The Experts below are selected from a list of 239784 Experts worldwide ranked by ideXlab platform
Francis G. Spinale - One of the best experts on this subject based on the ideXlab platform.
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Temporal disparity in the induction of matrix Metalloproteinases and tissue inhibitors of Metalloproteinases after thoracic aortic aneurysm formation
The Journal of thoracic and cardiovascular surgery, 2006Co-Authors: John R. Barbour, Robert E. Stroud, Abigail S. Lowry, Leslie L. Clark, Allyson M. Leone, Jeffery A. Jones, Francis G. Spinale, John S. IkonomidisAbstract:Background An important component of matrix remodeling during thoracic aortic aneurysm progression is the balance between matrix Metalloproteinases and their endogenous inhibitors (tissue inhibitors of Metalloproteinases). However, whether and to what degree matrix Metalloproteinase/tissue inhibitor of Metalloproteinases profiles change over time with an evolving thoracic aortic aneurysm remains unclear. Methods Descending thoracic aortic aneurysms were induced in mice (FVB strain, 15 minutes of 0.5 mol/L CaCl 2 exposure) and followed for 24 hours, 72 hours, 1week, 2 weeks, 4 weeks, or 8 weeks (each group, n=13). Thoracic aortic aneurysm size was determined by means of video micrometry, and immunoblotting was used to measure aortic matrix Metalloproteinase 2, 8, 9, and 12 and tissue inhibitor of Metalloproteinases 1 and 4 levels (expressed as a percentage of control values, n=13). Results Increased aortic diameter was detected by 72 hours and reached a maximal size at 4 weeks (135% ± 4% increase from baseline, P P P P P P P P Conclusions These findings show 2 phases of matrix Metalloproteinase abundance during murine thoracic aortic aneurysm formation. The late tissue inhibitor of Metalloproteinases 4 increase might explain prevention of further aortic dilation past 4 weeks. Unique matrix Metalloproteinase/tissue inhibitor of Metalloproteinases temporal relationships occurred during the natural history of thoracic aortic aneurysm progression that might hold both diagnostic and therapeutic relevance.
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a matrix Metalloproteinase induction activation system exists in the human left ventricular myocardium and is upregulated in heart failure
Circulation, 2000Co-Authors: Francis G. Spinale, Mytsi L Coker, Lena J Heung, Brian R Bond, Himali R Gunasinghe, Takuma Etoh, Aron T Goldberg, James L Zellner, Jackson A CrumbleyAbstract:Background—Matrix Metalloproteinases (MMPs) contribute to matrix remodeling in disease states such as tumor metastases. Extracellular matrix Metalloproteinase inducer (EMMPRIN) has been reported to...
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a matrix Metalloproteinase induction activation system exists in the human left ventricular myocardium and is upregulated in heart failure
Circulation, 2000Co-Authors: Francis G. Spinale, Mytsi L Coker, Lena J Heung, Brian R Bond, Himali R Gunasinghe, Takuma Etoh, Aron T Goldberg, James L Zellner, Jackson A CrumbleyAbstract:Background—Matrix Metalloproteinases (MMPs) contribute to matrix remodeling in disease states such as tumor metastases. Extracellular matrix Metalloproteinase inducer (EMMPRIN) has been reported to...
Jackson A Crumbley - One of the best experts on this subject based on the ideXlab platform.
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a matrix Metalloproteinase induction activation system exists in the human left ventricular myocardium and is upregulated in heart failure
Circulation, 2000Co-Authors: Francis G. Spinale, Mytsi L Coker, Lena J Heung, Brian R Bond, Himali R Gunasinghe, Takuma Etoh, Aron T Goldberg, James L Zellner, Jackson A CrumbleyAbstract:Background—Matrix Metalloproteinases (MMPs) contribute to matrix remodeling in disease states such as tumor metastases. Extracellular matrix Metalloproteinase inducer (EMMPRIN) has been reported to...
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a matrix Metalloproteinase induction activation system exists in the human left ventricular myocardium and is upregulated in heart failure
Circulation, 2000Co-Authors: Francis G. Spinale, Mytsi L Coker, Lena J Heung, Brian R Bond, Himali R Gunasinghe, Takuma Etoh, Aron T Goldberg, James L Zellner, Jackson A CrumbleyAbstract:Background—Matrix Metalloproteinases (MMPs) contribute to matrix remodeling in disease states such as tumor metastases. Extracellular matrix Metalloproteinase inducer (EMMPRIN) has been reported to...
Michio Sata - One of the best experts on this subject based on the ideXlab platform.
