland, gastrointestinal system, etc. The AF cell-free transcriptome is affected not only by normal physiologies, such as fetal sex, gestational age, and fetal maturity, but also by pathologic mechanisms such as maternal obesity, and genetic syndromes (Down, Edward, Turner, etc.), as well as pregnancy complications (preeclampsia, intrauterine growth restriction, preterm birth, etc.). cfRNA in the amniotic fluid originates from the placenta and fetal organs directly contacting the amniotic fluid as well as from the fetal plasma across the placenta. The AF transcriptome may reflect the fetal and placental development and therefore aid in the monitoring of normal and abnormal development.

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Satish, Latha, and Sandeep Kathju. "Cellular and Molecular Characteristics of Scarless versus Fibrotic Wound Healing." Dermatology Research and Practice 2010 (2010): 1–11. http://dx.doi.org/10.1155/2010/790234.

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The purpose of this paper is to compare and contrast the discrete biology differentiating fetal wound repair from its adult counterpart. Integumentary wound healing in mammalian fetuses is essentially different from wound healing in adult skin. Adult (postnatal) skin wound healing is a complex and well-orchestrated process spurred by attendant inflammation that leads to wound closure with scar formation. In contrast, fetal wound repair occurs with minimal inflammation, faster re-epithelialization, and without the accumulation of scar. Although research into scarless healing began decades ago, the critical molecular mechanisms driving the process of regenerative fetal healing remain uncertain. Understanding the molecular and cellular events during regenerative healing may provide clues that one day enable us to modulate adult wound healing and consequently reduce scarring.

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Ribitsch, Iris, Andrea Bileck, Monika Egerbacher, Simone Gabner, Rupert L. Mayer, Lukas Janker, Christopher Gerner, and Florien Jenner. "Fetal Immunomodulatory Environment Following Cartilage Injury—The Key to CARTILAGE Regeneration?" International Journal of Molecular Sciences 22, no. 23 (November 30, 2021): 12969. http://dx.doi.org/10.3390/ijms222312969.

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Fetal cartilage fully regenerates following injury, while in adult mammals cartilage injury leads to osteoarthritis (OA). Thus, in this study, we compared the in vivo injury response of fetal and adult ovine articular cartilage histologically and proteomically to identify key factors of fetal regeneration. In addition, we compared the secretome of fetal ovine mesenchymal stem cells (MSCs) in vitro with injured fetal cartilage to identify potential MSC-derived therapeutic factors. Cartilage injury caused massive cellular changes in the synovial membrane, with macrophages dominating the fetal, and neutrophils the adult, synovial cellular infiltrate. Correspondingly, proteomics revealed differential regulation of pro- and anti-inflammatory mediators and growth-factors between adult and fetal joints. Neutrophil-related proteins and acute phase proteins were the two major upregulated protein groups in adult compared to fetal cartilage following injury. In contrast, several immunomodulating proteins and growth factors were expressed significantly higher in the fetus than the adult. Comparison of the in vitro MSCs proteome with the in vivo fetal regenerative signature revealed shared upregulation of 17 proteins, suggesting their therapeutic potential. Biomimicry of the fetal paracrine signature to reprogram macrophages and modulate inflammation could be an important future research direction for developing novel therapeutics.

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Herbek, Savannah L., Marie C. Smithgall, Elisabeth A. Murphy, Robert E. Schwartz, Shuibing Chen, Laura E. Riley, Heidi Stuhlmann, Yawei J. Yang, and Ria Goswami. "Human Maternal-Fetal Interface Cellular Models to Assess Antiviral Drug Toxicity during Pregnancy." Reproductive Medicine 3, no. 4 (December 1, 2022): 303–19. http://dx.doi.org/10.3390/reprodmed3040024.

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Pregnancy is a period of elevated risk for viral disease severity, resulting in serious health consequences for both the mother and the fetus; yet antiviral drugs lack comprehensive safety and efficacy data for use among pregnant women. In fact, pregnant women are systematically excluded from therapeutic clinical trials to prevent potential fetal harm. Current FDA-recommended reproductive toxicity assessments are studied using small animals which often do not accurately predict the human toxicological profiles of drug candidates. Here, we review the potential of human maternal-fetal interface cellular models in reproductive toxicity assessment of antiviral drugs. We specifically focus on the 2- and 3-dimensional maternal placental models of different gestational stages and those of fetal embryogenesis and organ development. Screening of drug candidates in physiologically relevant human maternal-fetal cellular models will be beneficial to prioritize selection of safe antiviral therapeutics for clinical trials in pregnant women.

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Padron, Justin Gary, Nainoa D. Norman Ing, Po’okela K. Ng, and Claire E. Kendal-Wright. "Stretch Causes Cell Stress and the Downregulation of Nrf2 in Primary Amnion Cells." Biomolecules 12, no. 6 (May 31, 2022): 766. http://dx.doi.org/10.3390/biom12060766.

