Talk:Endocrine - Other Tissues
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Cite this page: Hill, M.A. (2019, June 27) Embryology Endocrine - Other Tissues. Retrieved from https://embryology.med.unsw.edu.au/embryology/index.php/Talk:Endocrine_-_Other_Tissues
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Note - This sub-heading shows an automated computer PubMed search using the listed sub-heading term. References appear in this list based upon the date of the actual page viewing. Therefore the list of references do not reflect any editorial selection of material based on content or relevance. In comparison, references listed on the content page and discussion page (under the publication year sub-headings) do include editorial selection based upon relevance and availability. (More? Pubmed Most Recent)
<pubmed limit=5>Adipose Embryology</pubmed>
J Mol Endocrinol. 2017 Oct;59(3):285-297. doi: 10.1530/JME-17-0046. Epub 2017 Jul 21. Adiponectin limits differentiation and trophoblast invasion in human endometrial cells. Duval F1, Dos Santos E1,2, Moindjie H1, Serazin V1,2, Swierkowski-Blanchard N1,3, Vialard F1,3, Dieudonné MN4. Author information Abstract Successful human embryo implantation requires a proper differentiation of endometrial stromal cells (ESCs) into decidual cells, during a process called decidualization. ESCs express specific molecules, such as prolactin, insulin-like growth factor-binding protein-1 (IGFBP-1) and connexin-43. Decidual cells are also involved in the control of trophoblast invasion, by secreting various factors, such as matrix metalloproteinases (MMPs) and tissue inhibitors of metalloproteinases (TIMPs). Adiponectin is an adipokine with insulin-sensitizing, anti-inflammatory and anti-proliferative effects. At the embryo-maternal interface, adiponectin promotes differentiation and invasion of human trophoblastic cells. We hypothesize that the effects of adiponectin on endometrium could counteract its pro-invasive effects previously described in the human trophoblast. In this context, we have firstly demonstrated that adiponectin downregulates IGFBP-1 and connexin-43 mRNA expressions, as well as prolactin secretion in ESCs, suggesting an anti-differentiative effect of adiponectin. Secondly, we found that invasive capacities of trophoblastic cell line HTR-8/SVneo are reduced in the presence of conditioned media from ESC cultured in the presence of adiponectin. Adiponectin's anti-invasive action is associated with a decreased activity of MMP-2 and MMP-9, and an increased TIMP-3 mRNA expression in ESCs. Finally, adiponectin receptors (ADIPOR1 and ADIPOR2) knockdown abolishes the anti-differentiative and anti-invasive effects of adiponectin in human ESCs. Altogether, our results suggest that adiponectin reduces the decidualization process and inversely induces the production of endometrial factors that limit trophoblast invasion. Thus, through a dual control in trophoblast and endometrial cells, adiponectin appears as a pivotal actor of the embryo implantation process. KEYWORDS: adiponectin; decidualization; embryo implantation; human endometrium; trophoblast invasion PMID: 28733350 DOI: 10.1530/JME-17-0046
Formation of a Neurosensory Organ by Epithelial Cell Slithering
Cell. 2015 Oct 8;163(2):394-405. doi: 10.1016/j.cell.2015.09.021. Epub 2015 Oct 1.
Kuo CS1, Krasnow MA2.
Epithelial cells are normally stably anchored, maintaining their relative positions and association with the basement membrane. Developmental rearrangements occur through cell intercalation, and cells can delaminate during epithelial-mesenchymal transitions and metastasis. We mapped the formation of lung neuroepithelial bodies (NEBs), innervated clusters of neuroendocrine/neurosensory cells within the bronchial epithelium, revealing a targeted mode of cell migration that we named "slithering," in which cells transiently lose epithelial character but remain associated with the membrane while traversing neighboring epithelial cells to reach cluster sites. Immunostaining, lineage tracing, clonal analysis, and live imaging showed that NEB progenitors, initially distributed randomly, downregulate adhesion and polarity proteins, crawling over and between neighboring cells to converge at diametrically opposed positions at bronchial branchpoints, where they reestablish epithelial structure and express neuroendocrine genes. There is little accompanying progenitor proliferation or apoptosis. Activation of the slithering program may explain why lung cancers arising from neuroendocrine cells are highly metastatic. Copyright © 2015 Elsevier Inc. All rights reserved.
