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2. Adipo-glial signaling mediates metabolic adaptation in peripheral nerve regeneration

Author

Sundaram, Venkat Krishnan, Schütza, Vlad, Schröter, Nele H., Backhaus, Aline, Bilsing, Annika, Joneck, Lisa, Seelbach, Anna, Mutschler, Clara, Gomez-Sanchez, Jose A., Schäffner, Erik, Sánchez, Eva Ernst, Akkermann, Dagmar, Paul, Christina, Schwagarus, Nancy, Müller, Silvana, Odle, Angela, Childs, Gwen, Ewers, David, Kungl, Theresa, Sitte, Maren, Salinas, Gabriela, Sereda, Michael W., Nave, Klaus-Armin, Schwab, Markus H., Ost, Mario, Arthur-Farraj, Peter, Stassart, Ruth M., and Fledrich, Robert

Published
2023
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5. Anterior Pituitary Transcriptomics Following a High-Fat Diet: Impact of Oxidative Stress on Cell Metabolism

Author

Miles, Tiffany K, primary, Odle, Angela K, additional, Byrum, Stephanie D, additional, Lagasse, Alex, additional, Haney, Anessa, additional, Ortega, Victoria G, additional, Bolen, Cole R, additional, Banik, Jewel, additional, Reddick, Milla M, additional, Herdman, Ashley, additional, MacNicol, Melanie C, additional, MacNicol, Angus M, additional, and Childs, Gwen V, additional

Published
2023
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8. Partial Leptin Reduction as an Insulin Sensitization and Weight Loss Strategy

Author

Zhao, Shangang, Zhu, Yi, Schultz, Robbie D., Li, Na, He, Zhenyan, Zhang, Zhuzhen, Caron, Alexandre, Zhu, Qingzhang, Sun, Kai, Xiong, Wei, Deng, Hui, Sun, Jia, Deng, Yingfeng, Kim, Min, Lee, Charlotte E., Gordillo, Ruth, Liu, Tiemin, Odle, Angela K., Childs, Gwen V., Zhang, Ningyan, Kusminski, Christine M., Elmquist, Joel K., Williams, Kevin W., An, Zhiqiang, and Scherer, Philipp E.

Published
2019
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9. Anterior Pituitary Transcriptomics Following a High-Fat Diet: Impact of Oxidative Stress on Cell Metabolism.

Author

Miles, Tiffany K, Odle, Angela K, Byrum, Stephanie D, Lagasse, Alex, Haney, Anessa, Ortega, Victoria G, Bolen, Cole R, Banik, Jewel, Reddick, Milla M, Herdman, Ashley, MacNicol, Melanie C, MacNicol, Angus M, and Childs, Gwen V

Subjects
PITUITARY cancer, OXIDATIVE stress, CELL metabolism
Abstract

Anterior pituitary cell function requires a high level of protein synthesis and secretion which depend heavily on mitochondrial adenosine triphosphate production and functional endoplasmic reticula. Obesity adds stress to tissues, requiring them to adapt to inflammation and oxidative stress, and adding to their allostatic load. We hypothesized that pituitary function is vulnerable to the stress of obesity. Here, we utilized a 10- to 15-week high-fat diet (HFD, 60%) in a thermoneutral environment to promote obesity, testing both male and female FVB.129P mice. We quantified serum hormones and cytokines, characterized the metabolic phenotype, and defined changes in the pituitary transcriptome using single-cell RNA-sequencing analysis. Weight gain was significant by 3 weeks in HFD mice, and by 10 weeks all HFD groups had gained 20 g. HFD females (15 weeks) had increased energy expenditure and decreased activity. All HFD groups showed increases in serum leptin and decreases in adiponectin. HFD caused increased inflammatory markers: interleukin-6, resistin, monocyte chemoattractant protein-1, and tumor necrosis factorα. HFD males and females also had increased insulin and increased TSH, and HFD females had decreased serum prolactin and growth hormone pulse amplitude. Pituitary single-cell transcriptomics revealed modest or no changes in pituitary cell gene expression from HFD males after 10 or 15 weeks or from HFD females after 10 weeks. However, HFD females (15 weeks) showed significant numbers of differentially expressed genes in lactotropes and pituitary stem cells. Collectively, these studies reveal that pituitary cells from males appear to be more resilient to the oxidative stress of obesity than females and identify the most vulnerable pituitary cell populations in females. [ABSTRACT FROM AUTHOR]

Published
2024
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10. Maternal undernutrition results in transcript changes in male offspring that may promote resistance to high fat diet induced weight gain.