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Nuclear-factor-E2-related factor 2 (Nrf2) is a key transcription factor for the regulation of cellular responses to cellular stress and inflammation, and its expression is significantly lower after spontaneous term labor in human fetal membranes. Pathological induction of inflammation can lead to adverse pregnancy outcomes such as pre-eclampsia, preterm labor, and fetal death. As stretch forces are known to act upon the fetal membranes in utero, we aimed to ascertain the effect of stretch on Nrf2 to increase our understanding of the role of this stimulus on cells of the amnion at term. Our results indicated a significant reduction in Nrf2 expression in stretched isolated human amnion epithelial cells (hAECs) that could be rescued with sulforaphane treatment. Downregulation of Nrf2 as a result of stretch was accompanied with activation of proinflammatory nuclear factor-kB (NF-kB) and increases in LDH activity, ROS, and HMGB1. This work supports stretch as a key modulator of cellular stress and inflammation in the fetal membranes. Our results showed that the modulation of the antioxidant response pathway in the fetal membranes through Nrf2 activation may be a viable approach to improve outcomes in pregnancy.

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Peterson, Suzanne E., J. Lee Nelson, Vijayakrishna K. Gadi, and Hilary S. Gammill. "Fetal cellular microchimerism in miscarriage and pregnancy termination." Chimerism 4, no. 4 (October 2013): 136–38. http://dx.doi.org/10.4161/chim.24915.

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Girard, Nadine J., and Charles A. Raybaud. "In Vivo MRI of Fetal Brain Cellular Migration." Journal of Computer Assisted Tomography 16, no. 2 (March 1992): 265–67. http://dx.doi.org/10.1097/00004728-199203000-00016.

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Goplerud, Jan M., and Maria Delivoria-Papadopoulos. "Principles in Cellular Oxygenation: Fetal and Neonatal Intestines." Clinics in Perinatology 13, no. 1 (March 1986): 191–96. http://dx.doi.org/10.1016/s0095-5108(18)30846-7.

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Ball, Andrew J., and Fred Levine. "Telomere-independent cellular senescence in human fetal cardiomyocytes." Aging Cell 4, no. 1 (February 2005): 21–30. http://dx.doi.org/10.1111/j.1474-9728.2004.00137.x.

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Zenclussen, Ana Claudia, Anne Schumacher, Maria Laura Zenclussen, Paul Wafula, and Hans-Dieter Volk. "Immunology of pregnancy: cellular mechanisms allowing fetal survival within the maternal uterus." Expert Reviews in Molecular Medicine 9, no. 10 (April 2007): 1–14. http://dx.doi.org/10.1017/s1462399407000294.

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AbstractPregnancy success remains a fascinating phenomenon to immunologists as it defies the immunological rules of rejection. Although it was previously thought that the maternal immune system does not see the fetus, it is now well documented that fetal cells reach the maternal body and encounter host immune cells. Natural tolerance mechanisms following this interaction remain to be fully elucidated. This article reviews the current literature on mechanisms of adaptive immunity, with emphasis on regulatory T cells and heme oxygenase 1 (HO-1). We propose a scenario in which regulatory T cells create a tolerant microenvironment at the fetal–maternal interface characterised by the presence of tolerance-associated molecules such as HO-1, which has been shown to be of vital importance for fetal survival.

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Iruloh, C. G., S. W. D'Souza, P. F. Speake, I. Crocker, W. Fergusson, P. N. Baker, C. P. Sibley, and J. D. Glazier. "Taurine transporter in fetal T lymphocytes and platelets: differential expression and functional activity." American Journal of Physiology-Cell Physiology 292, no. 1 (January 2007): C332—C341. http://dx.doi.org/10.1152/ajpcell.00634.2005.

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Transplacental transfer of taurine, a β-amino acid essential for fetal and neonatal development, constitutes the primary source of taurine for the fetus. Placental transport of taurine is compromised in pregnancies complicated by intrauterine growth restriction, resulting in a reduced concentration of taurine in cord plasma. This could impact on fetal cellular metabolism as taurine represents the most abundant intracellular amino acid in many fetal cell types. In the present study, we have used pure isolates of fetal platelets and T lymphocytes from cord blood of placentas, from normal, term pregnancies, as fetal cell types to examine the cellular uptake mechanisms for taurine by the system β transporter and have compared gene and protein expression for the taurine transporter protein (TAUT) in these two cell types. System β activity in fetal platelets was 15-fold higher compared with fetal T lymphocytes ( P < 0.005), mirroring greater TAUT mRNA expression in platelets than T lymphocytes ( P < 0.005). Cell-specific differences in TAUT protein moieties were detected with a doublet of 75 and 80 kDa in fetal platelets compared with 114 and 120 kDa in fetal T lymphocytes, with relatively higher expression in platelets. We conclude that greater system β activity in fetal platelets compared with T lymphocytes is the result of relatively greater TAUT mRNA and protein expression. This study represents the first characterization of amino acid transporters in fetal T lymphocytes.

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Chinnici, Cinzia Maria, Giandomenico Amico, Marcello Monti, Stefania Motta, Rosario Casalone, Sergio Li Petri, Marco Spada, Bruno Gridelli, and Pier Giulio Conaldi. "Isolation and Characterization of Multipotent Cells from Human Fetal Dermis." Cell Transplantation 23, no. 10 (October 2014): 1169–85. http://dx.doi.org/10.3727/096368913x668618.

