ArticleThe Journal of biological chemistry2014
Differential regulation of cellular senescence and differentiation by prolyl isomerase Pin1 in cardiac progenitor cells.
Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
19 citing papers in PubMed, 32 citations in OpenAlex.
- The role of CYP-sEH derived lipid mediators in regulating mitochondrial biology and cellular senescence: implications for the aging heart.Frontiers in pharmacology · 2024Review
- Shared and unique phosphoproteomics responses in skeletal muscle from exercise models and in hyperammonemic myotubes.iScience · 2022Article
- The role of cellular senescence in cardiac disease: basic biology and clinical relevance.Nature reviews. Cardiology · 2022Review
- Sustained and targeted delivery of siRNA/DP7-C nanoparticles from injectable thermosensitive hydrogel for hepatocellular carcinoma therapy.Cancer science · 2021Article
- PIN1 Protects Hair Cells and Auditory HEI-OC1 Cells against Senescence by Inhibiting the PI3K/Akt/mTOR Pathway.Oxidative medicine and cellular longevity · 2021Article
- Phosphorylation-Dependent Pin1 Isomerization of ATR: Its Role in Regulating ATR's Anti-apoptotic Function at Mitochondria, and the Implications in Cancer.Frontiers in cell and developmental biology · 2020Review
- Oncogenic Hijacking of the PIN1 Signaling Network.Frontiers in oncology · 2019Review
- Adult Cardiac Stem Cell Aging: A Reversible Stochastic Phenomenon?Oxidative medicine and cellular longevity · 2019Review
- Prolyl isomerase Pin1: a promoter of cancer and a target for therapy.Cell death & disease · 2018Review
- Effects of Melatonin and Its Underlying Mechanism on Ethanol-Stimulated Senescence and Osteoclastic Differentiation in Human Periodontal Ligament Cells and Cementoblasts.International journal of molecular sciences · 2018Article
- Pin1 facilitates isoproterenol‑induced cardiac fibrosis and collagen deposition by promoting oxidative stress and activating the MEK1/2‑ERK1/2 signal transduction pathway in rats.International journal of molecular medicine · 2018Article
- Peptidyl-Prolyl Isomerase 1 Regulates CaJournal of the American Heart Association · 2017Article
- Decline in cellular function of aged mouse c-kitThe Journal of physiology · 2017Article
- Pin1 induces the ADP-induced migration of human dental pulp cells through P2Y1 stabilization.Oncotarget · 2016Article
- Glutamine Regulates Cardiac Progenitor Cell Metabolism and Proliferation.Stem cells (Dayton, Ohio) · 2015Article
- c-kit(+) cells: the tell-tale heart of cardiac regeneration?Cellular and molecular life sciences : CMLS · 2015Review
- Forward Programming of Cardiac Stem Cells by Homogeneous Transduction with MYOCD plus TBX5.PloS one · 2015Article
- Pin1: a molecular orchestrator in the heart.Trends in cardiovascular medicine · 2014Review
- Phenotypic and proteomic characteristics of human dental pulp derived mesenchymal stem cells from a natal, an exfoliated deciduous, and an impacted third molar tooth.Stem cells international · 2014Article
Corrections and comments
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Authors and funding
14 authors at 2 institutions in 2 countries.
Funding
Abstract
Autologous c-kit(+) cardiac progenitor cells (CPCs) are currently used in the clinic to treat heart disease. CPC-based regeneration may be further augmented by better understanding molecular mechanisms of endogenous cardiac repair and enhancement of pro-survival signaling pathways that antagonize senescence while also increasing differentiation. The prolyl isomerase Pin1 regulates multiple signaling cascades by modulating protein folding and thereby activity and stability of phosphoproteins. In this study, we examine the heretofore unexplored role of Pin1 in CPCs. Pin1 is expressed in CPCs in vitro and in vivo and is associated with increased proliferation. Pin1 is required for cell cycle progression and loss of Pin1 causes cell cycle arrest in the G1 phase in CPCs, concomitantly associated with decreased expression of Cyclins D and B and increased expression of cell cycle inhibitors p53 and retinoblastoma (Rb). Pin1 deletion increases cellular senescence but not differentiation or cell death of CPCs. Pin1 is required for endogenous CPC response as Pin1 knock-out mice have a reduced number of proliferating CPCs after ischemic challenge. Pin1 overexpression also impairs proliferation and causes G2/M phase cell cycle arrest with concurrent down-regulation of Cyclin B, p53, and Rb. Additionally, Pin1 overexpression inhibits replicative senescence, increases differentiation, and inhibits cell death of CPCs, indicating that cell cycle arrest caused by Pin1 overexpression is a consequence of differentiation and not senescence or cell death. In conclusion, Pin1 has pleiotropic roles in CPCs and may be a molecular target to promote survival, enhance repair, improve differentiation, and antagonize senescence.
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