45 research outputs found
Role of myofibroblasts during normal tissue repair and excessive scarring: Interest of their assessment in nephropathies
Following injury, tissue repair process takes place involving inflammation, granulation tissue formation and scar constitution. Granulation tissue develops from the connective tissue surrounding the damaged area and contains vessels, inflammatory cells, fibroblasts and myofibroblasts. Myofibroblasts play an important role in many tissue injuries and fibrocontractive diseases. The process of normal wound repair after tissue injury follows a closely regulated sequence including the activation and the proliferation of fibroblastic cells. In pathological situations, the normal resolution stages are abrogated and the proliferation of myofibroblasts continues, inducing excessive accumulation of extracellular matrix. The differentiation of fibroblastic cells into myofibroblasts is an early event in the development of tissue fibrosis. Myofibroblastic cells express smooth muscle cytoskeletal markers (asmooth muscle actin in particular) and participate actively in the production of extracellular matrix. The evaluation of myofibroblast differentiation in renal biopsies would be useful for histopathologists to appreciate the intensity of tissue injury and particularly to predict the long term outcome of some nephropathies. Immunohistochemical studies for a-smooth muscle actin should be made systematically in renal tissue biopsies. Myofibroblastic differentiation appears to play a significant role in the progression of renal failure and seems to be a useful marker of progressive disease
Role of myofibroblasts during normal tissue repair and excessive scarring:Interest of their assessment in nephropathies
Following injury, tissue repair process takes
place involving inflammation, granulation tissue
formation and scar constitution. Granulation tissue
develops from the connective tissue surrounding the
damaged area and contains vessels, inflammatory cells,
fibroblasts and myofibroblasts. Myofibroblasts play an
important role in many tissue injuries and fibrocontractive
diseases. The process of normal wound
repair after tissue injury follows a closely regulated
sequence including the activation and the proliferation of
fibroblastic cells. In pathological situations, the normal
resolution stages are abrogated and the proliferation
of myofibroblasts continues, inducing excessive
accumulation of extracellular matrix. The differentiation
of fibroblastic cells into myofibroblasts is an early event
in the development of tissue fibrosis. Myofibroblastic
cells express smooth muscle cytoskeletal markers (asmooth
muscle actin in particular) and participate
actively in the production of extracellular matrix. The
evaluation of myofibroblast differentiation in renal
biopsies would be useful for histopathologists to
appreciate the intensity of tissue injury and particularly
to predict the long term outcome of some nephropathies.
Immunohistochemical studies for a-smooth muscle actin
should be made systematically in renal tissue biopsies.
Myofibroblastic differentiation appears to play a
significant role in the progression of renal failure and
seems to be a useful marker of progressive disease
Apoptosis during wound healing, fibrocontractive diseases and vascular wall injury
Following injury, tissue repair involves inflammation, granulation tissue formation and scar constitution. Granulation tissue develops from the connective tissue surrounding the damaged or missing area and contains mainly small vessels, inflammatory cells, fibroblasts and myofibroblasts. As the wound closes and evolves into a scar, there is a striking decrease in cellularity, including disappearance of typical myofibroblasts. The question arises as to what process is responsible for granulation tissue cell disappearance. Our results (in cutaneous wounds) and results of other laboratories (particularly in lungs and kidney) suggest that apoptosis is the mechanism responsible for the evolution of granulation tissue into a scar. During excessive scarring (hypertrophic scar or fibrosis), it is conceivable that the process of apoptosis cannot take place. After experimental endothelial injury in an artery, accumulation of smooth muscle cells participates in the formation of intimal thickening. Apoptotic features have been observed in cells of intimal thickening and also within human atherosclerotic plaques. In the case of atherosclerosis, apoptosis could be detrimental: since smooth muscle cells participate in plaque stability, apoptosis could lead to weakening and rupture of the plaque. These results underline the fact that both increased cell survival or excessive cell death can be associated with pathological disorders. Specific therapies devised to enhance or decrease the susceptibility of individual cell types to apoptosis development could modify the evolution of a variety of human diseases