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Role of emmprin/CD147 in tissue remodeling
- Source :
- Connective Tissue Research, Connective Tissue Research, Taylor & Francis, 2008, 49 (3), pp.175-9. ⟨10.1080/03008200802151722⟩
- Publication Year :
- 2008
-
Abstract
- Emmprin/CD147 is a cell membrane glycoprotein that belongs to the Ig superfamily and is involved in numerous physiological and pathological systems. Through its ability to interact with multiple partners within the cell surface and its potential to regulate the expression of several targets within the cell, emmprin may have different functions depending on the cell or tissue type. However, its role in tissue remodeling remains the most clearly demonstrated. Emmprin is able to induce, in the same cellular model, both the matrix metalloproteinases and the serine protease urokinase plasminogen activator, whose concerted action in the breakdown of the extracellular matrix (ECM) during various physiopathological situations has been reported. In addition, emmprin also promotes myofibroblasts' differentiation and tissue contraction through the induction of alpha smooth muscle actin, thus expanding on the mechanism by which emmprin remodels ECM.
- Subjects :
- Cellular differentiation
Cell
[SDV.BC]Life Sciences [q-bio]/Cellular Biology
Matrix metalloproteinase
Biochemistry
Extracellular matrix
Cell membrane
03 medical and health sciences
0302 clinical medicine
Rheumatology
Neoplasms
medicine
Animals
Humans
Orthopedics and Sports Medicine
Molecular Biology
Actin
030304 developmental biology
0303 health sciences
Chemistry
Cell Differentiation
Cell Biology
Urokinase-Type Plasminogen Activator
Matrix Metalloproteinases
Cell biology
Extracellular Matrix
medicine.anatomical_structure
030220 oncology & carcinogenesis
Enzyme Induction
Basigin
Cellular model
Myofibroblast
Subjects
Details
- ISSN :
- 16078438 and 03008207
- Volume :
- 49
- Issue :
- 3
- Database :
- OpenAIRE
- Journal :
- Connective tissue research
- Accession number :
- edsair.doi.dedup.....c389c2aaee3f424b3f61ed15b2bacf7b
- Full Text :
- https://doi.org/10.1080/03008200802151722⟩