Author

Miles, Tiffany K., Allensworth-James, Melody L., Odle, Angela K., Moreira, Ana Rita Silva, Haney, Anessa C., LaGasse, Alex N., Gies, Allen J., Byrum, Stephanie D., Riojas, Angelica M., MacNicol, Melanie C., MacNicol, Angus M., and Childs, Gwen V.

Subjects
WEIGHT gain, HIGH-fat diet, NON-alcoholic fatty liver disease, MATERNAL nutrition, EMBRYOLOGY, MALNUTRITION, LOW-calorie diet
Abstract

Maternal nutrition during embryonic development and lactation influences multiple aspects of offspring health. Using mice, this study investigates the effects of maternal caloric restriction (CR) during mid-gestation and lactation on offspring neonatal development and on adult metabolic function when challenged by a high fat diet (HFD). The CR maternal model produced male and female offspring that were significantly smaller, in terms of weight and length, and females had delayed puberty. Adult offspring born to CR dams had a sexually dimorphic response to the high fat diet. Compared to offspring of maternal control dams, adult female, but not male, CR offspring gained more weight in response to high fat diet at 10 weeks. In adipose tissue of male HFD offspring, maternal undernutrition resulted in blunted expression of genes associated with weight gain and increased expression of genes that protect against weight gain. Regardless of maternal nutrition status, HFD male offspring showed increased expression of genes associated with progression toward nonalcoholic fatty liver disease (NAFLD). Furthermore, we observed significant, sexually dimorphic differences in serum TSH. These data reveal tissue- and sex-specific changes in gene and hormone regulation following mild maternal undernutrition, which may offer protection against diet induced weight gain in adult male offspring. [ABSTRACT FROM AUTHOR]

Published
2024
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11. Musashi exerts control of gonadotrope target mRNA translation during the mouse estrous cycle

Author

Moreira, Ana Rita Silva, primary, Lim, Juchan, additional, Urbaniak, Alicja, additional, Banik, Jewel, additional, Bronson, Katherine, additional, Lagasse, Alex, additional, Hardy, Linda, additional, Haney, Anessa, additional, Allensworth, Melody, additional, Miles, Tiffany K, additional, Gies, Allen, additional, Byrum, Stephanie D, additional, Wilczynska, Ania, additional, Boehm, Ulrich, additional, Kharas, Michael, additional, Lengner, Christopher, additional, MacNicol, Melanie C, additional, Childs, Gwen V, additional, MacNicol, Angus M, additional, and Odle, Angela K, additional

Published
2023
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15. Leptin: A Metabolic Signal for the Differentiation of Pituitary Cells

Author

V., Childs, Gwen, K., Odle, Angela, C., MacNicol, Melanie, L., Allensworth-James, Melody, K., Miles, Tiffany, Noor, Akhter, M., Syed, hsin, and M., cNicol, Angus

Subjects
hormones, hormone substitutes, and hormone antagonists
Abstract

Pituitary cell function is impacted by metabolic states and therefore must receive signals that inform them about nutritional status or adiposity. A primary signal from adipocytes is leptin, which recent studies have shown regulates most pituitary cell types. Subsets of all pituitary cell types express leptin receptors and leptin has been shown to exert transcriptional control through classical JAK/STAT pathways. Recent studies show that leptin also signals through post-transcriptional pathways that involve the translational regulatory protein Musashi. Mechanistically, post-transcriptional control would permit rapid cellular regulation of critical pre-existing pituitary transcripts as energy states change. The chapter will review evidence for transcriptional and/or post-transcriptional regulation of leptin targets (including Gnrhr, activin, Fshb, Gh, Ghrhr, and Pou11f1) and the consequences of the loss of leptin signaling to gonadotrope and somatotrope functions.

