Tissues lose mechanical integrity when our body is injured.
To rapidly restore mechanical stability a multitude of cell types can jump into action by acquiring a reparative phenotype-the myofibroblast.
These cytoskeletal features not only enable the myofibroblast to remodel and contract the extracellular matrix but to adapt its activity to changes in the mechanical microenvironment.
Rapid repair comes at the cost of tissue contracture due to the inability of the myofibroblast to regenerate tissue.
More detailed during tissue repair in skin, connective tissue growth factor (CTGF/CCN2) is induced.
However, what the exact cell types are that express CTGF in normal and wounded skin remain controversial.
Scientists used transgenic knock-in mice in which the Pacific jellyfish Aequorea victoria enhanced green fluorescent protein (E-GFP) gene has been inserted between the endogenous CTGF promoter and gene.
Unwounded (day 0) and wounded (days 3 and 7) skin was examined for GFP to detect cells in which the CTGF promoter was active, alpha-smooth muscle actin (alpha-SMA) to detect myofibroblasts, and NG2 expression to detect pericytes.
In unwounded mice, CTGF expression was absent in epidermis and was present in a few cells in the dermis.
Upon wounding, CTGF expression was induced in the dermis.
Double immunolabeling revealed that CTGF-expressing cells also expressed alpha-SMA, indicating the CTGF was expressed in myofibroblasts.
A subset (~30%) of myofibroblasts were also NG2 positive, indicating that pericytes significantly contributed to the number of myofibroblasts in the wound.
Pericytes also expressed CTGF.
Collectively, these results indicate that CTGF expression in skin correlates with myofibroblast induction, and that CTGF-expressing pericytes are significant contributors to myofibroblast activity during cutaneous tissue repair.