Hyaluronan enhances cartilage repair through low grade tissue remodeling involving cytokines and matrix metalloproteinases

2004 ◽  
Vol 53 (10) ◽  
pp. 534-543 ◽  
Author(s):  
G. A. Homandberg ◽  
V. Ummadi ◽  
H. Kang
Keyword(s):  
Matrix Metalloproteinases ◽  
Cartilage Repair ◽  
Tissue Remodeling ◽  
Low Grade

MATRIX METALLOPROTEINASES AND ITS RELATED PROTEINS ARE PROGNOSTIC FACTORS OF LOW GRADE RENAL CELL CARCINOMA WITHOUT METASTASIS

2008 ◽  
Vol 179 (4S) ◽  
pp. 375-376
Author(s):  
Kenya Yamaguchi ◽  
Nozomu Kawata ◽  
Yusuke Nagane ◽  
Takumi Igarashi ◽  
Taketo Ichinose ◽  
...  
Keyword(s):  
Renal Cell Carcinoma ◽  
Prognostic Factors ◽  
Matrix Metalloproteinases ◽  
Cell Carcinoma ◽  
Renal Cell ◽  
Low Grade ◽  
Related Proteins

scholarly journals Adipose Tissue Remodeling as Homeostatic Inflammation

2011 ◽  
Vol 2011 ◽  
pp. 1-8 ◽  
Author(s):  
Michiko Itoh ◽  
Takayoshi Suganami ◽  
Rumi Hachiya ◽  
Yoshihiro Ogawa
Keyword(s):  
Fatty Acids ◽  
Adipose Tissue ◽  
Inflammatory Responses ◽  
Saturated Fatty Acids ◽  
Tissue Remodeling ◽  
Low Grade ◽  
Adipose Tissue Inflammation ◽  
Tissue Inflammation ◽  
Adipose Tissue Remodeling ◽  
Novel Therapeutic Strategies

Evidence has accumulated indicating that obesity is associated with a state of chronic, low-grade inflammation. Obese adipose tissue is characterized by dynamic changes in cellular composition and function, which may be referred to as “adipose tissue remodeling”. Among stromal cells in the adipose tissue, infiltrated macrophages play an important role in adipose tissue inflammation and systemic insulin resistance. We have demonstrated that a paracrine loop involving saturated fatty acids and tumor necrosis factor-α derived from adipocytes and macrophages, respectively, aggravates obesity-induced adipose tissue inflammation. Notably, saturated fatty acids, which are released from hypertrophied adipocytes via the macrophage-induced lipolysis, serve as a naturally occurring ligand for Toll-like receptor 4 complex, thereby activating macrophages. Such a sustained interaction between endogenous ligands derived from parenchymal cells and pathogen sensors expressed in stromal immune cells should lead to chronic inflammatory responses ranging from the basal homeostatic state to diseased tissue remodeling, which may be referred to as “homeostatic inflammation”. We, therefore, postulate that adipose tissue remodeling may represent a prototypic example of homeostatic inflammation. Understanding the molecular mechanism underlying homeostatic inflammation may lead to the identification of novel therapeutic strategies to prevent or treat obesity-related complications.

Matrix metalloproteinases and tissue remodeling in hypertrophic cardiomyopathy

2008 ◽  
Vol 156 (1) ◽  
pp. 85-91 ◽  
Author(s):  
Vanessa Roldán ◽  
Francisco Marín ◽  
Juan R. Gimeno ◽  
Francisco Ruiz-Espejo ◽  
Josefa González ◽  
...  
Keyword(s):  
Hypertrophic Cardiomyopathy ◽  
Matrix Metalloproteinases ◽  
Tissue Remodeling

Ovarian tissue remodeling: role of matrix metalloproteinases and their inhibitors

2002 ◽  
Vol 191 (1) ◽  
pp. 45-56 ◽  
Author(s):  
Michael F. Smith ◽  
William A. Ricke ◽  
Leanne J. Bakke ◽  
Mark P.D. Dow ◽  
George W. Smith
Keyword(s):  
Matrix Metalloproteinases ◽  
Ovarian Tissue ◽  
Tissue Remodeling

scholarly journals Extracellular Matrix Degradation and Tissue Remodeling in Periprosthetic Loosening and Osteolysis: Focus on Matrix Metalloproteinases, Their Endogenous Tissue Inhibitors, and the Proteasome

2013 ◽  
Vol 2013 ◽  
pp. 1-18 ◽  
Author(s):  
Spyros A. Syggelos ◽  
Alexios J. Aletras ◽  
Ioanna Smirlaki ◽  
Spyros S. Skandalis
Keyword(s):  
Extracellular Matrix ◽  
Matrix Metalloproteinases ◽  
Molecular Mechanisms ◽  
Total Joint Replacement ◽  
Proteolytic Enzymes ◽  
Tissue Remodeling ◽  
Wear Particle ◽  
Matrix Degradation ◽  
Tissue Inhibitors ◽  
Extracellular Matrix Degradation

The leading complication of total joint replacement is periprosthetic osteolysis, which often results in aseptic loosening of the implant, leading to revision surgery. Extracellular matrix degradation and connective tissue remodeling around implants have been considered as major biological events in the periprosthetic loosening. Critical mediators of wear particle-induced inflammatory osteolysis released by periprosthetic synovial cells (mainly macrophages) are inflammatory cytokines, chemokines, and proteolytic enzymes, mainly matrix metalloproteinases (MMPs). Numerous studies reveal a strong interdependence of MMP expression and activity with the molecular mechanisms that control the composition and turnover of periprosthetic matrices. MMPs can either actively modulate or be modulated by the molecular mechanisms that determine the debris-induced remodeling of the periprosthetic microenvironment. In the present study, the molecular mechanisms that control the composition, turnover, and activity of matrix macromolecules within the periprosthetic microenvironment exposed to wear debris are summarized and presented. Special emphasis is given to MMPs and their endogenous tissue inhibitors (TIMPs), as well as to the proteasome pathway, which appears to be an elegant molecular regulator of specific matrix macromolecules (including specific MMPs and TIMPs). Furthermore, strong rationale for potential clinical applications of the described molecular mechanisms to the treatment of periprosthetic loosening and osteolysis is provided.

Sign in / Sign up

Export Citation Format

Share Document