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We report that cells from human fetal dermis, termed here multipotent fetal dermal cells, can be isolated with high efficiency by using a nonenzymatic, cell outgrowth method. The resulting cell population was consistent with the definition of mesenchymal stromal cells by the International Society for Cellular Therapy. As multipotent fetal dermal cells proliferate extensively, with no loss of multilineage differentiation potential up to passage 25, they may be an ideal source for cell therapy to repair damaged tissues and organs. Multipotent fetal dermal cells were not recognized as targets by T lymphocytes in vitro, thus supporting their feasibility for allogenic transplantation. Moreover, the expansion protocol did not affect the normal phenotype and karyotype of cells. When compared with adult dermal cells, fetal cells displayed several advantages, including a greater cellular yield after isolation, the ability to proliferate longer, and the retention of differentiation potential. Interestingly, multipotent fetal dermal cells expressed the pluripotency marker SSEA4 (90.56 ± 3.15% fetal vs. 10.5 ± 8.5% adult) and coexpressed mesenchymal and epithelial markers (>80% CD90+/CK18+ cells), coexpression lacking in the adult counterparts isolated under the same conditions. Multipotent fetal dermal cells were able to form capillary structures, as well as differentiate into a simple epithelium in vitro, indicating skin regeneration capabilities.

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Yamane, Toshiyuki. "Cellular Basis of Embryonic Hematopoiesis and Its Implications in Prenatal Erythropoiesis." International Journal of Molecular Sciences 21, no. 24 (December 8, 2020): 9346. http://dx.doi.org/10.3390/ijms21249346.

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Primitive erythrocytes are the first hematopoietic cells observed during ontogeny and are produced specifically in the yolk sac. Primitive erythrocytes express distinct hemoglobins compared with adult erythrocytes and circulate in the blood in the nucleated form. Hematopoietic stem cells produce adult-type (so-called definitive) erythrocytes. However, hematopoietic stem cells do not appear until the late embryonic/early fetal stage. Recent studies have shown that diverse types of hematopoietic progenitors are present in the yolk sac as well as primitive erythroblasts. Multipotent hematopoietic progenitors that arose in the yolk sac before hematopoietic stem cells emerged likely fill the gap between primitive erythropoiesis and hematopoietic stem-cell-originated definitive erythropoiesis and hematopoiesis. In this review, we discuss the cellular origin of primitive erythropoiesis in the yolk sac and definitive hematopoiesis in the fetal liver. We also describe mechanisms for developmental switches that occur during embryonic and fetal erythropoiesis and hematopoiesis, particularly focusing on recent studies performed in mice.

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Ptasznik, Andrzej, Gillian M. Beattie, Martin I. Mally, Vincenzo Cirulli, Ana Lopez, and Alberto Hayek. "Phosphatidylinositol 3-Kinase Is a Negative Regulator of Cellular Differentiation." Journal of Cell Biology 137, no. 5 (June 2, 1997): 1127–36. http://dx.doi.org/10.1083/jcb.137.5.1127.

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Phosphatidylinositol 3-kinase (PI3K) has been shown to be an important mediator of intracellular signal transduction in mammalian cells. We show here, for the first time, that the blockade of PI3K activity in human fetal undifferentiated cells induced morphological and functional endocrine differentiation. This was associated with an increase in mRNA levels of insulin, glucagon, and somatostatin, as well as an increase in the insulin protein content and secretion in response to secretagogues. Blockade of PI3K also increased the proportion of pluripotent precursor cells coexpressing multiple hormones and the total number of terminally differentiated cells originating from these precursor cells. We examined whether any of the recently described modulators of endocrine differentiation could participate in regulating PI3K activity in fetal islet cells. The activity of PI3K was inversely correlated with the hepatocyte growth factor/scatter factor–induced downregulation or nicotinamideinduced upregulation of islet-specific gene expression, giving support to the role of PI3K, as a negative regulator of endocrine differentiation. In conclusion, our results provide a mechanism for the regulation of hormone-specific gene expression during human fetal neogenesis. They also suggest a novel function for PI3K, as a negative regulator of cellular differentiation.

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Gallacher, Lisa, Barbara Murdoch, Dongmei Wu, Francis Karanu, Fraser Fellows, and Mickie Bhatia. "Identification of novel circulating human embryonic blood stem cells." Blood 96, no. 5 (September 1, 2000): 1740–47. http://dx.doi.org/10.1182/blood.v96.5.1740.

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Abstract Using murine models, primitive hematopoietic cells capable of repopulation have been shown to reside in various anatomic locations, including the aortic gonad mesonephros, fetal liver, and bone marrow. These sites are thought to be seeded by stem cells migrating through fetal circulation and would serve as ideal targets for in utero cellular therapy. In humans, however, it is unknown whether similar stem cells exist. Here, we identify circulating hematopoeitic cells present during human in utero development that are capable of multilineage repopulation in immunodeficient NOD/SCID (nonobese diabetic/severe combined immunodeficient) mice. Using limiting dilution analysis, the frequency of these fetal stem cells was found to be 1 in 3.2 × 105, illustrating a 3- and 22-fold enrichment compared with full-term human cord blood and circulating adult mobilized–peripheral blood, respectively. Comparison of in vivo differentiation and proliferative capacity demonstrated that circulating fetal stem cells are intrinsically distinct from hematopoietic stem cells found later in human development and those derived from the fetal liver or fetal bone marrow compartment at equivalent gestation. Taken together, these studies demonstrate the existence of unique circulating stem cells in early human embryonic development that provide a novel and previously unexplored source of pluripotent stem cell targets for cellular and gene-based fetal therapies.

