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Journal ArticleDOI

Urotensin II inhibits the proliferation but not the differentiation of cardiac side population cells

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TLDR
The results revealed that UII did inhibit the proliferation of CSPs through up-regulation of phosphorylated c-Jun N-terminal protein kinase (JNK), although it didn't affect the differentiation of cultured C SPs.
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This article is published in Peptides.The article was published on 2011-05-01. It has received 9 citations till now. The article focuses on the topics: Myocyte & Urotensin-II.

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Journal ArticleDOI

International Union of Basic and Clinical Pharmacology. XCII. Urotensin II, Urotensin II–Related Peptide, and Their Receptor: From Structure to Function

TL;DR: The current knowledge concerning the pleiotropic actions of UII is reviewed and the possible use of antagonists for future therapeutic applications are discussed.
Journal ArticleDOI

The Role of Cardiac Side Population Cells in Cardiac Regeneration.

TL;DR: A review of the current literature on the progenitor cell properties and therapeutic potential of cardiac side population cells demonstrates the great promise cSPCs hold as targets for new regenerative strategies.
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UII and UT in grouper: cloning and effects on the transcription of hormones related to growth control

TL;DR: Results collectively indicate that the UII/UT system may play a role in the promotion of the growth of the orange-spotted grouper.
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Urotensin II inhibited the proliferation of cardiac side population cells in mice during pressure overload by JNK-LRP6 signalling.

TL;DR: It is shown that urotensin II regulates the proliferation of CSPs by c‐Jun N‐terminal kinase (JNK) and low density lipoprotein receptor‐related protein 6 (LRP6) signalling during pressure overload.
Journal ArticleDOI

Role of PKA in the process of neonatal cardiomyocyte hypertrophy induced by urotensin II

TL;DR: The results suggest that UII induces cardiomyocytehypertrophy through the PKA-mediated upregulation of PLN phosphorylation at Ser16, which provides a new experimental foundation for the prevention and/or treatment of cardiac hypertrophy.
References
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Journal ArticleDOI

Mitogen-activated protein (MAP) kinase pathways: regulation and physiological functions.

TL;DR: Nonenzymatic mechanisms that impact MAP kinase functions and findings from gene disruption studies are highlighted and particular emphasis is on ERK1/2.
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Isolation and functional properties of murine hematopoietic stem cells that are replicating in vivo.

TL;DR: It is discovered that display of Hoechst fluorescence simultaneously at two emission wavelengths revealed a small and distinct subset of whole bone marrow cells that had phenotypic markers of multipotential HSC, which were shown in competitive repopulation experiments to contain the vast majority of HSC activity from murine bone marrow and to be enriched at least 1,000-fold for in vivo reconstitution activity.
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Dystrophin expression in the mdx mouse restored by stem cell transplantation

TL;DR: Results suggest that the transplantation of different stem cell populations, using the procedures of bone marrow transplantation, might provide an unanticipated avenue for treating muscular dystrophy as well as other diseases where the systemic delivery of therapeutic cells to sites throughout the body is critical.
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Serine/threonine protein kinases and apoptosis.

TL;DR: This minireview will focus on the role of protein kinases in apoptosis, which has been implicated both in the upstream induction phase of apoptosis and in the downstream execution stage, as the direct targets for caspases.
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