Hi,
please find here enclosed a possible answer to Your question and some PDF.
As initially described in granulation tissue and nodules of Dupuytren’s disease, myofibroblasts share morphological features in common with fibroblasts and smooth muscle cells (1,2).
IHC demonstrates heterogeneous cytoskeletal phenotypes among myofibroblasts in terms of intermediate filament protein, smooth muscle actin, and smoth muscle myosin expression. In normal tissue, in granulation tissue, and in pathological tissue 5 cytoskeletal phenotypes have been reported (3,4).
- phenotype V: cells expressing only vimentin
- phenotype VA: cells expressing vimentin and -smooth muscle actin
- phenotype VAD: cells expressing vimentin and -smooth muscle actin, and desmin
- phenotype VD: cells expressing vimentin and desmin
- phenotype VA (D) M: cells expressing vimentin and -smooth muscle actin, and smooth muscle
myosin heavy chains, with and without desmin.
These five phenotypes are readily defined in frozen/paraffin section using immunohistochemistry with commercially available antibodies, in single, double and triple staining.
This heterogeneity could reflect different functional needs since all of these stromal cells participate in visceral contraction or extracellular matrix remodelling (5). Another interpretation proposes that most spindle cells in normal tissues cited as being myofibroblasts might be closer to pericytes, smooth muscle cells, or stromal cells with myoid features of variable degrees that correspond to functional demands (6).
Myofibroblast are present in normal tissues and are involved in repair phenomena, in organ fibrosis (lung fibrosis, liver cirrhosis etc), in “Quasi neoplastic” proliferations (e.g. superficial and deep fibromatosis, myxomas), in the stromal response to neoplasia. Neoplasms of myofibroblasts have been described, but are an uncommon event.
It is to be stressed that myofibroblasts and/or stromal cells with myoid features are not stable in terms of cytoskeletal phenotypes. In normal, abnormal, and pathological conditions, the V phenotype may change into phenotype VA, VAD, VD, and, eventually, into VA (D) M, but terminal smooth muscle differentiation (smooth muscle metaplasia) is never attained.
In conclusion, the myofibroblast still remains an enigmatic cell, one that appears and disappears after completion of its function or, more rarely, one that may persist in certain pathologic conditions.
PDF of paper 7-9 are recent reviews on myofibroblasts in liver fibrosis, in myocardial infarction and in tumoral stroma and are good examples of the complex role of these cells.
1) Gabbiani G et al. Experientia 1971;27:549.
2) Gabbiani G and Majno G. Am J Pathol 1972;66:131.
3) Desmouliere A and Gabbiani G. 1994;29:195.
4) Chiavegato A et al. Virchows Archiv 1995;426:77.
5) Sappino AP et al. Lab Invest 1990;63:144.
6) Eyden BP et al. J Submicroscop Cytol Pathol. 1994;26:347
7) Brenner DA et al. Fibrogenesis & Tissue Repair 2012;5(Suppl 1):S17.
8) Turner NA and Porter KE. Fibrogenesis & Tissue Repair 2013;6:5.
9) Polanska UM. J Cell Physiol 2013;228:1651.
Hi,
please find here enclosed a possible answer to Your question and some PDF.
As initially described in granulation tissue and nodules of Dupuytren’s disease, myofibroblasts share morphological features in common with fibroblasts and smooth muscle cells (1,2).
IHC demonstrates heterogeneous cytoskeletal phenotypes among myofibroblasts in terms of intermediate filament protein, smooth muscle actin, and smoth muscle myosin expression. In normal tissue, in granulation tissue, and in pathological tissue 5 cytoskeletal phenotypes have been reported (3,4).
- phenotype V: cells expressing only vimentin
- phenotype VA: cells expressing vimentin and -smooth muscle actin
- phenotype VAD: cells expressing vimentin and -smooth muscle actin, and desmin
- phenotype VD: cells expressing vimentin and desmin
- phenotype VA (D) M: cells expressing vimentin and -smooth muscle actin, and smooth muscle
myosin heavy chains, with and without desmin.
These five phenotypes are readily defined in frozen/paraffin section using immunohistochemistry with commercially available antibodies, in single, double and triple staining.
This heterogeneity could reflect different functional needs since all of these stromal cells participate in visceral contraction or extracellular matrix remodelling (5). Another interpretation proposes that most spindle cells in normal tissues cited as being myofibroblasts might be closer to pericytes, smooth muscle cells, or stromal cells with myoid features of variable degrees that correspond to functional demands (6).
Myofibroblast are present in normal tissues and are involved in repair phenomena, in organ fibrosis (lung fibrosis, liver cirrhosis etc), in “Quasi neoplastic” proliferations (e.g. superficial and deep fibromatosis, myxomas), in the stromal response to neoplasia. Neoplasms of myofibroblasts have been described, but are an uncommon event.
It is to be stressed that myofibroblasts and/or stromal cells with myoid features are not stable in terms of cytoskeletal phenotypes. In normal, abnormal, and pathological conditions, the V phenotype may change into phenotype VA, VAD, VD, and, eventually, into VA (D) M, but terminal smooth muscle differentiation (smooth muscle metaplasia) is never attained.
In conclusion, the myofibroblast still remains an enigmatic cell, one that appears and disappears after completion of its function or, more rarely, one that may persist in certain pathologic conditions.
PDF of paper 7-9 are recent reviews on myofibroblasts in liver fibrosis, in myocardial infarction and in tumoral stroma and are good examples of the complex role of these cells.
1) Gabbiani G et al. Experientia 1971;27:549.
2) Gabbiani G and Majno G. Am J Pathol 1972;66:131.
3) Desmouliere A and Gabbiani G. 1994;29:195.
4) Chiavegato A et al. Virchows Archiv 1995;426:77.
5) Sappino AP et al. Lab Invest 1990;63:144.
6) Eyden BP et al. J Submicroscop Cytol Pathol. 1994;26:347
7) Brenner DA et al. Fibrogenesis & Tissue Repair 2012;5(Suppl 1):S17.
8) Turner NA and Porter KE. Fibrogenesis & Tissue Repair 2013;6:5.
9) Polanska UM. J Cell Physiol 2013;228:1651.
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