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Gallacher, Lisa, Barbara Murdoch, Dongmei Wu, Francis Karanu, Fraser Fellows, and Mickie Bhatia. "Identification of novel circulating human embryonic blood stem cells." Blood 96, no. 5 (September 1, 2000): 1740–47. http://dx.doi.org/10.1182/blood.v96.5.1740.h8001740_1740_1747.

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Using murine models, primitive hematopoietic cells capable of repopulation have been shown to reside in various anatomic locations, including the aortic gonad mesonephros, fetal liver, and bone marrow. These sites are thought to be seeded by stem cells migrating through fetal circulation and would serve as ideal targets for in utero cellular therapy. In humans, however, it is unknown whether similar stem cells exist. Here, we identify circulating hematopoeitic cells present during human in utero development that are capable of multilineage repopulation in immunodeficient NOD/SCID (nonobese diabetic/severe combined immunodeficient) mice. Using limiting dilution analysis, the frequency of these fetal stem cells was found to be 1 in 3.2 × 105, illustrating a 3- and 22-fold enrichment compared with full-term human cord blood and circulating adult mobilized–peripheral blood, respectively. Comparison of in vivo differentiation and proliferative capacity demonstrated that circulating fetal stem cells are intrinsically distinct from hematopoietic stem cells found later in human development and those derived from the fetal liver or fetal bone marrow compartment at equivalent gestation. Taken together, these studies demonstrate the existence of unique circulating stem cells in early human embryonic development that provide a novel and previously unexplored source of pluripotent stem cell targets for cellular and gene-based fetal therapies.

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D’Antonio, Matteo, Jennifer P. Nguyen, Timothy D. Arthur, Hiroko Matsui, Margaret K. R. Donovan, Agnieszka D’Antonio-Chronowska, and Kelly A. Frazer. "In heart failure reactivation of RNA-binding proteins is associated with the expression of 1,523 fetal-specific isoforms." PLOS Computational Biology 18, no. 2 (February 28, 2022): e1009918. http://dx.doi.org/10.1371/journal.pcbi.1009918.

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Reactivation of fetal-specific genes and isoforms occurs during heart failure. However, the underlying molecular mechanisms and the extent to which the fetal program switch occurs remains unclear. Limitations hindering transcriptome-wide analyses of alternative splicing differences (i.e. isoform switching) in cardiovascular system (CVS) tissues between fetal, healthy adult and heart failure have included both cellular heterogeneity across bulk RNA-seq samples and limited availability of fetal tissue for research. To overcome these limitations, we have deconvoluted the cellular compositions of 996 RNA-seq samples representing heart failure, healthy adult (heart and arteria), and fetal-like (iPSC-derived cardiovascular progenitor cells) CVS tissues. Comparison of the expression profiles revealed that reactivation of fetal-specific RNA-binding proteins (RBPs), and the accompanied re-expression of 1,523 fetal-specific isoforms, contribute to the transcriptome differences between heart failure and healthy adult heart. Of note, isoforms for 20 different RBPs were among those that reverted in heart failure to the fetal-like expression pattern. We determined that, compared with adult-specific isoforms, fetal-specific isoforms encode proteins that tend to have more functions, are more likely to harbor RBP binding sites, have canonical sequences at their splice sites, and contain typical upstream polypyrimidine tracts. Our study suggests that compared with healthy adult, fetal cardiac tissue requires stricter transcriptional regulation, and that during heart failure reversion to this stricter transcriptional regulation occurs. Furthermore, we provide a resource of cardiac developmental stage-specific and heart failure-associated genes and isoforms, which are largely unexplored and can be exploited to investigate novel therapeutics for heart failure.

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SHOHAT, BATYA, MICHAEL HIRSCH, OVADIA JARDENA, JOSHUA HENRY, ISKA LEVY, and NATHAN TRAININ. "Cellular Immune Aspects of the Human Fetal-Maternal Relationship." American Journal of Reproductive Immunology and Microbiology 11, no. 4 (August 1986): 125–29. http://dx.doi.org/10.1111/j.1600-0897.1986.tb00045.x.

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Verner, Glenn Helen, Elissa Epel, Marius Lahti-Pulkkinen, Eero Kajantie, Claudia Buss, Jue Lin, Elizabeth Blackburn, Katri Räikkönen, Pathik Wadhwa, and Sonja Entringer. "Maternal psychological resilience during pregnancy and fetal cellular aging." Psychoneuroendocrinology 107 (September 2019): 35. http://dx.doi.org/10.1016/j.psyneuen.2019.07.097.

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WOOD, C., and D. BARKOE. "Fetal pulmonary immunoreactive adrenocorticotropin: Molecular weight and cellular localization." Journal of the Society for Gynecologic Investigation 5, no. 1 (January 1998): 44A. http://dx.doi.org/10.1016/s1071-5576(97)86098-4.

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Wood, Charles E., David Barkoe, Angeline The, Howard Newman, Timothy A. Cudd, Scott Purinton, and Maria I. Castro. "Fetal pulmonary immunoreactive adrenocorticotropin: molecular weight and cellular localization." Regulatory Peptides 73, no. 3 (February 1998): 191–96. http://dx.doi.org/10.1016/s0167-0115(98)00004-4.

