M
Michael J. Banda
Researcher at University of California, San Francisco
Publications - 37
Citations - 6381
Michael J. Banda is an academic researcher from University of California, San Francisco. The author has contributed to research in topics: Wound healing & Proteolysis. The author has an hindex of 27, co-authored 37 publications receiving 6277 citations. Previous affiliations of Michael J. Banda include University of California, Berkeley.
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Journal ArticleDOI
Wound Macrophages Express TGF-α and Other Growth Factors in Vivo: Analysis by mRNA Phenotyping
TL;DR: Macrophages isolated from a wound site, and not exposed to cell culture conditions, expressed messenger RNA transcripts for TGF-alpha, T GF-beta, platelet-derived growth factor A-chain, and insulin-like growth factor-1 by a novel method for RNA analysis.
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Oxygen tension regulates the expression of angiogenesis factor by macrophages
David R. Knighton,Thomas K. Hunt,Heinz Scheuenstuhl,Betty J. Halliday,Zena Werb,Michael J. Banda +5 more
TL;DR: The control of angiogenesis in wound healing may be the result of macrophages responding to tissue oxygen tension without the necessity of interacting with other cell types or biochemical signals.
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Large induction of keratinocyte growth factor expression in the dermis during wound healing
Sabine Werner,Kevin G. Peters,Michael T. Longaker,Frances Fuller-Pace,Michael J. Banda,Lewis T. Williams +5 more
TL;DR: The results suggest that basal keratinocytes are stimulated by dermally derived KGF during wound healing and implicate a unique role of this member of the FGF family in wound repair.
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Secretion of metalloproteinases by stimulated capillary endothelial cells. II. Expression of collagenase and stromelysin activities is regulated by endogenous inhibitors.
TL;DR: It is shown that enzyme activities of procollagenase and prostromelysin are revealed after conditioned medium is analyzed by gel filtration chromatography or by electrophoresis on sodium dodecyl sulfate-substrate gels, suggesting that endogenous inhibitors regulate the expression of metalloproteinases secreted by endothelial cells.
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Degradation of connective tissue matrices by macrophages. I. Proteolysis of elastin, glycoproteins, and collagen by proteinases isolated from macrophages.
TL;DR: The data indicate that macrophages at inflammatory sites contain and secrete proteolytic enzymes that could degrade the extracellular matrix, and human granulocyte elastase effectively degraded the matrix glycoproteins, elastin, and, to a lesser extent, collagens.