Selective endothelial growth inhibition by tetracyclines that inhibit collagenase

Christopher Guerin; John Laterra; Taras Masnyk; Lorne M. Golub; Henry Brem

doi:10.1016/0006-291X(92)91118-A

Selective endothelial growth inhibition by tetracyclines that inhibit collagenase

Christopher Guerin, John Laterra, Taras Masnyk, Lorne M. Golub, Henry Brem

School of Medicine

Research output: Contribution to journal › Article › peer-review

54 Scopus citations

Abstract

The potential of angiogenesis inhibitors as therapy for human diseases is limited by a lack of clinically available agents. We investigated the mechanism of the anti-angiogenesis effects of minocycline, a commonly used drug, and several derivatives. Endothelial cell proliferation was inhibited by several of these compounds. We found that inhibition was associated with inhibition of collagenase, did not require antibiotic activity, and was not related to cytotoxicity. Other microvessel-associated cells were unaffected. This endothelial antiproliferative effect is a potential mechanism of the anti-angiogenic activity of minocycline.

Original language	English (US)
Pages (from-to)	740-745
Number of pages	6
Journal	Biochemical and Biophysical Research Communications
Volume	188
Issue number	2
DOIs	https://doi.org/10.1016/0006-291X(92)91118-A
State	Published - Oct 30 1992

ASJC Scopus subject areas

Biophysics
Biochemistry
Molecular Biology
Cell Biology

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10.1016/0006-291X(92)91118-A

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title = "Selective endothelial growth inhibition by tetracyclines that inhibit collagenase",

abstract = "The potential of angiogenesis inhibitors as therapy for human diseases is limited by a lack of clinically available agents. We investigated the mechanism of the anti-angiogenesis effects of minocycline, a commonly used drug, and several derivatives. Endothelial cell proliferation was inhibited by several of these compounds. We found that inhibition was associated with inhibition of collagenase, did not require antibiotic activity, and was not related to cytotoxicity. Other microvessel-associated cells were unaffected. This endothelial antiproliferative effect is a potential mechanism of the anti-angiogenic activity of minocycline.",

author = "Christopher Guerin and John Laterra and Taras Masnyk and Golub, {Lorne M.} and Henry Brem",

note = "Funding Information: +This work was supported by grants from the NIH (C.G., J.L., H.B., and L.M.G.) and the Poole and Kent Foundation (H-B.). We thank J. Goodman of the Ohio State University School of Medicine for F98 cells, and G. Bulkley of the Johns Hopkins University School of Medicine for porcine aortic endothelial cells. We thank Pamela Talalay for her assistance in preparation of the manuscript.",

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doi = "10.1016/0006-291X(92)91118-A",

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T1 - Selective endothelial growth inhibition by tetracyclines that inhibit collagenase

AU - Guerin, Christopher

AU - Laterra, John

AU - Masnyk, Taras

AU - Golub, Lorne M.

AU - Brem, Henry

N1 - Funding Information: +This work was supported by grants from the NIH (C.G., J.L., H.B., and L.M.G.) and the Poole and Kent Foundation (H-B.). We thank J. Goodman of the Ohio State University School of Medicine for F98 cells, and G. Bulkley of the Johns Hopkins University School of Medicine for porcine aortic endothelial cells. We thank Pamela Talalay for her assistance in preparation of the manuscript.

PY - 1992/10/30

Y1 - 1992/10/30

N2 - The potential of angiogenesis inhibitors as therapy for human diseases is limited by a lack of clinically available agents. We investigated the mechanism of the anti-angiogenesis effects of minocycline, a commonly used drug, and several derivatives. Endothelial cell proliferation was inhibited by several of these compounds. We found that inhibition was associated with inhibition of collagenase, did not require antibiotic activity, and was not related to cytotoxicity. Other microvessel-associated cells were unaffected. This endothelial antiproliferative effect is a potential mechanism of the anti-angiogenic activity of minocycline.

AB - The potential of angiogenesis inhibitors as therapy for human diseases is limited by a lack of clinically available agents. We investigated the mechanism of the anti-angiogenesis effects of minocycline, a commonly used drug, and several derivatives. Endothelial cell proliferation was inhibited by several of these compounds. We found that inhibition was associated with inhibition of collagenase, did not require antibiotic activity, and was not related to cytotoxicity. Other microvessel-associated cells were unaffected. This endothelial antiproliferative effect is a potential mechanism of the anti-angiogenic activity of minocycline.

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Selective endothelial growth inhibition by tetracyclines that inhibit collagenase

Abstract

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