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  1. Article ; Online: The wide reach of fatty acids and their metabolites.

    Boeldt, Derek S / Joss-Moore, Lisa

    Molecular and cellular endocrinology

    2022  Volume 560, Page(s) 111823

    MeSH term(s) Fatty Acids/metabolism ; Fatty Acids, Omega-3
    Chemical Substances Fatty Acids ; Fatty Acids, Omega-3
    Language English
    Publishing date 2022-11-18
    Publishing country Ireland
    Document type Editorial
    ZDB-ID 187438-x
    ISSN 1872-8057 ; 0303-7207
    ISSN (online) 1872-8057
    ISSN 0303-7207
    DOI 10.1016/j.mce.2022.111823
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  2. Article ; Online: Perinatal Research Society's Young Investigator Workshop Prepares the Next Generation of Investigators.

    Joss-Moore, Lisa A / Lane, Robert H / Rozance, Paul J / Bird, Ian / Albertine, Kurt H

    Reproductive sciences (Thousand Oaks, Calif.)

    2022  Volume 29, Issue 4, Page(s) 1271–1277

    Abstract: Sustaining impactful research within the field of perinatal biology requires training and retention of the next generations of physician-scientists and basic-scientists. Professional societies such as the Perinatal Research Society (PRS) have a unique ... ...

    Abstract Sustaining impactful research within the field of perinatal biology requires training and retention of the next generations of physician-scientists and basic-scientists. Professional societies such as the Perinatal Research Society (PRS) have a unique role to play in training and retention of perinatal biologists. Here we report outcomes for an innovative Young Investigator Training Workshop created for the PRS. The PRS Workshop uses immersive, active-writing, and active-oral presentation design, with one-on-one feedback from NIH-funded faculty-mentors drawn from the PRS membership. Young investigator data were collected by anonymous surveys of young investigators, NIH RePORTER, and individual young investigator follow-up. Ninety-seven young investigators attended the Workshops over the period 2013-2018. Young investigators were physician- (73%) and PhD- (27%) scientists at the rank of clinical fellow/postdoctoral fellow (27%) or instructor/assistant professor (73%). Participation by underrepresented minority (URM) young investigators was 14%. Young investigators received NIH and non-NIH funding, with 80% of young investigators receiving new funding since the Workshop that they attended. NIH funding was received by 31% of young investigators in the form of K-series awards, R01 equivalents, and other NIH awards. In conclusion, our PRS young investigator Workshop serves as a model to facilitate training of emerging physician- and basic-scientists by scientific societies.
    MeSH term(s) Biomedical Research ; Humans ; Mentors ; Research Personnel ; United States
    Language English
    Publishing date 2022-01-12
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2276411-2
    ISSN 1933-7205 ; 1933-7191
    ISSN (online) 1933-7205
    ISSN 1933-7191
    DOI 10.1007/s43032-021-00836-4
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    Zs.A 4113: Show issues Location:
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  3. Article ; Online: Antenatal Steroids and Cord Blood T-cell Glucocorticoid Receptor DNA Methylation and Exon 1 Splicing.

    Carpenter, Jeanette R / Jablonski, Kathleen A / Koncinsky, Jordan / Varner, Michael W / Gyamfi-Bannerman, Cynthia / Joss-Moore, Lisa A

    Reproductive sciences (Thousand Oaks, Calif.)

    2022  Volume 29, Issue 5, Page(s) 1513–1523

    Abstract: Antenatal administration of glucocorticoids such as betamethasone (BMZ) during the late preterm period improves neonatal respiratory outcomes. However, glucocorticoids may elicit programming effects on immune function and gene regulation. Here, we test ... ...

