Matthew Plotkin
University of Arkansas for Medical Sciences
16 Papers
218 Citations
Matthew Plotkin is an academic researcher from University of Arkansas for Medical Sciences. The author has contributed to research in topics: Endothelial stem cell & Mesenchymal stem cell. The author has an hindex of 11, co-authored 16 publications. Previous affiliations of Matthew Plotkin include New York Medical College & John L. Scott.
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Papers
Kidney-derived mesenchymal stem cells contribute to vasculogenesis, angiogenesis and endothelial repair
Jun Chen,Hyeong Cheon Park,Hyeong Cheon Park,Francesco Addabbo,Jie Ni,Edward Pelger,Houwei Li,Matthew Plotkin,Michael S. Goligorsky +8 more
TL;DR: It is shown that kidney mesenchymal stem cells are capable of differentiation toward endothelial and smooth muscle cell lineages in vitro and in vivo, support new blood vessel formation in favorable conditions and promote functional recovery of an ischemic kidney.
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Microparticles from kidney-derived mesenchymal stem cells act as carriers of proangiogenic signals and contribute to recovery from acute kidney injury.
Hoon Young Choi,Sung Jin Moon,Brian B. Ratliff,Sun Hee Ahn,Ara Jung,Mirae Lee,Seol Ae Lee,Beom Jin Lim,Beom Seok Kim,Matthew Plotkin,Sung Kyu Ha,Hyeong Cheon Park +11 more
TL;DR: The hypothesis that KMSC-derived MPs may act as a source of proangiogenic signals and confer renoprotective effects in ischemic kidneys is supported.
INK4a knockout mice exhibit increased fibrosis under normal conditions and in response to unilateral ureteral obstruction.
TL;DR: Results confirm that p16(INK4a) controls cell proliferation and matrix production and mitigates fibrosis following injury and suggest that the mechanism involves a role in limiting inflammation and cell proliferation.
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INK4a deletion results in improved kidney regeneration and decreased capillary rarefaction after ischemia-reperfusion injury.
TL;DR: Results suggest that the absence of p16(INK4a) and p19(ARF) following IRI has a protective effect on the kidney through improved epithelial and microvascular repair, in part by enhancing the mobilization of myeloid cells into the kidney.
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Depletion of senescent-like neuronal cells alleviates cisplatin-induced peripheral neuropathy in mice.
Scarlett Acklin,Manchao Zhang,Wuying Du,Xin Zhao,Matthew Plotkin,Jianhui Chang,Judith Campisi,Judith Campisi,Daohong Zhou,Daohong Zhou,Fen Xia +10 more
TL;DR: It is shown that cisplatin induces senescent-like neuronal cells in primary culture and in mouse dorsal root ganglia (DRG), and that clearance of DRG senescent neuronal cells reverses CIPN, suggesting that sencess-like neurons play a role in CIPn pathogenesis.