Published
2022

18. Chemotherapy induced oxidative stress in the ovary: drug-dependent mechanisms and potential interventions†

Author

Trujillo, Madison, Odle, Angela K, Aykin-Burns, Nukhet, and Allen, Antiño R

Abstract

Cancer incidence and relative survival are expected to increase over the next few decades. With the majority of patients receiving combinatorial chemotherapy, an increasing proportion of patients experience long-term side effects from treatment—including reproductive disorders and infertility. A limited number of studies have examined mechanisms of single-agent chemotherapy-induced gonadotoxicity, with chemotherapy-induced oxidative stress being implicated in the loss of reproductive functions. Current methods of female fertility preservation are costly, invasive, only moderately successful, and seldom presented to cancer patients. The potential of antioxidants to alleviate chemotherapy has been overlooked at a time when it is becoming increasingly important to develop strategies to protect reproductive functions during chemotherapy. This review will summarize the importance of reactive oxygen species homeostasis in reproduction, chemotherapy-induced mitochondrial dysfunction in oocytes, chemotherapy-induced oxidative stress, and several promising natural adjuvants.Chemotherapy-induced oxidative stress has long-lasting and devastating impacts on female fertility and reproduction; while there is a devastating lack of affordable and effective interventions available, antioxidants are potential adjuvants.Graphical AbstractFigure prepared using BioRender.com

Published
2023
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27. Control of the Anterior Pituitary Cell Lineage Regulator POU1F1 by the Stem Cell Determinant Musashi

Author

Allensworth-James, Melody, primary, Banik, Jewel, additional, Odle, Angela, additional, Hardy, Linda, additional, Lagasse, Alex, additional, Moreira, Ana Rita Silva, additional, Bird, Jordan, additional, Thomas, Christian L, additional, Avaritt, Nathan, additional, Kharas, Michael G, additional, Lengner, Christopher J, additional, Byrum, Stephanie D, additional, MacNicol, Melanie C, additional, Childs, Gwen V, additional, and MacNicol, Angus M, additional

Published
2020
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38. SAT-298 Integrative Single-Cell Transcriptomic and Epigenomic Landscape of Mouse Anterior Pituitary Cell Types

Author

Ruf-Zamojski, Frederique Murielle, primary, Zamojski, Michel A, primary, Nudelman, German, primary, Ge, Yongchao, primary, Mendelev, Natalia, primary, Smith, Gregory R, primary, Zhou, Xiang, primary, Toufaily, Chirine, primary, Schang, Gauthier, primary, Gambino, Luisina Ongaro, primary, Liu, Hanqing, primary, Gomez Castanon, Rosa G, primary, Moriwaki, Mika, primary, Nair, Venugopalan, primary, Pincas, Hanna, primary, Nery, Joseph R, primary, Bartlett, Anna, primary, Alridge, Andrew, primary, Odle, Angela Katherine, primary, Childs, Gwen V, primary, Turgeon, Judith L, primary, Welt, Corrine Kolka, primary, Ecker, Joseph R, primary, Bernard, Daniel J, primary, and Sealfon, Stuart C, primary

Published
2020
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40. SAT-284 Musashi Exerts Translational Control Within Anterior Pituitary Cells of the POU1F1 Lineage

Author

Allensworth, Melody Lyn, primary, Odle, Angela Katherine, primary, Moreira, Ana Rita Silva, primary, Lim, Juchan, primary, Banik, Jewel, primary, Haney, Anessa, primary, Lagasse, Alex, primary, Hardy, Linda, primary, Byrum, Stephanie, primary, Avaritt, Nathan, primary, MacNicol, Melanie C, primary, Childs, Gwen V, primary, and MacNicol, Angus M, primary

Published
2020
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41. SAT-292 Musashi: A Novel Regulator of the Gonadotrope Transcriptome

Author

Moreira, Ana Rita Silva, primary, Lagasse, Alexandra N, primary, Haney, Anessa C, primary, Avaritt, Nathan, primary, Byrum, Stephanie, primary, Boehm, Ulrich, primary, Kharas, Michael G, primary, Lengner, Christopher J, primary, MacNicol, Melanie C, primary, Childs, Gwen V, primary, MacNicol, Angus M, primary, and Odle, Angela Katherine, primary

Published
2020
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48. Control of the Anterior Pituitary Cell Lineage Regulator POU1F1 by the Stem Cell Determinant Musashi.