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Green, David W., Gregory S. Watson, Jolanta A. Watson, Jong-Min Lee, and Han-Sung Jung. "Simulated embryonic and fetal cellular dynamics inside structured biomaterials." Applied Materials Today 11 (June 2018): 291–307. http://dx.doi.org/10.1016/j.apmt.2017.12.007.

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Buzsàki, G., J. Czopf, I. KondÀkor, A. Björklund, and F. H. Gage. "Cellular activity of intracerebrally transplanted fetal hippocampus during behavior." Neuroscience 22, no. 3 (September 1987): 871–83. http://dx.doi.org/10.1016/0306-4522(87)92966-6.

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Lissauer, D., K. Piper, O. Goodyear, P. A. H. Moss, and M. D. Kilby. "Maternal cellular immunity to fetal HY antigens during pregnancy." Journal of Reproductive Immunology 90, no. 2 (August 2011): 144. http://dx.doi.org/10.1016/j.jri.2011.06.026.

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Ono, Katsuhiko, and Koki Kawamura. "Cellular migration in the pontine stream of fetal mouse." Neuroscience Research Supplements 9 (January 1989): 53. http://dx.doi.org/10.1016/0921-8696(89)90620-8.

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Jordan, Craig T., John P. McKearn, and Ihor R. Lemischka. "Cellular and developmental properties of fetal hematopoietic stem cells." Cell 61, no. 6 (June 1990): 953–63. http://dx.doi.org/10.1016/0092-8674(90)90061-i.

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Neel, H. Bryan, Stephen G. Harner, Brian J. Broker, and David Reiter. "Fetal Wound Healing." Otolaryngology–Head and Neck Surgery 110, no. 6 (June 1994): 547–49. http://dx.doi.org/10.1177/019459989411000612.

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Wound healing research has produced some startling discoveries during the past decade. Foremost among these is the observation that cutaneous wounds created and healed in utero are histologically indistinguishable from intact, unwounded tissue. Observers have documented that the acute inflammatory response and endogenous immunoglobullns that characterize healing in human beings after birth are absent in the fetal wound. Determination of the cellular and biochemical differences between fetal and postdelivery wound healing offers the promise of Improved control over the process of tissue repair. Another promise of fetal wound healing research is the option of in utero repair of defects such as cieft lip and palate. We review what is known at present about fetal wound healing.

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Mateos, Rosa María, Gema Jiménez, Carmen Álvarez-Gil, Francisco Visiedo, Fátima Rivera-Rodríguez, Celeste Santos-Rosendo, Antonia Rodriguez-Pareja, Germán Perdomo, and Alfonso M. Lechuga-Sancho. "Excess Hydrocortisone Hampers Placental Nutrient Uptake Disrupting Cellular Metabolism." BioMed Research International 2018 (October 9, 2018): 1–11. http://dx.doi.org/10.1155/2018/5106174.

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Low birth weight increases neonatal morbidity and mortality, and surviving infants have increased risk of metabolic and cardiovascular disturbances later in life, as well as other neurological, psychiatric, and immune complications. A gestational excess of glucocorticoids (GCs) is a well-known cause for fetal growth retardation, but the biological basis for this association remains elusive. Placental growth is closely related to fetal growth. The placenta is the main regulator of nutrient transport to the fetus, resulting from the difference between placental nutrient uptake and the placenta’s own metabolism. The aim of this study was to analyze how excess hydrocortisone affects placental glucose and lipid metabolism. Human placenta explants from term physiological pregnancies were cultured for 18 hours under different hydrocortisone concentrations (2.75, 5.5, and 55 mM; 1, 2, and 20 mg/ml). Placental glucose and lipid uptake and the metabolic partitioning of fatty acids were quantified by isotopic techniques, and expression of specific glucose transporter GLUT1 was quantified by western blot. Cell viability was assessed by MTT, immunohistochemistry and caspase activity. We found that excess hydrocortisone impairs glucose uptake and lipoprotein lipase (LPL) activity, coincident with a GC-dose dependent inhibition of fatty acid oxidation and esterification. None of the experimental conditions showed an increased cell death. In conclusion, our results show that GC overexposure exerts a dysfunctional effect on lipid transport and metabolism and glucose uptake in human placental explants. These findings could well be directly related to a reduced placental growth and possibly to a reduced supply of nutrients to the fetus and the consequent fetal growth retardation and metabolic programming.

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Karamlou, Tara, George D. Giraud, Donogh McKeogh, Sonnet S. Jonker, Irving Shen, Ross M. Ungerleider, and Kent L. Thornburg. "Right ventricular remodeling in response to volume overload in fetal sheep." American Journal of Physiology-Heart and Circulatory Physiology 316, no. 5 (May 1, 2019): H985—H991. http://dx.doi.org/10.1152/ajpheart.00439.2018.