    Abstract Antenatal administration of glucocorticoids such as betamethasone (BMZ) during the late preterm period improves neonatal respiratory outcomes. However, glucocorticoids may elicit programming effects on immune function and gene regulation. Here, we test the hypothesis that exposure to antenatal BMZ alters cord blood immune cell composition in association with altered DNA methylation and alternatively expressed Exon 1 transcripts of the glucocorticoid receptor (GR) gene in cord blood CD4
    MeSH term(s) Betamethasone ; DNA Methylation ; Exons ; Female ; Fetal Blood/metabolism ; Glucocorticoids/pharmacology ; Humans ; Infant, Newborn ; Pregnancy ; Premature Birth/metabolism ; Receptors, Glucocorticoid/genetics ; Receptors, Glucocorticoid/metabolism
    Chemical Substances Glucocorticoids ; Receptors, Glucocorticoid ; Betamethasone (9842X06Q6M)
    Language English
    Publishing date 2022-02-10
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 2276411-2
    ISSN 1933-7205 ; 1933-7191
    ISSN (online) 1933-7205
    ISSN 1933-7191
    DOI 10.1007/s43032-022-00859-5
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  4. Article ; Online: Postnatal growth restriction impairs rat lung structure and function.

    Zhao, James / Ballard, Craig / Cohen, Adrienne J / Ringham, Ben / Zhao, Brooke / Wang, Haimei / Zuspan, Katie / Rebentisch, Andrew / Locklear, Brent A / Dahl, MarJanna / Maschek, J Alan / Cox, James E / Joss-Moore, Lisa A

    Anatomical record (Hoboken, N.J. : 2007)

    2023  

    Abstract: The negative impact of nutritional deficits in the development of bronchopulmonary dysplasia is well recognized, yet mechanisms by which nutrition alters lung outcomes and nutritional strategies that optimize development and protect the lung remain ... ...

    Abstract The negative impact of nutritional deficits in the development of bronchopulmonary dysplasia is well recognized, yet mechanisms by which nutrition alters lung outcomes and nutritional strategies that optimize development and protect the lung remain elusive. Here, we use a rat model to assess the isolated effects of postnatal nutrition on lung structural development without concomitant lung injury. We hypothesize that postnatal growth restriction (PGR) impairs lung structure and function, critical mediators of lung development, and fatty acid profiles at postnatal day 21 in the rat. Rat pups were cross-fostered at birth to rat dams with litter sizes of 8 (control) or 16 (PGR). Lung structure and function, as well as serum and lung tissue fatty acids, and lung molecular mediators of development, were measured. Male and female PGR rat pups had thicker airspace walls, decreased lung compliance, and increased tissue damping. Male rats also had increased lung elastance, increased lung elastin protein abundance, and lysol oxidase expression, and increased elastic fiber deposition. Female rat lungs had increased conducting airway resistance and reduced levels of docosahexaenoic acid in lung tissue. We conclude that PGR impairs lung structure and function in both male and female rats, with sex-divergent changes in lung molecular mediators of development.
    Language English
    Publishing date 2023-07-28
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2269667-2
    ISSN 1932-8494 ; 1932-8486
    ISSN (online) 1932-8494
    ISSN 1932-8486
    DOI 10.1002/ar.25297
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  5. Article ; Online: A Pediatric Department's Innovative Grant Writing Workshops.

    Joss-Moore, Lisa A / Keenan, Heather T / Bale, James F / Dean, J Michael / Albertine, Kurt H

    The Journal of pediatrics

    2018  Volume 197, Page(s) 5–7.e1

    MeSH term(s) Female ; Financing, Organized ; Hospital Departments ; Humans ; Male ; Pediatrics/education ; Physicians ; Staff Development/methods ; Writing
    Language English
    Publishing date 2018-05-22
    Publishing country United States
    Document type Editorial
    ZDB-ID 3102-1
    ISSN 1097-6833 ; 0022-3476
    ISSN (online) 1097-6833
    ISSN 0022-3476
    DOI 10.1016/j.jpeds.2018.02.060
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  6. Article ; Online: Uteroplacental Insufficiency with Hypoxia Upregulates Placental PPARγ-KMT5A Axis in the Rat.