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Increased expression of membrane type 1 matrix Metalloproteinase and matrix Metalloproteinase-2 with tumor dedifferentiation in hepatocellular carcinomas
Human pathology, 1999Co-Authors: Riko Ogata, Takuji Torimura, Motoaki Kin, Takato Ueno, Yukio Tateishi, Ryoko Kuromatsu, Yoshihiro Shimauchi, Masaharu Sakamoto, Seisyu Tamaki, Michio SataAbstract:Abstract Destruction of the extracellular matrices is required for tumor invasion and metastasis. Matrix Metalloproteinase-2 degrades type IV collagen and laminin, major components of the basement membrane. Membrane type 1 matrix Metalloproteinase activates the latent form of matrix Metalloproteinase-2. We studied changes in membrane type 1 matrix Metalloproteinase and matrix Metalloproteinase-2 expression in relation to the tumor differentiation of hepatocellular carcinomas. Activity of matrix Metalloproteinase-2 was also evaluated in hepatocellular carcinomas and noncancerous tissues. Overall, 37 hepatocellular carcinomas were studied. Expression of membrane type 1 matrix Metalloproteinase and matrix Metalloproteinase-2 was determined by either immunohistochemistry ( n = 37) or in situ hybridization ( n = 6). Changes in membrane type 1 matrix Metalloproteinase and matrix Metalloproteinase-2 expression were evaluated in relation to tumor differentiation. Gelatinolytic activities were analyzed by gelatin zymography ( n = 4). Membrane type 1 matrix Metalloproteinase and matrix Metalloproteinase-2 were detected in hepatoma cells and stromal cells. In addition, these matrix Metalloproteinases were detected in the same hepatoma cells. Increased expression of membrane type 1 matrix Metalloproteinase and matrix Metalloproteinase-2 was associated with tumor dedifferentiation. The active form of matrix Metalloproteinase-2 was more strongly expressed by hepatocellular carcinomas than by noncancerous tissues. These findings indicate that increased expression of membrane type 1 matrix Metalloproteinase and matrix Metalloproteinase-2 was associated with tumor dedifferentiation, suggesting that these matrix Metalloproteinases are intimately involved in the invasion of hepatocellular carcinomas.
John S. Ikonomidis - One of the best experts on this subject based on the ideXlab platform.
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Temporal disparity in the induction of matrix Metalloproteinases and tissue inhibitors of Metalloproteinases after thoracic aortic aneurysm formation
The Journal of thoracic and cardiovascular surgery, 2006Co-Authors: John R. Barbour, Robert E. Stroud, Abigail S. Lowry, Leslie L. Clark, Allyson M. Leone, Jeffery A. Jones, Francis G. Spinale, John S. IkonomidisAbstract:Background An important component of matrix remodeling during thoracic aortic aneurysm progression is the balance between matrix Metalloproteinases and their endogenous inhibitors (tissue inhibitors of Metalloproteinases). However, whether and to what degree matrix Metalloproteinase/tissue inhibitor of Metalloproteinases profiles change over time with an evolving thoracic aortic aneurysm remains unclear. Methods Descending thoracic aortic aneurysms were induced in mice (FVB strain, 15 minutes of 0.5 mol/L CaCl 2 exposure) and followed for 24 hours, 72 hours, 1week, 2 weeks, 4 weeks, or 8 weeks (each group, n=13). Thoracic aortic aneurysm size was determined by means of video micrometry, and immunoblotting was used to measure aortic matrix Metalloproteinase 2, 8, 9, and 12 and tissue inhibitor of Metalloproteinases 1 and 4 levels (expressed as a percentage of control values, n=13). Results Increased aortic diameter was detected by 72 hours and reached a maximal size at 4 weeks (135% ± 4% increase from baseline, P P P P P P P P Conclusions These findings show 2 phases of matrix Metalloproteinase abundance during murine thoracic aortic aneurysm formation. The late tissue inhibitor of Metalloproteinases 4 increase might explain prevention of further aortic dilation past 4 weeks. Unique matrix Metalloproteinase/tissue inhibitor of Metalloproteinases temporal relationships occurred during the natural history of thoracic aortic aneurysm progression that might hold both diagnostic and therapeutic relevance.
Motoharu Seiki - One of the best experts on this subject based on the ideXlab platform.
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processing of a precursor of 72 kilodalton type iv collagenase gelatinase a by a recombinant membrane type 1 matrix Metalloproteinase
Cancer Research, 1996Co-Authors: Takeshi Kinoshita, Takahisa Takino, Michiyasu Itoh, Toshifumi Akizawa, Hiroshi Sato, Motoharu SeikiAbstract:Membrane-type 1 matrix Metalloproteinase that is associated with the proteolytic activation of progelatinase A was expressed as a recombinant fusion protein in Escherichia coli . The recombinant enzyme cleaved the propeptide sequence of gelatinase A in a sequence-specific manner. A mutant progelatinase A that has a substitution of Asn66-Leu to Ile-Val was not processed at all. The processing was blocked by tissue inhibitor of Metalloproteinases-2 or BB-94 but not by tissue inhibitor of Metalloproteinases-1. Thus, membrane-type 1 matrix Metalloproteinase is a direct activator of progelatinase A without requiring additional proteases.
