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Peter R. Brink

Researcher at Stony Brook University

Publications -  285
Citations -  11424

Peter R. Brink is an academic researcher from Stony Brook University. The author has contributed to research in topics: Connexin & Gap junction. The author has an hindex of 56, co-authored 283 publications receiving 10654 citations. Previous affiliations of Peter R. Brink include Columbia University & Syracuse University.

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Human Mesenchymal Stem Cells as a Gene Delivery System to Create Cardiac Pacemakers

TL;DR: It is demonstrated that genetically modified hMSCs can express functional HCN2 channels in vitro and in vivo, mimicking overexpression ofHCN2 genes in cardiac myocytes, and represent a novel delivery system for pacemaker genes into the heart or other electrical syncytia.
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Mesenchymal stem cells support migration, extracellular matrix invasion, proliferation, and survival of endothelial cells in vitro.

TL;DR: Medium conditioned by hMSC spheroids was more effective in stimulation of umbilical vein endothelial cell proliferation, migration, and basement membrane invasion than medium conditioned by a monolayer of hMSCs, suggesting that culturing of h MSCs as three‐dimensional cellular aggregates provides a method to concentrate proangiogenic factors secreted by hmsCs and allows for reduction of serum concentration in conditioned medium.
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Gap Junctions in Vascular Tissues Evaluating the Role of Intercellular Communication in the Modulation of Vasomotor Tone

TL;DR: The thesis of this review is that the presence of gap junctions, in concert with the autonomic nervous system, pacemaker cells, myogenic mechanisms, and/or electrotonic current spread, confers a plasticity, adaptability, and flexibility to vasculature that may well account for the observed diversity in regulation and function of vascular tissues throughout the vascular tree.
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Connexin-specific cell-to-cell transfer of short interfering RNA by gap junctions.

TL;DR: The novel hypothesis that non‐hybridized and possible hybridized forms of siRNA can move between mammalian cells through connexin‐specific gap junctions is supported.
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Selectivity of Connexin-Specific Gap Junctions Does Not Correlate With Channel Conductance

TL;DR: A new model for connexin channel conductance and permselectivity based on electrostatic interactions is suggested and is not consistent with the conventional simple aqueous pore model of a gap junction channel.