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  1. Article: Vertebrate cardiac regeneration: evolutionary and developmental perspectives.

    Cutie, Stephen / Huang, Guo N

    Cell regeneration (London, England)

    2021  Volume 10, Issue 1, Page(s) 6

    Abstract: Cardiac regeneration is an ancestral trait in vertebrates that is lost both as more recent vertebrate lineages evolved to adapt to new environments and selective pressures, and as members of certain species developmentally progress towards their adult ... ...

    Abstract Cardiac regeneration is an ancestral trait in vertebrates that is lost both as more recent vertebrate lineages evolved to adapt to new environments and selective pressures, and as members of certain species developmentally progress towards their adult forms. While higher vertebrates like humans and rodents resolve cardiac injury with permanent fibrosis and loss of cardiac output as adults, neonates of these same species can fully regenerate heart structure and function after injury - as can adult lower vertebrates like many teleost fish and urodele amphibians. Recent research has elucidated several broad factors hypothesized to contribute to this loss of cardiac regenerative potential both evolutionarily and developmentally: an oxygen-rich environment, vertebrate thermogenesis, a complex adaptive immune system, and cancer risk trade-offs. In this review, we discuss the evidence for these hypotheses as well as the cellular participators and molecular regulators by which they act to govern heart regeneration in vertebrates.
    Language English
    Publishing date 2021-03-01
    Publishing country China
    Document type Journal Article ; Review
    ZDB-ID 2682438-3
    ISSN 2045-9769
    ISSN 2045-9769
    DOI 10.1186/s13619-020-00068-y
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Vertebrate cardiac regeneration

    Stephen Cutie / Guo N. Huang

    Cell Regeneration, Vol 10, Iss 1, Pp 1-

    evolutionary and developmental perspectives

    2021  Volume 10

    Abstract: Abstract Cardiac regeneration is an ancestral trait in vertebrates that is lost both as more recent vertebrate lineages evolved to adapt to new environments and selective pressures, and as members of certain species developmentally progress towards their ...

    Abstract Abstract Cardiac regeneration is an ancestral trait in vertebrates that is lost both as more recent vertebrate lineages evolved to adapt to new environments and selective pressures, and as members of certain species developmentally progress towards their adult forms. While higher vertebrates like humans and rodents resolve cardiac injury with permanent fibrosis and loss of cardiac output as adults, neonates of these same species can fully regenerate heart structure and function after injury – as can adult lower vertebrates like many teleost fish and urodele amphibians. Recent research has elucidated several broad factors hypothesized to contribute to this loss of cardiac regenerative potential both evolutionarily and developmentally: an oxygen-rich environment, vertebrate thermogenesis, a complex adaptive immune system, and cancer risk trade-offs. In this review, we discuss the evidence for these hypotheses as well as the cellular participators and molecular regulators by which they act to govern heart regeneration in vertebrates.
    Keywords Heart ; Regeneration ; Development ; Evolution ; Cardiomyocyte proliferation ; Cell cycle arrest ; Medicine (General) ; R5-920 ; Biology (General) ; QH301-705.5
    Language English
    Publishing date 2021-03-01T00:00:00Z
    Publisher SpringerOpen
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  3. Article: Hormonal control of cardiac regenerative potential.

    Amram, Alexander V / Cutie, Stephen / Huang, Guo N

    Endocrine connections

    2020  Volume 10, Issue 1, Page(s) R25–R35

    Abstract: Research conducted across phylogeny on cardiac regenerative responses following heart injury implicates endocrine signaling as a pivotal regulator of both cardiomyocyte proliferation and heart regeneration. Three prominently studied endocrine factors are ...

    Abstract Research conducted across phylogeny on cardiac regenerative responses following heart injury implicates endocrine signaling as a pivotal regulator of both cardiomyocyte proliferation and heart regeneration. Three prominently studied endocrine factors are thyroid hormone, vitamin D, and glucocorticoids, which canonically regulate gene expression through their respective nuclear receptors thyroid hormone receptor, vitamin D receptor, and glucocorticoid receptor. The main animal model systems of interest include humans, mice, and zebrafish, which vary in cardiac regenerative responses possibly due to the differential onsets and intensities of endocrine signaling levels throughout their embryonic to postnatal organismal development. Zebrafish and lower vertebrates tend to retain robust cardiac regenerative capacity into adulthood while mice and other higher vertebrates experience greatly diminished cardiac regenerative potential in their initial postnatal period that is sustained throughout adulthood. Here, we review recent progress in understanding how these three endocrine signaling pathways regulate cardiomyocyte proliferation and heart regeneration with a particular focus on the controversial findings that may arise from different assays, cellular-context, age, and species. Further investigating the role of each endocrine nuclear receptor in cardiac regeneration from an evolutionary perspective enables comparative studies between species in hopes of extrapolating the findings to novel therapies for human cardiovascular disease.
    Language English
    Publishing date 2020-12-14
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 2668428-7
    ISSN 2049-3614
    ISSN 2049-3614
    DOI 10.1530/EC-20-0503
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: In vitro and in vivo roles of glucocorticoid and vitamin D receptors in the control of neonatal cardiomyocyte proliferative potential.

