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  1. Article ; Online: APJ+ cells in the SHF contribute to the cells of aorta and pulmonary trunk through APJ signaling

    Baral, Kamal / D’amato, Gaetano / Kuschel, Bryce / Bogan, Frank / Jones, Brendan W. / Large, Colton L. / Whatley, Jeffery D. / Red-Horse, Kristy / Sharma, Bikram

    Developmental Biology. 2023 June, v. 498 p.77-86

    2023  

    Abstract: Outflow tract (OFT) develops from cardiac progenitor cells in the second heart field (SHF) domain. APJ, a G-Protein Coupled Receptor, is expressed by cardiac progenitors in the SHF. By lineage tracing APJ+SHF cells, we show that these cardiac progenitors ...

    Abstract Outflow tract (OFT) develops from cardiac progenitor cells in the second heart field (SHF) domain. APJ, a G-Protein Coupled Receptor, is expressed by cardiac progenitors in the SHF. By lineage tracing APJ+SHF cells, we show that these cardiac progenitors contribute to the cells of OFT, which eventually give rise to aorta and pulmonary trunk/artery upon its morphogenesis. Furthermore, we show that early APJ ​+ ​cells give rise to both aorta and pulmonary cells but late APJ ​+ ​cells predominantly give rise to pulmonary cells. APJ is expressed by the outflow tract progenitors in the SHF but its role is unclear. We performed knockout studies to determine the role of APJ in SHF cell proliferation and survival. Our data suggested that APJ knockout in the SHF reduced the proliferation of SHF progenitors, while there was no significant impact on survival. In addition, we show that ectopic overexpression of WNT in these cells disrupted aorta and pulmonary morphogenesis from OFT. Overall, our study has identified APJ ​+ ​progenitor population within the SHF that give rise to aorta and pulmonary trunk/artery cells. Furthermore, we show that APJ signaling stimulates proliferation of these cells in the SHF.
    Keywords G-proteins ; aorta ; cell proliferation ; heart ; morphogenesis ; Second heart field (SHF) ; APJ signaling ; WNT signaling ; Outflow tract development
    Language English
    Dates of publication 2023-06
    Size p. 77-86.
    Publishing place Elsevier Inc.
    Document type Article ; Online
    ZDB-ID 1114-9
    ISSN 1095-564X ; 0012-1606
    ISSN (online) 1095-564X
    ISSN 0012-1606
    DOI 10.1016/j.ydbio.2023.04.003
    Database NAL-Catalogue (AGRICOLA)

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    In stock of ZB MED Bonn / Germany

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  2. Article: Hypoxia regulate developmental coronary angiogenesis potentially through VEGFR2- and SOX17-mediated signaling.

    Vitali, Halie E / Kuschel, Bryce / Sherpa, Chhiring / Jones, Brendan W / Jacob, Nisha / Madiha, Syeda A / Elliott, Sam / Dziennik, Eddie / Kreun, Lily / Conatser, Cora / Bhetwal, Bhupal P / Sharma, Bikram

    bioRxiv : the preprint server for biology

    2023  

    Abstract: Background: Coronary vessels in embryonic mouse heart arises from multiple progenitor population including sinus venosus (SV), endocardium, and proepicardium. ELA/APJ signaling is shown to regulate coronary growth from SV pathway within the ... ...

    Abstract Background: Coronary vessels in embryonic mouse heart arises from multiple progenitor population including sinus venosus (SV), endocardium, and proepicardium. ELA/APJ signaling is shown to regulate coronary growth from SV pathway within the subepicardium, whereas VEGF-A/VEGF-R2 pathways is implicated to regulate coronary growth from endocardium pathway. Our previous study show hypoxia as a potential signaling cue to stimulate overall coronary growth and expansion within the myocardium. However, the role of hypoxia and its downstream signaling pathways in the regulation of coronary vessel development is not known. In this study, we investigated the role of hypoxia in coronary vessel development and have identified SOX17- and VEGF-R2-mediated signaling as a potential downstream pathway of hypoxia in the regulation of coronary vessel development.
    Results: We show that hypoxia gain-of-function in the myocardium through upregulation of HIF-1α disrupts the normal pattern of coronary angiogenesis in developing mouse hearts and displays phenotype that is reminiscent of accelerated coronary growth. We show that VEGF-R2 expression is increased in coronary endothelial cells under hypoxia gain-of-function
    Conclusion: Collectively, our data provide strong phenotypic evidence to show that hypoxia might regulate coronary growth in the developing mouse heart potentially through VEGF-R2- and SOX17-mediated downstream signaling pathways.
    Language English
    Publishing date 2023-08-16
    Publishing country United States
    Document type Preprint
    DOI 10.1101/2023.08.16.553531
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: APJ+ cells in the SHF contribute to the cells of aorta and pulmonary trunk through APJ signaling.

    Baral, Kamal / D'amato, Gaetano / Kuschel, Bryce / Bogan, Frank / Jones, Brendan W / Large, Colton L / Whatley, Jeffery D / Red-Horse, Kristy / Sharma, Bikram

    Developmental biology

    2023  Volume 498, Page(s) 77–86

    Abstract: Outflow tract (OFT) develops from cardiac progenitor cells in the second heart field (SHF) domain. APJ, a G-Protein Coupled Receptor, is expressed by cardiac progenitors in the SHF. By lineage tracing APJ+SHF cells, we show that these cardiac progenitors ...

    Abstract Outflow tract (OFT) develops from cardiac progenitor cells in the second heart field (SHF) domain. APJ, a G-Protein Coupled Receptor, is expressed by cardiac progenitors in the SHF. By lineage tracing APJ+SHF cells, we show that these cardiac progenitors contribute to the cells of OFT, which eventually give rise to aorta and pulmonary trunk/artery upon its morphogenesis. Furthermore, we show that early APJ ​+ ​cells give rise to both aorta and pulmonary cells but late APJ ​+ ​cells predominantly give rise to pulmonary cells. APJ is expressed by the outflow tract progenitors in the SHF but its role is unclear. We performed knockout studies to determine the role of APJ in SHF cell proliferation and survival. Our data suggested that APJ knockout in the SHF reduced the proliferation of SHF progenitors, while there was no significant impact on survival. In addition, we show that ectopic overexpression of WNT in these cells disrupted aorta and pulmonary morphogenesis from OFT. Overall, our study has identified APJ ​+ ​progenitor population within the SHF that give rise to aorta and pulmonary trunk/artery cells. Furthermore, we show that APJ signaling stimulates proliferation of these cells in the SHF.
    MeSH term(s) Heart ; Signal Transduction ; Stem Cells ; Pulmonary Artery ; Aorta ; Myocardium ; Gene Expression Regulation, Developmental
    Language English
    Publishing date 2023-04-08
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 1114-9
    ISSN 1095-564X ; 0012-1606
    ISSN (online) 1095-564X
    ISSN 0012-1606
    DOI 10.1016/j.ydbio.2023.04.003
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.B 508: Show issues Location:
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