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The fetal myocardium is known to be sensitive to hemodynamic load, responding to systolic overload with cellular hypertrophy, proliferation, and accelerated maturation. However, the fetal cardiac growth response to primary volume overload is unknown. We hypothesized that increased venous return would stimulate fetal cardiomyocyte proliferation and terminal differentiation, particularly in the right ventricle (RV). Vascular catheters and pulmonary artery flow probes were implanted in 16 late-gestation fetal sheep: a right carotid artery-jugular vein (AV) fistula was surgically created in nine fetuses, and sham operations were performed on seven fetuses. Instrumented fetuses were studied for 1 wk before hearts were dissected for component analysis or cardiomyocyte dispersion for cellular measurements. Within 1 day of AV fistula creation, RV output was 20% higher in experimental than sham fetuses ( P < 0.0001). Circulating atrial natriuretic peptide levels were elevated fivefold in fetuses with an AV fistula ( P < 0.002). On the terminal day, RV-to-body weight ratios were 35% higher in the AV fistula group ( P < 0.05). Both left ventricular and RV cardiomyocytes grew longer in fetuses with an AV fistula ( P < 0.02). Cell cycle activity was depressed by >50% [significant in left ventricle ( P < 0.02), but not RV ( P < 0.054)]. Rates of terminal differentiation were unchanged. Based on these studies, we speculate that atrial natriuretic peptide suppressed fetal cardiomyocyte cell cycle activity. Unlike systolic overload, fetal diastolic load appears to drive myocyte enlargement, but not cardiomyocyte proliferation or maturation. These changes could predispose to RV dysfunction later in life. NEW & NOTEWORTHY Adaptation of the fetal heart to changes in cardiac load allows the fetus to maintain adequate blood flow to its systemic and placental circulations, which is necessary for the well-being of the fetus. Addition of arterial-venous fistula flow to existing venous return increased right ventricular stroke volume and output. The fetal heart compensated by cardiomyocyte elongation without accelerated cellular maturation, while cardiomyocyte proliferation decreased. Even transient volume overload in utero alters myocardial structure and cardiomyocyte endowment.

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Wood, Charles E., and Maureen Keller-Wood. "Current paradigms and new perspectives on fetal hypoxia: implications for fetal brain development in late gestation." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 317, no. 1 (July 1, 2019): R1—R13. http://dx.doi.org/10.1152/ajpregu.00008.2019.

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The availability of oxygen to the fetus is limited by the route taken by oxygen from the atmosphere to fetal tissues, aided or diminished by pregnancy-associated changes in maternal physiology and, ultimately, a function of atmospheric pressure and composition of the mother’s inspired gas. Much of our understanding of the fetal physiological response to hypoxia comes from experiments designed to elucidate the cardiovascular and endocrine responses to transient hypoxia. Complementing this work is equally impactful research into the origins of intrauterine growth restriction in which animal models designed to restrict the transfer of oxygen from the maternal to the fetal circulation were used. A common assumption has been that outcomes measured after a period of hypoxia are related to cellular deprivation of oxygen and reoxygenation: an assumption based on a focus on what we can see “under the streetlights.” Recent studies demonstrate that availability of oxygen may not tell the whole story. Transient hypoxia in the fetal sheep stimulates transcriptomics responses that mirror inflammation. This response is accompanied by the appearance of bacteria in the fetal brain and other tissues, likely resulting from a hypoxia-stimulated release of bacteria from the placenta. The appearance of bacteria in the fetus after transient hypoxia complements the recent discovery of bacterial DNA in the normal human placenta and in the tissues of fetal sheep. An understanding of the mechanism of the physiological, cellular, and molecular responses to hypoxia requires an appreciation of stimuli other than cellular oxygen deprivation: stimuli that we would have never known about without looking “between the streetlights,” illuminating direct responses to the manipulated variables.

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Friedman, S. "Fetal Plasma Levels of Cellular Fibronectin as a Measure of Fetal Endothelial Involvement in Preeclampsia." Obstetrics & Gynecology 89, no. 1 (January 1997): 46–48. http://dx.doi.org/10.1016/s0029-7844(96)00382-1.

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42

Kajdy, Anna, Jan Modzelewski, Aneta Cymbaluk-Płoska, Ewa Kwiatkowska, Magdalena Bednarek-Jędrzejek, Dariusz Borowski, Katarzyna Stefańska, Michał Rabijewski, Andrzej Torbé, and Sebastian Kwiatkowski. "Molecular Pathways of Cellular Senescence and Placental Aging in Late Fetal Growth Restriction and Stillbirth." International Journal of Molecular Sciences 22, no. 8 (April 18, 2021): 4186. http://dx.doi.org/10.3390/ijms22084186.

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Abnormally accelerated, premature placental senescence plays a crucial role in the genesis of pregnancy pathologies. Abnormal growth in the third trimester can present as small for gestational age fetuses or fetal growth restriction. One differs from the other by the presence of signs of placental insufficiency and the risk of stillbirth. The majority of stillbirths occur in normally grown fetuses and are classified as “unexplained”, which often leads to conclusions that they were unpreventable. The main characteristic of aging is a gradual decline in the function of cells, tissues, and organs. These changes result in the accumulation of senescent cells in mitotic tissues. These cells begin the aging process that disrupts tissues’ normal functions by affecting neighboring cells, degrading the extracellular matrix, and reducing tissues’ regeneration capacity. Different degrees of abnormal placentation result in the severity of fetal growth restriction and its sequelae, including fetal death. This review aims to present the current knowledge and identify future research directions to understand better placental aging in late fetal growth restriction and unexplained stillbirth. We hypothesized that the final diagnosis of placental insufficiency can be made only using markers of placental senescence.

