• Publications
  • Influence
p38 MAP kinase inhibition enables proliferation of adult mammalian cardiomyocytes.
It is shown that adult mammalian cardiomyocytes can divide and p38 is established as a key negative regulator ofCardiomyocyte proliferation and inhibition of p38 in adult cardiomers promotes cytokinesis. Expand
International Union of Basic and Clinical Pharmacology. XCIV. Adhesion G Protein–Coupled Receptors
This review covers all major biologic aspects of Adhesion GPCRs, including evolutionary origins, interaction partners, signaling, expression, physiologic functions, and therapeutic potential. Expand
FGF1/p38 MAP kinase inhibitor therapy induces cardiomyocyte mitosis, reduces scarring, and rescues function after myocardial infarction.
Mammalian cardiomyocytes have limited proliferation potential, and acutely injured mammalian hearts do not regenerate adequately. Instead, injured myocardium develops fibrosis and scarring. Here weExpand
FGF1/p38 MAP kinase inhibitor therapy induces cardiomyocyte mitosis, reduces scarring, and rescues function after myocardial infarction
The data indicate that FGF1 and p38 MAP kinase, proteins involved in cardiomyocyte proliferation and angiogenesis during development, may be delivered therapeutically to enhance cardiac regeneration. Expand
The SRF target gene Fhl2 antagonizes RhoA/MAL-dependent activation of SRF.
Using large-scale expression profiling combined with bioinformatic and biochemical approaches, an autoregulatory mechanism is identified to selectively regulate subsets of RhoA-activated SRF target genes, including Fhl2, encoding a transcriptional cofactor that is highly expressed in the heart. Expand
New non-viral method for gene transfer into primary cells.
Efficient transfer of DNA expression vectors and siRNA oligonucleotides into a variety of primary cell types from different species utilizing the Nucleofector technology, including human B-CLL cells,human CD34+ cells, human lymphocytes, rat cardiomyocytes, human, porcine, and bovine chondrocytes, and rat neurons are shown. Expand
Gpr126 Functions in Schwann Cells to Control Differentiation and Myelination via G-Protein Activation
A model in which Gpr126 functions in SCs for proper development and myelination is supported and evidence that these functions are mediated via G-protein-signaling pathways is provided. Expand
The GSK-3 inhibitor BIO promotes proliferation in mammalian cardiomyocytes.
The demonstration of a second role for BIO suggests that the maintenance of stem cell self-renewal and the induction of proliferation in differentiated cardiomyocytes may share common molecular pathways. Expand
Spatially Resolved Genome-wide Transcriptional Profiling Identifies BMP Signaling as Essential Regulator of Zebrafish Cardiomyocyte Regeneration.
It is found that genetic or chemical inhibition of BMP signaling in zebrafish reduces cardiomyocyte dedifferentiation and proliferation, ultimately compromising myocardial regeneration, while bmp2b overexpression is sufficient to enhance it. Expand
Hypoxia-inducible factor induces local thyroid hormone inactivation during hypoxic-ischemic disease in rats.
A mechanism of metabolic regulation during hypoxic-ischemic injury is suggested in which HIF-1 reduces local thyroid hormone signaling through induction of D3, suggesting that hypoxia-induced D3 may reduce metabolic rate in hypoxic tissues. Expand