Orthodontic tensile strain induces angiogenesis via type IV collagen degradation by matrix metalloproteinase-12

2017 ◽  
Vol 52 (5) ◽  
pp. 842-852 ◽  
Author(s):  
T. Narimiya ◽  
S. Wada ◽  
H. Kanzaki ◽  
M. Ishikawa ◽  
A. Tsuge ◽  
...  
Keyword(s):  
Matrix Metalloproteinase ◽  
Tensile Strain ◽  
Type Iv Collagen ◽  
Collagen Degradation ◽  
Type Iv ◽  
Matrix Metalloproteinase 12

scholarly journals Nonenzymatic glycation of type IV collagen and matrix metalloproteinase susceptibility

1997 ◽  
Vol 52 (5) ◽  
pp. 1302-1312 ◽  
Author(s):  
Joni D. Mott ◽  
Raja G. Khalifah ◽  
Hideaki Nagase ◽  
Charles F. Shield ◽  
Julie K. Hudson ◽  
...  
Keyword(s):  
Matrix Metalloproteinase ◽  
Type Iv Collagen ◽  
Nonenzymatic Glycation ◽  
Type Iv

scholarly journals Regulation of proteinases during mouse peri-implantation development: urokinase-type plasminogen activator expression and cross talk with matrix metalloproteinase 9

Reproduction ◽  
2011 ◽  
Vol 141 (2) ◽  
pp. 227-239 ◽  
Author(s):  
M G Martínez-Hernández ◽  
L A Baiza-Gutman ◽  
A Castillo-Trápala ◽  
D Randall Armant
Keyword(s):  
Matrix Metalloproteinase ◽  
Mrna Expression ◽  
Plasminogen Activator ◽  
Type Iv Collagen ◽  
Matrix Metalloproteinase 9 ◽  
Trophoblast Cells ◽  
Type Iv ◽  
Type Plasminogen Activator ◽  
Urokinase Type Plasminogen Activator ◽  
Metalloproteinase 9

Trophoblast cells express urokinase-type plasminogen activator (PLAU) and may depend on its activity for endometrial invasion and tissue remodeling during peri-implantation development. However, the developmental regulation, tissue distribution, and function of PLAU are not completely understood. In this study, the expression of PLAU and its regulation by extracellular matrix proteins was examined by RT-PCR, immunocytochemistry, and plasminogen–casein zymography in cultured mouse embryos. There was a progressive increase inPlaumRNA expression in blastocysts cultured on gestation days 4–8. Tissue-type plasminogen activator (55 kDa) and PLAU (a triplet of 40, 37, and 31 kDa) were present in conditioned medium and embryo lysates, and were adsorbed to the culture plate surface. The temporal expression pattern of PLAU, according to semi-quantitative gel zymography, was similar in non-adhering embryos and embryos cultured on fibronectin, laminin, or type IV collagen, although type IV collagen and laminin upregulatedPlaumRNA expression. Immunofluorescence revealed PLAU on the surface of the mural trophectoderm and in non-spreading giant trophoblast cells. Exogenous human plasminogen was transformed to plasmin by cultured embryos and activated endogenous matrix metalloproteinase 9 (MMP9). Indeed, the developmental expression profile of MMP9 was similar to that of PLAU. Our data suggest that the intrinsic developmental program predominantly regulates PLAU expression during implantation, and that PLAU could be responsible for activation of MMP9, leading to localized matrix proteolysis as trophoblast invasion commences.

scholarly journals Type IV collagen degradation in the myocardial basement membrane after unloading of the failing heart by a left ventricular assist device

2007 ◽  
Vol 87 (11) ◽  
pp. 1125-1137 ◽  
Author(s):  
Annette H Bruggink ◽  
Matthijs F M van Oosterhout ◽  
Nicolaas de Jonge ◽  
Jack P M Cleutjens ◽  
Dick F van Wichen ◽  
...  
Keyword(s):  
Basement Membrane ◽  
Left Ventricular Assist Device ◽  
Ventricular Assist Device ◽  
Type Iv Collagen ◽  
Left Ventricular ◽  
Collagen Degradation ◽  
Assist Device ◽  
Ventricular Assist ◽  
Type Iv ◽  
Left Ventricular Assist

scholarly journals Role of type IV collagen and matrix metalloproteinase-9 in remodeling of the left ventricular in coronary artery disease