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Kuijk, Ewart, Francis Blokzijl, Myrthe Jager, Nicolle Besselink, Sander Boymans, Susana M. Chuva de Sousa Lopes, Ruben van Boxtel, and Edwin Cuppen. "Early divergence of mutational processes in human fetal tissues." Science Advances 5, no. 5 (May 2019): eaaw1271. http://dx.doi.org/10.1126/sciadv.aaw1271.

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A developing human fetus needs to balance rapid cellular expansion with maintaining genomic stability. Here, we accurately quantified and characterized somatic mutation accumulation in fetal tissues by analyzing individual stem cells from human fetal liver and intestine. Fetal mutation rates were about fivefold higher than in tissue-matched adult stem cells. The mutational landscape of fetal intestinal stem cells resembled that of adult intestinal stem cells, while the mutation spectrum of fetal liver stem cells is distinct from stem cells of the fetal intestine and the adult liver. Our analyses indicate that variation in mutational mechanisms, including oxidative stress and spontaneous deamination of methylated cytosines, contributes to the observed divergence in mutation accumulation patterns and drives genetic mosaicism in humans.

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WARRINGTON, JANET A., ARCHANA NAIR, MAMATHA MAHADEVAPPA, and MAYA TSYGANSKAYA. "Comparison of human adult and fetal expression and identification of 535 housekeeping/maintenance genes." Physiological Genomics 2, no. 3 (April 27, 2000): 143–47. http://dx.doi.org/10.1152/physiolgenomics.2000.2.3.143.

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Warrington, Janet A., Archana Nair, Mamatha Mahadevappa, and Maya Tsyganskaya. Comparison of human adult and fetal expression and identification of 535 housekeeping/maintenance genes. Physiol Genomics 2: 143–147, 2000.—Gene expression levels of about 7,000 genes were measured in 11 different human adult and fetal tissues using high-density oligonucleotide arrays to identify genes involved in cellular maintenance. The tissues share a set of 535 transcripts that are turned on early in fetal development and stay on throughout adulthood. Because our goal was to identify genes that are involved in maintaining cellular function in normal individuals, we minimized the effect of individual variation by screening mRNA pooled from many individuals. This information is useful for establishing average expression levels in normal individuals. Additionally, we identified transcripts uniquely expressed in each of the 11 tissues.

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Dewing, Jennifer M., Vinay Saunders, Ita O’Kelly, and David I. Wilson. "Defining cardiac cell populations and relative cellular composition of the early fetal human heart." PLOS ONE 17, no. 11 (November 30, 2022): e0259477. http://dx.doi.org/10.1371/journal.pone.0259477.

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While the adult human heart is primarily composed of cardiomyocytes, fibroblasts, endothelial and smooth muscle cells, the cellular composition during early development remains largely unknown. Reliable identification of fetal cardiac cell types using protein markers is critical to understand cardiac development and delineate the cellular composition of the developing human heart. This is the first study to use immunohistochemistry (IHC), flow cytometry and RT-PCR analyses to investigate the expression and specificity of commonly used cardiac cell markers in the early human fetal heart (8–12 post-conception weeks). The expression of previously reported protein markers for the detection of cardiomyocytes (Myosin Heavy Chain (MHC) and cardiac troponin I (cTnI), fibroblasts (DDR2, THY1, Vimentin), endothelial cells (CD31) and smooth muscle cells (α-SMA) were assessed. Two distinct populations of cTnI positive cells were identified through flow cytometry, with MHC positive cardiomyocytes showing high cTnI expression (cTnIHigh) while MHC negative non-myocytes showed lower cTnI expression (cTnILow). cTnI expression in non-myocytes was further confirmed by IHC and RT-PCR analyses, suggesting troponins are not cardiomyocyte-specific and may play distinct roles in non-muscle cells during early development. Vimentin (VIM) was expressed in cultured ventricular fibroblast populations and flow cytometry revealed VIMHigh and VIMLow cell populations in the fetal heart. MHC positive cardiomyocytes were VIMLow whilst CD31 positive endothelial cells were VIMHigh. Using markers investigated within this study, we characterised fetal human cardiac populations and estimate that 75–80% of fetal cardiac cells are cardiomyocytes and are MHC+/cTnIHigh/VIMLow, whilst non-myocytes comprise 20–25% of total cells and are MHC-/cTnILow/VIMHigh, with CD31+ endothelial cells comprising ~9% of this population. These findings show distinct differences from those reported for adult heart.

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Das, Utpala G., Robert E. Schroeder, William W. Hay, and Sherin U. Devaskar. "Time-dependent and tissue-specific effects of circulating glucose on fetal ovine glucose transporters." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 276, no. 3 (March 1, 1999): R809—R817. http://dx.doi.org/10.1152/ajpregu.1999.276.3.r809.