    Barrett, Emily / Loverin, Amy / Wang, Haimei / Carlson, Michelle / Larsen, Tricia D / Almeida, Mariana M / Whitman, Jenna / Baack, Michelle L / Joss-Moore, Lisa A

    Reproductive sciences (Thousand Oaks, Calif.)

    2021  Volume 28, Issue 5, Page(s) 1476–1488

    Abstract: The placenta represents a critical node in fetal lipid acquisition, yet the mechanisms by which the placenta handles lipids under normal and pathologic conditions are incompletely understood. A key player in placental lipid handling is peroxisome ... ...

    Abstract The placenta represents a critical node in fetal lipid acquisition, yet the mechanisms by which the placenta handles lipids under normal and pathologic conditions are incompletely understood. A key player in placental lipid handling is peroxisome proliferator-activated receptor gamma (PPARγ). PPARγ influences global gene expression via its regulation of the epigenetic modifier lysine methyltransferase 5A (KMT5A), which places a methyl group on histone 4 lysine 20 (H4K20me) of target genes. Here we test the hypothesis that KMT5A is present in both the human and rat placentas and is affected by uteroplacental insufficiency (UPI) in the rat in association with increased placental lipid accumulation. We assessed levels and localization of KMT5A, as well as lipid droplet accumulation, in human placental tissue collected from maternal donors after delivery by planned cesarean section. Using a rat model of UPI, we also evaluated the effects of UPI on lipid accumulation, PPARγ, KMT5A, and H4K20me in the rat placenta. In this study, we show for the first time the presence and activity of KMT5A, in human and in rat placentas. We also demonstrate that in the rat placenta, UPI increases hypoxia, KMT5a expression, and activity in association with increased lipid accumulation in placenta supporting male fetuses. Placental PPARγ-KMT5A axis may be an important mediator of placental lipid handling.
    MeSH term(s) Animals ; Disease Models, Animal ; Female ; Humans ; Hypoxia/metabolism ; Lipid Accumulation Product ; Methyltransferases/metabolism ; PPAR gamma/metabolism ; Placenta Diseases/metabolism ; Pregnancy ; Rats, Sprague-Dawley ; Signal Transduction ; Up-Regulation ; Uterine Diseases/metabolism ; Rats
    Chemical Substances PPAR gamma ; PPAR gamma, rat ; Methyltransferases (EC 2.1.1.-)
    Language English
    Publishing date 2021-01-04
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 2276411-2
    ISSN 1933-7205 ; 1933-7191
    ISSN (online) 1933-7205
    ISSN 1933-7191
    DOI 10.1007/s43032-020-00434-w
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  7. Article ; Online: Epigenetics and the developmental origins of disease: the key to unlocking the door of personalized medicine.

    Joss-Moore, Lisa A / Lane, Robert H

    Epigenomics

    2012  Volume 4, Issue 5, Page(s) 471–473

    MeSH term(s) Biomarkers/analysis ; DNA Methylation ; Environmental Exposure/adverse effects ; Epigenesis, Genetic ; Female ; Genetic Predisposition to Disease ; Humans ; Precision Medicine ; Pregnancy ; Prenatal Exposure Delayed Effects/genetics ; Prenatal Exposure Delayed Effects/pathology
    Chemical Substances Biomarkers
    Language English
    Publishing date 2012-10
    Publishing country England
    Document type Editorial ; Research Support, N.I.H., Extramural
    ISSN 1750-192X
    ISSN (online) 1750-192X
    DOI 10.2217/epi.12.53
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  8. Article ; Online: Epigenetic contributions to the developmental origins of adult lung disease.

    Joss-Moore, Lisa A / Lane, Robert H / Albertine, Kurt H

    Biochemistry and cell biology = Biochimie et biologie cellulaire

    2014  Volume 93, Issue 2, Page(s) 119–127

    Abstract: Perinatal insults, including intrauterine growth restriction, preterm birth, maternal exposure to toxins, or dietary deficiencies produce deviations in the epigenome of lung cells. Occurrence of perinatal insults often coincides with the final stages of ... ...