An updated view of leptin on implantation and pregnancy: a review
Physiol Res. 2014;63(5):543-57. Epub 2014 Jun 5.
Herrid M1, Palanisamy SK, Ciller UA, Fan R, Moens P, Smart NA, McFarlane JR.
The hormone leptin, which is thought to be primarily produced by adipose tissue, is a polypeptide that was initially characterized by its ability to regulate food intake and energy metabolism. Leptin appears to signal the status of body energy stores to the brain, resulting in the regulation of food intake and whole-body energy expenditure. Subsequently, it was recognized as a cytokine with a wide range of peripheral actions and is involved in the regulation of a number of physiological systems including reproduction. In the fed state, leptin circulates in the plasma in proportion to body adiposity in all species studied to date. However other factors such as sex, age, body mass index (BMI), sex steroids and pregnancy may also affect leptin levels in plasma. In pregnant mice and humans, the placenta is also a major site of leptin expression. Leptin circulates in biological fluids both as free protein and in a form that is bound to the soluble isoform of its receptor or other binding proteins such as one of the immunoglobulin superfamily members Siglec-6 (OB-BP1). Although the actions of leptin in the control of reproductive function are thought to be exerted mainly via the hypothalamic-pituitary-gonadal axis, there have also been reports of local direct effects of leptin at the peripheral level, however, these data appear contradictory. Therefore, there is a need to summarize the current status of research outcomes and analyze the possible reasons for differing results and thus provide researchers with new insight in designing experiments to investigate leptin effect on reproduction. Most importantly, our recent experimental data suggesting that reproductive performance is improved by decreasing concentrations of peripheral leptin was unexpected and cannot be explained by hypotheses drawn from the experiments of excessive exogenous leptin administration to normal animals or ob/ob mice.
|Leptin effects on female reproduction|
|Target Tissue||Biological Process||Biological Function||Mechanism|
|Hypothalamus||GnRH secretion||Regulation of LH and FSH secretion||Indirectly via kisspeptin|
|Pituitary||Estrous cycles and ovulation||FSH and LH release; LH plasticity and cyclicity|
|Ovary||Ovarian steroidogenesis||Estrogen production||P450 aromatase; P450-17α hydroxylase|
|Ovary||Folliculogenesis||Low leptin promotes follicle development||Promotes the transition of primordial to primary follicles|
|Embryo||Embryogenesis||Biophysical effect on embryo growth and quality||Stimulates proliferation|
|Uterus||Angiogenesis||Stimulates metalloproteinase activity||Inhibits terminal differentiation of committed giant cells|
|Table modified from:<pubmed>24908087</pubmed>|
Adipokines and the Female Reproductive Tract
Int J Endocrinol. 2014;2014:232454. Epub 2014 Feb 18.
Reverchon M, Ramé C, Bertoldo M, Dupont J.
It is well known that adipose tissue can influence puberty, sexual maturation, and fertility in different species. Adipose tissue secretes molecules called adipokines which most likely have an endocrine effect on reproductive function. It has been revealed over the last few years that adipokines are functionally implicated at all levels of the reproductive axis including the gonad and hypothalamic-pituitary axis. Many studies have shown the presence and the role of the adipokines and their receptors in the female reproductive tract of different species. These adipokines regulate ovarian steroidogenesis, oocyte maturation, and embryo development. They are also present in the uterus and placenta where they could create a favorable environment for embryonic implantation and play a key role in maternal-fetal metabolism communication and gestation. Reproductive functions are strongly dependent on energy balance, and thereby metabolic abnormalities can lead to the development of some pathophysiologies such as polycystic ovary syndrome (PCOS). Adipokines could be a link between reproduction and energy metabolism and could partly explain some infertility related to obesity or PCOS.
The fat controller: adipocyte development
PLoS Biol. 2012 Nov;10(11):e1001436. doi: 10.1371/journal.pbio.1001436. Epub 2012 Nov 27.
Stephens JM. Source Adipocyte Biology Laboratory, Pennington Biomedical Research Center, Louisiana State University, Baton Rouge, Louisiana, United States of America.