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To determine the cellular adaptations to fetal hyperglycemia and hypoglycemia, we examined the time-dependent effects on basal (GLUT-1 and GLUT-3) and insulin-responsive (GLUT-4) glucose transporter proteins by quantitative Western blot analysis in fetal ovine insulin-insensitive (brain and liver) and insulin-sensitive (myocardium, skeletal muscle, and adipose) tissues. Maternal glucose infusions causing fetal hyperglycemia resulted in a transient 30% increase in brain GLUT-1 but not GLUT-3 levels and a decline in liver and adipose GLUT-1 and myocardial and skeletal muscle GLUT-1 and GLUT-4 levels compared with gestational age-matched controls. Maternal insulin infusions leading to fetal hypoglycemia caused a decline in brain GLUT-3, an increase in brain GLUT-1, and a subsequent decline in liver GLUT-1, with no significant change in insulin-sensitive myocardium, skeletal muscle, and adipose tissue GLUT-1 or GLUT-4 concentrations, compared with gestational age-matched sham controls. We conclude that fetal glucose transporters are subject to a time-dependent and tissue- and isoform-specific differential regulation in response to altered circulating glucose and/or insulin concentrations. These cellular adaptations in GLUT-1 (and GLUT-3) are geared toward protecting the conceptus from perturbations in substrate availability, and the adaptations in GLUT-4 are geared toward development of fetal insulin resistance.

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Maloyan, Alina, Sribalasubashini Muralimanoharan, Steven Huffman, Laura A. Cox, Peter W. Nathanielsz, Leslie Myatt, and Mark J. Nijland. "Identification and comparative analyses of myocardial miRNAs involved in the fetal response to maternal obesity." Physiological Genomics 45, no. 19 (October 1, 2013): 889–900. http://dx.doi.org/10.1152/physiolgenomics.00050.2013.

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Human and animal studies show that suboptimal intrauterine environments lead to fetal programming, predisposing offspring to disease in later life. Maternal obesity has been shown to program offspring for cardiovascular disease (CVD), diabetes, and obesity. MicroRNAs (miRNAs) are small, noncoding RNA molecules that act as key regulators of numerous cellular processes. Compelling evidence links miRNAs to the control of cardiac development and etiology of cardiac pathology; however, little is known about their role in the fetal cardiac response to maternal obesity. Our aim was to sequence and profile the cardiac miRNAs that are dysregulated in the hearts of baboon fetuses born to high fat/high fructose-diet (HFD) fed mothers for comparison with fetal hearts from mothers eating a regular diet. Eighty miRNAs were differentially expressed. Of those, 55 miRNAs were upregulated and 25 downregulated with HFD. Twenty-two miRNAs were mapped to human; 14 of these miRNAs were previously reported to be dysregulated in experimental or human CVD. We used an Ingenuity Pathway Analysis to integrate miRNA profiling and bioinformatics predictions to determine miRNA-regulated processes and genes potentially involved in fetal programming. We found a correlation between miRNA expression and putative gene targets involved in developmental disorders and CVD. Cellular death, growth, and proliferation were the most affected cellular functions in response to maternal obesity. Thus, the current study reveals significant alterations in cardiac miRNA expression in the fetus of obese baboons. The epigenetic modifications caused by adverse prenatal environment may represent one of the mechanisms underlying fetal programming of CVD.

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McCain, Megan L. "Organs-on-chips take baby steps." Science Translational Medicine 11, no. 492 (May 15, 2019): eaax1713. http://dx.doi.org/10.1126/scitranslmed.aax1713.

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Hepper, Peter G., and Leo R. Leader. "Fetal Habituation." Fetal and Maternal Medicine Review 8, no. 2 (May 1996): 109–23. http://dx.doi.org/10.1017/s0965539500001534.

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One aim of obstetric practice is to ensure the wellbeing of the fetus. This is by no means an easy task and recent years have seen the development of a variety of tests, with varying degrees of success, to evaluate fetal health.Fetal wellbeing may be assessed at a variety of levels: genetic/cellular, physical/structural or functional. Ideally the evaluation of fetal health should provide information about the functional outcome of any particular condition, especially the performance of the central nervous system. Current tests may not do this. Thus, whilst tests of the fetal chromosomal or genetic constitution may determine the presence of particular genetic/chromosomal conditions, they may not predict functional outcome especially the functioning of the cerebral cortices, the ultimate arbiter of excellence in man. For example, Down's syndrome may be accurately diagnosed by analysis of fetal cells to detect the presence of Trisomy 21 but this in itself provides little information on the subsequent functional performance of the individual. The development of tests of fetal heart function such as antenatal cardiotocography have provided a means of assessing cardiac function and, to a certain extent, the functioning of parts of the autonomic nervous system. However such tests can only indirectly assess cortical function.

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Helmo, Fernanda Rodrigues, Juliana Reis Machado, Camila Souza de Oliveira Guimarães, Vicente de Paula Antunes Teixeira, Marlene Antônia dos Reis, and Rosana Rosa Miranda Corrêa. "Fetal Wound Healing Biomarkers." Disease Markers 35 (2013): 939–44. http://dx.doi.org/10.1155/2013/567353.

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Fetal skin has the intrinsic capacity for wound healing, which is not correlated with the intrauterine environment. This intrinsic ability requires biochemical signals, which start at the cellular level and lead to secretion of transforming factors and expression of receptors, and specific markers that promote wound healing without scar formation. The mechanisms and molecular pathways of wound healing still need to be elucidated to achieve a complete understanding of this remodeling system. The aim of this paper is to discuss the main biomarkers involved in fetal skin wound healing as well as their respective mechanisms of action.

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Journal articles on the topic 'Cellule Fetali'

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