    Abstract Perinatal insults, including intrauterine growth restriction, preterm birth, maternal exposure to toxins, or dietary deficiencies produce deviations in the epigenome of lung cells. Occurrence of perinatal insults often coincides with the final stages of lung development. The result of epigenome disruptions in response to perinatal insults during lung development may be long-term structural and functional impairment of the lung and development of lung disease. Understanding the contribution of epigenetic mechanisms to life-long lung disease following perinatal insults is the focus of the developmental origins of adult lung disease field. DNA methylation, histone modifications, and microRNA changes are all observed in various forms of lung disease. However, the perinatal contribution to such epigenetic mechanisms is poorly understood. Here we discuss the developmental origins of adult lung disease, the interplay between perinatal events, lung development and disease, and the role that epigenetic mechanisms play in connecting these events.
    MeSH term(s) Adult ; Animals ; DNA Methylation/genetics ; Disease Models, Animal ; Epigenesis, Genetic ; Female ; Gene Expression Regulation, Developmental ; Histones/genetics ; Humans ; Lung/embryology ; Lung Diseases/embryology ; Male ; Mice ; MicroRNAs/genetics ; Pregnancy ; Rats ; Sheep
    Chemical Substances Histones ; MicroRNAs
    Language English
    Publishing date 2014-10-13
    Publishing country Canada
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 54104-7
    ISSN 1208-6002 ; 0829-8211
    ISSN (online) 1208-6002
    ISSN 0829-8211
    DOI 10.1139/bcb-2014-0093
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  9. Article ; Online: Maternal Tobacco Smoke Exposure Causes Sex-Divergent Changes in Placental Lipid Metabolism in the Rat.

    Weinheimer, Claudia / Wang, Haimei / Comstock, Jessica M / Singh, Purneet / Wang, Zhengming / Locklear, Brent A / Goodwin, Kasi L / Maschek, J Alan / Cox, James E / Baack, Michelle L / Joss-Moore, Lisa A

    Reproductive sciences (Thousand Oaks, Calif.)

    2020  Volume 27, Issue 2, Page(s) 631–643

    Abstract: Maternal tobacco smoke exposure (MTS) affects fetal acquisition of long-chain polyunsaturated fatty acids (LCPUFA) and increases the risk of obesity and cardio-metabolic disease in the offspring. Alterations in fetal LCPUFA acquisition in maternal ... ...

    Abstract Maternal tobacco smoke exposure (MTS) affects fetal acquisition of long-chain polyunsaturated fatty acids (LCPUFA) and increases the risk of obesity and cardio-metabolic disease in the offspring. Alterations in fetal LCPUFA acquisition in maternal smoking are mediated by the placenta. The handling of LCPUFA by the placenta involves protein-mediated transfer and storage. Molecular mediators of placental LCPUFA handling include PPARγ and the fatty acid transport proteins. We previously demonstrated, in a rat model, that MTS results in programming of adult-onset obesity and metabolic disease in male, but not female, offspring. In this study, we test the hypothesis that in utero MTS exposure alters placental structure, placental LCPUFA handling, and fetal fatty acid levels, in a sex-divergent manner. We exposed pregnant rats to tobacco smoke from embryonic day 11 to term gestation. We measured placental and fetal fatty acid profiles, the systolic/diastolic ratio (SD ratio), placental histology, and expression of molecular mediators in the placenta. Our primary finding is that MTS alters fatty acid profiles in male, but not female fetuses and placenta, including increasing the ratio of omega-6 to omega-3 fatty acids. MTS also increased SD ratio in male, but not female placenta. In contrast, the expression of PPARγ and FATPs was upregulated in female, but not male placenta. We conclude that MTS causes sex-divergent changes in placental handling of LCPUFA in the rat. We speculate that our results demonstrate an adaptive response to MTS by the female placenta.
    MeSH term(s) Animals ; Estradiol/metabolism ; Estriol/metabolism ; Female ; Lipid Metabolism/drug effects ; Male ; Maternal Exposure/adverse effects ; PPAR gamma/metabolism ; Placenta/drug effects ; Placenta/metabolism ; Placenta/pathology ; Pregnancy ; Rats, Sprague-Dawley ; Sex Factors ; Nicotiana/toxicity
    Chemical Substances PPAR gamma ; Estradiol (4TI98Z838E) ; Estriol (FB33469R8E)
    Language English
    Publishing date 2020-01-06
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2276411-2
    ISSN 1933-7205 ; 1933-7191
    ISSN (online) 1933-7205
    ISSN 1933-7191
    DOI 10.1007/s43032-019-00065-w
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  10. Article ; Online: Maternal high-fat diet up-regulates type-1 cannabinoid receptor with estrogen signaling changes in a sex- and depot- specific manner in white adipose tissue of adult rat offspring.