2019 ◽  
pp. 83-87
Author(s):  
M. A. Popov ◽  
D. V. Shumakov ◽  
D. I. Zybin ◽  
L. E. Gurevich ◽  
V. E. Ashevskaya ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Matrix Metalloproteinase ◽  
Type Iv Collagen ◽  
Basal Membrane ◽  
Left Ventricular ◽  
Type Iv ◽  
Artery Disease ◽  
Metalloproteinase 9

Currently, the analysis of the fibrosis severity during the restructuring of the surrounding extracellular matrix (ECM) is studied in most of the research works devoted to “cardiac remodeling”. At the same time, the role of the basal membrane of cardiomyocytes in heart diseases was not studied. The basal membrane of cardiomyocytes is a highly organized layer of the ECM which is located on the outer side of the sarcolemma. Degradation of ECM components is carried out by different types of matrix metalloproteinases (MMP), which have proteolytic activity and are actively involved in the process of ECM remodeling, destroying its components such as collagen, elastin, fibronectin, glycosaminoglycans and other structural components.Aim. To evaluate the ECM status in patients with coronary artery disease and its effect on left ventricular myocardial remodeling.Material and methods. Morphological and immunohistochemical (IHC) examination of left ventricular myocardial biopsies was performed in 16 patients undergoing left ventricular reconstruction in combination with coronary artery bypass grafting.Results. The IHC study revealed the accumulation of matrix metalloproteinase-9 in the cytoplasm of cardiomyocytes. This accumulation was combined with partial or complete destruction of the basal membranes (BM) of cardiomyocytes formed by type IV collagen.Conclusion. Type IV collagen destruction in basal membranes of left ventricular cardiomyocyteswasrevealed. It iscausedbytheactionofmatrixmetalloproteinase-9, which accumulates in the cell cytoplasm.

scholarly journals P123 Type I collagen degradation fragments and type IV collagen formation/degradation ratio are serological biomarkers for stricturing (Montreal B2) Crohn’s disease

2021 ◽  
Vol 15 (Supplement_1) ◽  
pp. S214-S215
Author(s):  
A R Bourgonje ◽  
M Alexdottir ◽  
R Loveikyte ◽  
A C Bay-Jensen ◽  
H M van Dullemen ◽  
...  
Keyword(s):  
Crohn’S Disease ◽  
Type Iv Collagen ◽  
Type I Collagen ◽  
Collagen Degradation ◽  
Type I ◽  
Discriminative Power ◽  
Collagen Formation ◽  
Type Iv ◽  
Montreal Classification ◽  
Serological Biomarkers

Abstract Background Crohn’s disease (CD) is characterized by increased extracellular matrix (ECM) remodeling, which is a key pathophysiological mechanism underlying intestinal stricture formation and other fibrotic disease complications. Alterations in intestinal ECM turnover may be reflected by products of collagen formation and degradation that are released into the systemic circulation. In this study, we aimed to investigate associations between serological biomarkers of collagen turnover and disease behavior subtypes according to the Montreal classification in patients with CD. Methods Serological biomarkers of collagen formation (PRO-C3, PRO-C4) and matrix metalloproteinase (MMP)-mediated collagen degradation (reC1M, C3M, C4M, C4G, C6Ma3) were measured using neo-epitope solid-phase competitive enzyme-linked immunosorbent assay (ELISA) technology in 101 patients with CD (Montreal B1: n=47; B2: n=28; B3: n=26) who were characterized according to the Montreal classification. Logistic regression modelling and receiver operating characteristics (ROC) statistics were used to assess discriminative power. Results Specific fragments of MMP-2,9,13-mediated degradation of type I collagen (reC1M) were significantly reduced in patients with stricturing (Montreal B2) disease compared to other disease phenotypes (B1 and B3) (P<0.001). Ratios of type IV collagen formation and degradation (PRO-C4/C4M) were significantly elevated in Montreal B2 patients (P<0.001). No differences in remaining serological biomarkers were observed between the different Montreal subtypes. Both reC1M and PRO-C4/C4M ratios demonstrated high discriminative power to distinguish inflammatory CD (B1) from stricturing (B2) CD, also after adjustment for confounding factors (area under the curve [AUC] 0.85 and 0.84, respectively). Conclusion Elevated degradation of type I collagen and excessive (relative) formation of type IV collagen strongly associate with stricturing CD (Montreal B2) and accurately discriminate it from inflammatory CD (Montreal B1). Therefore, reC1M and PRO-C4/C4M ratios could serve as serological biomarkers for stricturing CD. Our results should be validated in additional prospective, larger patient cohorts to corroborate these findings.

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