Obesity is a condition characterized by excess adipose tissue that results from positive energy balance and is the most common metabolic disorder in the industrialized world. The obesity epidemic shows no sign of slowing, and it is increasingly a global problem. Serious clinical problems associated with obesity include an increased risk for type 2 diabetes, atherosclerosis, and cancer. Hence, understanding the origin and development of adipocytes and adipose tissue will be critical to the analysis and treatment of metabolic diseases. Historically, albeit incorrectly, adipocytes were thought to be inert cells whose singular function was lipid storage. It is now known that adipocytes have other critical functions; the most important include sensitivity to insulin and the ability to produce and secrete adipocyte-specific endocrine hormones that regulate energy homeostasis in other tissues. Today, adipocytes are recognized as critical regulators of whole-body metabolism and known to be involved in the pathogenesis of a variety of metabolic diseases. All cells come from other cells and many cells arise from precursor cells. Adipocytes are not created from other adipocytes, but they arise from precursor cells. In the last two decades, scientists have discovered the function of many proteins that influence the ability of precursor cells to become adipocytes. If the expansion of the adipose tissue is the problem, it seems logical that adipocyte development inhibitors could be a viable anti-obesity therapeutic. However, factors that block adipocyte development and limit adipocyte expansion also impair metabolic health. This notion may be counterintuitive, but several lines of evidence support the idea that blocking adipocyte development is unhealthy. For this reason it is clear that we need a better understanding of adipocyte development.
Concepts of neuroendocrine cardiology and neuroendocrine immunology, chemistry and biology of signal molecules
Neurochem Res. 2010 Dec;35(12):2001-17. Epub 2010 Nov 3.
Galoyan A. HKh Buniatian Institute of Biochemistry, NAS RA, 5/1 Sevak Str, Yerevan 0014, Armenia. firstname.lastname@example.org
Abstract Discovery of neurosecretion of cardioactive neurohormones produced by hypothalamic nuclei (NSO and NPV), as well as the biosynthesis of several immunomodulators (signal molecules of the neuroendocrine immune system of brain), deciphering of their chemical structure and study of their biological properties led to the foundation of two important trends of neurobiology: neuroendocrine immunology and cardiology. Hormone formation by atrium ganglionary nerve cells and auriculum establishment of neurohumoral interactions between hypothalamic and atrium neurosecretion indicated the existence of the system neuroendocrine hypothalamus--endocrine heart. Study of their biological properties promoted creation of powerful neurohormonal preparations for the treatment of immune, cardio-vascular, neurodegenerative, infectious and tumor diseases. Concepts suggested by us on neuroendocrine cardiology and immunology, create large perspectives for development of the theory and its implementation in medicine. PMID 21042849
17928643 12631561, 12831171
Neuroendocrine cells in the developing human lung: morphologic and functional considerations
Pediatr Pulmonol. 1985 May-Jun;1(3 Suppl):S21-9.
Cutz E, Gillan JE, Bryan AC.
The structure, distribution, and frequency of neuroendocrine (NE) cells in human fetal lung from early stages of development to term are described. Neuroendocrine cells were studied by electron microscopy and immunostaining for serotonin and bombesin, recently identified markers of these cells in human lung. The differentiation of NE cells within the airway epithelium proceeded centrifugally and followed the development of the bronchial tree. The first NE cells, identified at 8 weeks' gestation, appeared well-differentiated compared with adjacent epithelial cells, and were immunoreactive for serotonin. The first bombesin-immunoreactive cells were detected at 10 weeks' gestation. Fetal lungs from midgestation contained several ultrastructurally distinct NE cell types, distributed singly and in groups. Serotonin-immunoreactive cells were more frequent during early stages of development and were predominantly located in larger airways. Bombesin-immunoreactive cells became more numerous towards term and were concentrated in small peripheral airways. The well-differentiated appearance and large number of NE cells in fetal lung, and their increase in number towards term, suggest an important role for these cells during intrauterine life and neonatal adaptation. Whether this role involves neurohormonal regulation of fetal-neonatal pulmonary circulation or local (paracrine) or endocrine function requires further investigation.
Neuroendocrinelike (small granule) epithelial cells of the lung
Environ Health Perspect. 1984 Apr;55:271-95.
DiAugustine RP, Sonstegard KS.