    de Almeida, Mariana Macedo / Dias-Rocha, Camilla P / Reis-Gomes, Clara F / Wang, Haimei / Cordeiro, Aline / Pazos-Moura, Carmen C / Joss-Moore, Lisa / Trevenzoli, Isis H

    European journal of nutrition

    2020  Volume 60, Issue 3, Page(s) 1313–1326

    Abstract: Purpose: Obesity and high-fat (HF) diet are associated with over activation of the endocannabinoid system (ECS). We have demonstrated that maternal HF diet induces early obesity and modulates cannabinoid signaling in visceral (VIS) and subcutaneous (SUB) ...

    Abstract Purpose: Obesity and high-fat (HF) diet are associated with over activation of the endocannabinoid system (ECS). We have demonstrated that maternal HF diet induces early obesity and modulates cannabinoid signaling in visceral (VIS) and subcutaneous (SUB) white adipose tissue (WAT) in weanling rat offspring. We hypothesized that perinatal maternal HF diet would program the expression of ECS in adipose tissue in a long-term way in parallel to alterations in epigenetic markers and sex hormone signaling.
    Methods: Progenitor female rats received control diet (C, 9% fat) or isocaloric high-fat diet (HF, 28% fat) for 8 weeks before mating, gestation, and lactation. All pups were weaned to C diet and they were euthanized at 180 days old.
    Results: Maternal HF diet induced overweight and increased SUB WAT mass of male and female adult offspring. Maternal HF diet induced hypertrophy of VIS and SUB adipocytes only in female offspring associated with increased type 1 cannabinoid receptor protein (CB1) and mRNA (Cnr1) levels. These changes were associated with increased estrogen receptor α binding to Cnr1 promoter in SUB WAT of adult female offspring, which may contribute to higher expression of Cnr1.
    Conclusion: Increased CB1 signaling in adipose tissue might contribute to higher adiposity programmed by maternal HF diet because endocannabinoids stimulate the accumulation of fat in the adipose tissue. Our findings provide molecular insights into sex-specific targets for anti-obesity therapies based on the endocannabinoid system.
    MeSH term(s) Adipose Tissue/metabolism ; Adipose Tissue, White/metabolism ; Adiposity ; Animals ; Diet, High-Fat/adverse effects ; Estrogens ; Female ; Male ; Maternal Nutritional Physiological Phenomena ; Pregnancy ; Rats ; Receptors, Cannabinoid/metabolism
    Chemical Substances Estrogens ; Receptors, Cannabinoid
    Language English
    Publishing date 2020-07-15
    Publishing country Germany
    Document type Journal Article
    ZDB-ID 1466536-0
    ISSN 1436-6215 ; 1436-6207
    ISSN (online) 1436-6215
    ISSN 1436-6207
    DOI 10.1007/s00394-020-02318-w
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