Entrance in mitosis of adult cardiomyocytes in ischemic pig hearts after plasmid-mediated rhVEGF165 gene transfer

Laguens, Rubén M.; Meckert, Patricia Cabeza; Janavel, Gustavo Vera; Valle, Héctor Del; Lascano, Elena C.; Negroni, Jorge A.; Werba, P; Cuniberti, Luis; Martinez, V.; Melo, Cynthia de Freitas; Papouchado, Mariana; Ojeda, Ricardo A.; Criscuolo, Marcelo; Crottogini, Alberto J.

doi:10.1038/sj.gt.3301844

Cited by 57 publications

(53 citation statements)

References 16 publications

(21 reference statements)

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“…21 Virally mediated overexpression of vascular endothelial growth factor conferred a fivefold increase in cardiomyocyte mitotic index following left circumflex coronary artery ligation. 17 In vitro studies with isolated rodent cardiomyocytes have supported these observations that terminally differentiated cardiomyocytes can be stimulated to proliferate. Murine cardiomyocytes overexpressing Bcl-2 demonstrated an increase in mitotic index from 30 to 75 per million nuclei, 22 and adenoviral-mediated overexpression of FGF-2 in neonatal rat ventricular myocytes demonstrated a 140-fold increase in mitotic index.…”

Section: Cdc5 Promotes Cardiomyocyte Division Sd Williams Et Alsupporting

confidence: 49%

“…Although others have reported incomplete transverse splitting of cardiomyocytes in vivo following genetic manipulation, 17 our observation of adjacent daughter cells arising from a single cell strongly suggests cytokinesis in vitro. To quantitate the extent of cell division within the cultured cardiomyocyte population, we calculated mitotic indices for neonatal rat cardiomyocytes co-infected with AdE1A/E1B and AdCDC5 48 h after infection.…”

Section: Overexpression Of E1a/e1b and Hcdc5 Results In An Increase Imentioning

confidence: 70%

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Adenoviral delivery of human CDC5 promotes G2/M progression and cell division in neonatal ventricular cardiomyocytes

et al. 2006

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Heart failure results from the cumulative death of cardiomyocytes, and the inability of remaining cells to regenerate. Efforts toward transcriptional reprogramming of cardiomyocytes by overexpressing E1A or E2F1 have been limited by the inability of cardiomyocytes to enter and complete mitosis. Human CDC5 (hCDC5), a component of the pre-mRNA splicing complex, has been shown to regulate G2/M transit in asynchronously dividing cells. We now show that co-infection of recombinant adenoviruses expressing E1A/E1B and hCDC5 promotes cell cycle re-entry and G2/M progression in post-mitotic cardiomyocytes. Co-expression of E1A/E1B and hCDC5 induced nuclear localization of cyclin-dependent kinase 1 and cyclin B1, and was sufficient to promote mitotic entry as determined by an increase in mitotic index only in co-infected cells. E1A/E1B and hCDC5 promoted cell division, as evidenced by an increase in the number of cardiomyocytes following co-infection. Thus, overexpression of E1A/E1B and hCDC5 resulted in cell cycle re-entry, DNA synthesis, cell division, and an increase in cardiomyocyte number, suggesting the formation of new cardiomyocytes. These studies suggest that G1/S-phase transcriptional regulators, in combination with pre-mRNA splicing factors, such as CDC5, that regulate rate-limiting G2/M target genes may prove useful in developing therapies to stimulate myocardial regeneration. Gene Therapy (2006) 13, 837-843.

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Section: Cdc5 Promotes Cardiomyocyte Division Sd Williams Et Alsupporting

confidence: 49%

Section: Overexpression Of E1a/e1b and Hcdc5 Results In An Increase Imentioning

confidence: 70%

Adenoviral delivery of human CDC5 promotes G2/M progression and cell division in neonatal ventricular cardiomyocytes

et al. 2006

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“…[30][31][32] VEGF drives angiogenesis in a wide variety of tissues and lesions including tumors, and can induce vasculogenesis in adult rat muscle. 18 We did not detect smooth muscle b-actin and CD31-double staining with multiple layers in AAVH9-VEGF-transduced mice, which might have been due to the short time course and low dose of VEGF treatment.…”

Section: Aavh9-vegf Promotes Angiogenesismentioning

confidence: 99%

Adeno-associated viral vector-mediated hypoxia-regulated VEGF gene transfer promotes angiogenesis following focal cerebral ischemia in mice

Shen

Fan

et al. 2007

Gene Ther

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“…[16][17][18][19] VEGF is one of such growth factors that can be used in combination with transplanted stem cells to improve therapeutic efficiency of cellular transplantation. VEGF is an angiogenetic growth factor acting as a potent mitogen and survival factor for endothelial cells, 20,21 smooth muscle cells, 22,23 hepatocytes 24 and cardiomyocytes, 25,26 and also known for neuroprotective effect against brain injury. 27,28 Several recent studies have also shown that VEGF promoted cell survival pathways and blocked cell death in the ALS animal model.…”

Section: Introductionmentioning

confidence: 99%

Intrathecal transplantation of human neural stem cells overexpressing VEGF provide behavioral improvement, disease onset delay and survival extension in transgenic ALS mice

et al. 2009

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Entrance in mitosis of adult cardiomyocytes in ischemic pig hearts after plasmid-mediated rhVEGF165 gene transfer

Cited by 57 publications

References 16 publications

Adenoviral delivery of human CDC5 promotes G2/M progression and cell division in neonatal ventricular cardiomyocytes

Adenoviral delivery of human CDC5 promotes G2/M progression and cell division in neonatal ventricular cardiomyocytes

Adeno-associated viral vector-mediated hypoxia-regulated VEGF gene transfer promotes angiogenesis following focal cerebral ischemia in mice

Intrathecal transplantation of human neural stem cells overexpressing VEGF provide behavioral improvement, disease onset delay and survival extension in transgenic ALS mice

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