Author

Allensworth-James, Melody, Banik, Jewel, Odle, Angela, Hardy, Linda, Lagasse, Alex, Moreira, Ana Rita Silva, Bird, Jordan, Thomas, Christian L, Avaritt, Nathan, Kharas, Michael G, Lengner, Christopher J, Byrum, Stephanie D, MacNicol, Melanie C, Childs, Gwen V, and MacNicol, Angus M

Subjects
STEM cells, LEPTIN receptors, SOMATOTROPIN, NUCLEOTIDE sequence, TRANSCRIPTION factors
Abstract

The adipokine leptin regulates energy homeostasis through ubiquitously expressed leptin receptors. Leptin has a number of major signaling targets in the brain, including cells of the anterior pituitary (AP). We have previously reported that mice lacking leptin receptors in AP somatotropes display growth hormone (GH) deficiency, metabolic dysfunction, and adult-onset obesity. Among other targets, leptin signaling promotes increased levels of the pituitary transcription factor POU1F1, which in turn regulates the specification of somatotrope, lactotrope, and thyrotrope cell lineages within the AP. Leptin's mechanism of action on somatotropes is sex dependent, with females demonstrating posttranscriptional control of Pou1f1 messenger RNA (mRNA) translation. Here, we report that the stem cell marker and mRNA translational control protein, Musashi1, exerts repression of the Pou1f1 mRNA. In female somatotropes, Msi1 mRNA and protein levels are increased in the mouse model that lacks leptin signaling (Gh -CRE Lepr -null), coincident with lack of POU1f1 protein, despite normal levels of Pou1f1 mRNA. Single-cell RNA sequencing of pituitary cells from control female animals indicates that both Msi1 and Pou1f1 mRNAs are expressed in Gh -expressing somatotropes, and immunocytochemistry confirms that Musashi1 protein is present in the somatotrope cell population. We demonstrate that Musashi interacts directly with the Pou1f1 mRNA 3′ untranslated region and exerts translational repression of a Pou1f1 mRNA translation reporter in a leptin-sensitive manner. Musashi immunoprecipitation from whole pituitary reveals coassociated Pou1f1 mRNA. These findings suggest a mechanism in which leptin stimulation is required to reverse Musashi-mediated Pou1f1 mRNA translational control to coordinate AP somatotrope function with metabolic status. [ABSTRACT FROM AUTHOR]

Published
2021
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49. The Importance of Leptin to Reproduction.

Author

Childs, Gwen V, Odle, Angela K, MacNicol, Melanie C, and MacNicol, Angus M

Subjects
LEPTIN, GONADOTROPIN, MESSENGER RNA, GONADOTROPIN releasing hormone, KISSPEPTIN neurons, LUTEINIZING hormone releasing hormone receptors, GROWTH factors
Abstract

A healthy nutritional state is required for all aspects of reproduction and is signaled by the adipokine leptin. Leptin acts in a relatively narrow concentration range: too much or too little will compromise fertility. The leptin signal timing is important to prepubertal development in both sexes. In the brain, leptin acts on ventral premammillary neurons which signal kisspeptin (Kiss1) neurons to stimulate gonadotropin releasing hormone (GnRH) neurons. Suppression of Kiss1 neurons occurs when agouti-related peptide neurons are activated by reduced leptin, because leptin normally suppresses these orexigenic neurons. In the pituitary, leptin stimulates production of GnRH receptors (GnRHRs) and follicle-stimulating hormone at midcycle, by activating pathways that derepress actions of the messenger ribonucleic acid translational regulatory protein Musashi. In females, rising estrogen stimulates a rise in serum leptin, which peaks at midcycle, synchronizing with nocturnal luteinizing hormone pulses. The normal range of serum leptin levels (10-20 ng/mL) along with gonadotropins and growth factors promote ovarian granulosa and theca cell functions and oocyte maturation. In males, the prepubertal rise in leptin promotes testicular development. However, a decline in leptin levels in prepubertal boys reflects inhibition of leptin secretion by rising androgens. In adult males, leptin levels are 10% to 50% of those in females, and high leptin inhibits testicular function. The obesity epidemic has elucidated leptin resistance pathways, with too much leptin in either sex leading to infertility. Under conditions of balanced nutrition, however, the secretion of leptin is timed and regulated within a narrow level range that optimizes its trophic effects. [ABSTRACT FROM AUTHOR]

Published
2021
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