    Cutie, Stephen / Payumo, Alexander Y / Lunn, Dominic / Huang, Guo N

    Journal of molecular and cellular cardiology

    2020  Volume 142, Page(s) 126–134

    Abstract: Cardiomyocyte (CM) proliferative potential varies considerably across species. While lower vertebrates and neonatal mammals retain robust capacities for CM proliferation, adult mammalian CMs lose proliferative potential due to cell-cycle withdrawal and ... ...

    Abstract Cardiomyocyte (CM) proliferative potential varies considerably across species. While lower vertebrates and neonatal mammals retain robust capacities for CM proliferation, adult mammalian CMs lose proliferative potential due to cell-cycle withdrawal and polyploidization, failing to mount a proliferative response to regenerate lost CMs after cardiac injury. The decline of murine CM proliferative potential occurs in the neonatal period when the endocrine system undergoes drastic changes for adaptation to extrauterine life. We recently demonstrated that thyroid hormone (TH) signaling functions as a primary factor driving CM proliferative potential loss in vertebrates. Whether other hormonal pathways govern this process remains largely unexplored. Here we showed that agonists of glucocorticoid receptor (GR) and vitamin D receptor (VDR) suppressed neonatal CM proliferation. We next examined CM nucleation and proliferation in neonatal mutant mice lacking GR or VDR specifically in CMs, but we observed no difference between mutant and control littermates at postnatal day 14. Additionally, we generated compound mutant mice that lack GR or VDR and express dominant-negative TH receptor alpha in their CMs, and similarly observed no increase in CM proliferative potential compared to dominant-negative TH receptor alpha mice alone. Thus, although GR and VDR activation is sufficient to inhibit CM proliferation, they seem to be dispensable for neonatal CM cell-cycle exit and polyploidization in vivo. In addition, given the recent report that VDR activation in zebrafish promotes CM proliferation and tissue regeneration, our results suggest distinct roles of VDR in zebrafish and rodent CM cell-cycle regulation.
    Language English
    Publishing date 2020-04-11
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 80157-4
    ISSN 1095-8584 ; 0022-2828
    ISSN (online) 1095-8584
    ISSN 0022-2828
    DOI 10.1016/j.yjmcc.2020.04.013
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 426: Show issues Location:
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  5. Article ; Online: Unconventional Functions of Muscles in Planarian Regeneration.

    Cutie, Stephen / Hoang, Alison T / Payumo, Alexander Y / Huang, Guo N

    Developmental cell

    2017  Volume 43, Issue 6, Page(s) 657–658

    Abstract: Muscles are traditionally considered in the context of force generation. Scimone et al. (2017), reporting in Nature, now examine muscles in a developmental setting and find unexpected roles for distinct planarian muscle fibers. The authors show that ... ...

    Abstract Muscles are traditionally considered in the context of force generation. Scimone et al. (2017), reporting in Nature, now examine muscles in a developmental setting and find unexpected roles for distinct planarian muscle fibers. The authors show that muscles provide patterning signals to promote regeneration and guide tissue growth after injury.
    MeSH term(s) Animals ; Body Patterning/physiology ; Cell Differentiation/physiology ; Muscle Fibers, Skeletal/physiology ; Muscles/physiology ; Planarians/physiology ; Regeneration/physiology
    Language English
    Publishing date 2017--18
    Publishing country United States
    Document type Journal Article ; Review ; Comment
    ZDB-ID 2054967-2
    ISSN 1878-1551 ; 1534-5807
    ISSN (online) 1878-1551
    ISSN 1534-5807
    DOI 10.1016/j.devcel.2017.12.006
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 5742: Show issues Location:
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  6. Article ; Online: (with research data) Mutations in different pigmentation genes are associated with parallel melanism in island flycatchers.

    Uy, J Albert C / Cooper, Elizabeth A / Cutie, Stephen / Concannon, Moira R / Poelstra, Jelmer W / Moyle, Robert G / Filardi, Christopher E

    Proceedings. Biological sciences

    2016  Volume 283, Issue 1834

    Abstract: The independent evolution of similar traits across multiple taxa provides some of the most compelling evidence of natural selection. Little is known, however, about the genetic basis of these convergent or parallel traits: are they mediated by identical ... ...