The presence of neuroendocrinelike epithelial cells in the lung of numerous species has been demonstrated by light and electron microscopy. Histochemical methods used to identify these cells have included staining with silver, amine-type fluorescence (APUD cell), periodic acid Schiff (PAS)-lead hematoxylin, and immunohistochemical localization of neuron-specific enolase. Cytoplasmic dense core vesicles (70-200 nm in diameter) have served as the major ultrastructural characteristic. Lung neuroendocrinelike cells have been shown to occur in fetal and adult mammals as solitary-type cells or as distinct organoids known as neuroepithelial bodies ( NEBs ). Although the frequency of both populations is considered low, solitary-type cells with dense-core granules can be found in as high as 5% of epithelial cells in the cricoid region of the guinea-pig larynx. The solitary cells can be found throughout the airways of mammals, whereas the NEBs are confined to the intrapulmonary airways. Unmyelinated fibers have been traced from the lamina propria and into the NEB, where they ramified between the component cells of the NEB. The function of lung neuroendocrinelike cells is not known, but morphological and cytochemical studies suggest that the NEBs are intrapulmonary chemoreceptors that can respond to changes in airway gas composition. Hypoxia or hypercapnia has been shown to decrease the amine cytofluorescence in these organoids and apparently to increase the exocytosis of dense core vesicles from the basal region of the cell. Immunohistochemical studies have suggested that some lung epithelial cells may contain a known neuropeptide(s), but further investigation is needed to confirm the presence of such compounds in lung neuroendocrinelike cells and their physiochemical properties. Apparent hyperplasia of lung neuroendocrinelike cells can occur readily in hamsters treated with diethylnitrosamine. It has been postulated that human lung tumors with endocrinelike properties, namely, bronchial carcinoids and lung small cell carcinomas, may originate from lung neuroendocrinelike cells. However, a more plausible explanation, based on cytokinetic studies of epithelial neuroendocrinelike cells in the lung and other organs, is that these cells originate from a nonneuroendocrine population. Interaction of such a progenitor cell population with selected carcinogens may lead to stimulation of the rate of normal differentiation or, alternately, to selection of an abnormal route of differentiation that possesses a neuroendocrine phenotype.
Copyright: Reproduced with permission from Environmental Health Perspectives (EHP) is a publication of the U.S. Government. Publication of EHP lies in the public domain and is therefore without copyright.
Neuroendocrine cells of the lung. An overview of morphologic characteristics and development
Exp Lung Res. 1982 Nov;3(3-4):185-208.
The detailed morphology of pulmonary neuroendocrine (NE) cells has been defined only during the last decade. The purpose of this paper is to review the main morphologic features of the NE cells, to review the methods and techniques used for their identification, and to discuss the development and functional significance of these cells. The main emphasis is on NE cells in human lung, but where appropriate, studies in animal lungs are also included. NE cells are present in the airway epithelium of human and various animal species and occur singly as well as in clusters called neuroepithelial bodies (NEB). The general cytochemical features (common to both single NE cells and NEB) include cytoplasmic argyrophilia, fluorogenic amine content, positive staining with lead-hematoxylin, and masked metachromasia. These staining properties are similar to those found in APUD cells scattered in various tissues. More specific cell markers are immunoreactivity to peptide hormones (bombesin, calcitonin, leu-enkephalin) identified so far in NE cells of human lung, and immunoreactivity to serotonin found in both human and animal lungs. At the ultrastructural level, NE cells are characterized by the presence of cytoplasmic dense core granules (90-150 nm in diameter), which are considered the storage site of amine and peptide hormones. The distinctive feature of NEB, not found with single NE cells, is the presence of nonmyelinated nerve endings in contact with granulated cells, and positive staining for acetylcholinesterase. The single NE cells are scattered throughout the tracheobronchial epithelium, whereas NEB are found only within the intrapulmonary airways. In postnatal lungs, both the single NE cells and NEB appear concentrated in small peripheral airways. In developing human lung, the first NE cells appear at 8 weeks' gestation, when all other epithelial cells are still undifferentiated. The development and cytodifferentiation of NE cells progresses in a centrifugal direction. By the end of the glandular period, single and groups of NE cells are found along the entire length of primitive bronchial epithelium. Based on differences in the size and morphology of cytoplasmic granules, three distinct types of NE cells can be recognized. During terminal stages of development, NE cells appear in small peripheral airways and primitive saccules. The functional considerations include the possible role of NE cells as endocrine, paracrine, or receptosecretory cells involved in neurohormonal regulation of pulmonary vascular or bronchial responses, and possible function of NEB as intrapulmonary hypoxia-sensitive chemoreceptors. PMID 6188605