    Abstract The independent evolution of similar traits across multiple taxa provides some of the most compelling evidence of natural selection. Little is known, however, about the genetic basis of these convergent or parallel traits: are they mediated by identical or different mutations in the same genes, or unique mutations in different genes? Using a combination of candidate gene and reduced representation genomic sequencing approaches, we explore the genetic basis of and the evolutionary processes that mediate similar plumage colour shared by isolated populations of the Monarcha castaneiventris flycatcher of the Solomon Islands. A genome-wide association study (GWAS) that explicitly controlled for population structure revealed that mutations in known pigmentation genes are the best predictors of parallel plumage colour. That is, entirely black or melanic birds from one small island share an amino acid substitution in the melanocortin-1 receptor (MC1R), whereas similarly melanic birds from another small island over 100 km away share an amino acid substitution in a predicted binding site of agouti signalling protein (ASIP). A third larger island, which separates the two melanic populations, is inhabited by birds with chestnut bellies that lack the melanic MC1R and ASIP allelic variants. Formal FST outlier tests corroborated the results of the GWAS and suggested that strong, directional selection drives the near fixation of the MC1R and ASIP variants across islands. Our results, therefore, suggest that selection acting on different mutations with large phenotypic effects can drive the evolution of parallel melanism, despite the relatively small population size on islands.
    MeSH term(s) Agouti Signaling Protein/genetics ; Amino Acid Substitution ; Animals ; Feathers/physiology ; Genetic Association Studies ; Islands ; Melanesia ; Mutation ; Pigmentation/genetics ; Receptor, Melanocortin, Type 1/genetics ; Songbirds/genetics
    Chemical Substances Agouti Signaling Protein ; Receptor, Melanocortin, Type 1
    Language English
    Publishing date 2016-07-13
    Publishing country England
    Document type Journal Article ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, Non-U.S. Gov't
    ZDB-ID 209242-6
    ISSN 1471-2954 ; 0080-4649 ; 0962-8452 ; 0950-1193
    ISSN (online) 1471-2954
    ISSN 0080-4649 ; 0962-8452 ; 0950-1193
    DOI 10.1098/rspb.2016.0731
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1364: Show issues Location:
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  7. Article ; Online: Evidence for hormonal control of heart regenerative capacity during endothermy acquisition.

    Hirose, Kentaro / Payumo, Alexander Y / Cutie, Stephen / Hoang, Alison / Zhang, Hao / Guyot, Romain / Lunn, Dominic / Bigley, Rachel B / Yu, Hongyao / Wang, Jiajia / Smith, Megan / Gillett, Ellen / Muroy, Sandra E / Schmid, Tobias / Wilson, Emily / Field, Kenneth A / Reeder, DeeAnn M / Maden, Malcom / Yartsev, Michael M /
    Wolfgang, Michael J / Grützner, Frank / Scanlan, Thomas S / Szweda, Luke I / Buffenstein, Rochelle / Hu, Guang / Flamant, Frederic / Olgin, Jeffrey E / Huang, Guo N

    Science (New York, N.Y.)

    2019  Volume 364, Issue 6436, Page(s) 184–188

    Abstract: Tissue regenerative potential displays striking divergence across phylogeny and ontogeny, but the underlying mechanisms remain enigmatic. Loss of mammalian cardiac regenerative potential correlates with cardiomyocyte cell-cycle arrest and ... ...

    Abstract Tissue regenerative potential displays striking divergence across phylogeny and ontogeny, but the underlying mechanisms remain enigmatic. Loss of mammalian cardiac regenerative potential correlates with cardiomyocyte cell-cycle arrest and polyploidization as well as the development of postnatal endothermy. We reveal that diploid cardiomyocyte abundance across 41 species conforms to Kleiber's law-the ¾-power law scaling of metabolism with bodyweight-and inversely correlates with standard metabolic rate, body temperature, and serum thyroxine level. Inactivation of thyroid hormone signaling reduces mouse cardiomyocyte polyploidization, delays cell-cycle exit, and retains cardiac regenerative potential in adults. Conversely, exogenous thyroid hormones inhibit zebrafish heart regeneration. Thus, our findings suggest that loss of heart regenerative capacity in adult mammals is triggered by increasing thyroid hormones and may be a trade-off for the acquisition of endothermy.
    MeSH term(s) Animals ; Body Temperature Regulation ; Cell Cycle Checkpoints ; Cell Proliferation ; Diploidy ; Heart/physiology ; Mice ; Myocytes, Cardiac/classification ; Myocytes, Cardiac/physiology ; Phylogeny ; Polyploidy ; Receptors, Thyroid Hormone/genetics ; Receptors, Thyroid Hormone/physiology ; Regeneration/drug effects ; Regeneration/genetics ; Regeneration/physiology ; Signal Transduction ; Thyroid Hormones/pharmacology ; Thyroid Hormones/physiology ; Zebrafish
    Chemical Substances Receptors, Thyroid Hormone ; Thyroid Hormones
    Language English
    Publishing date 2019-03-07
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 128410-1
    ISSN 1095-9203 ; 0036-8075
    ISSN (online) 1095-9203
    ISSN 0036-8075
    DOI 10.1126/science.aar2038
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

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