Expression of smooth muscle actin in cells involved in distraction osteogenesis in a rat model

Abstract

Distraction osteogenesis has proven to be of great value for the treatment of a variety of musculoskeletal problems. Little is still known, however, about the phenotypic changes in the cells participating in the bone formation process, induced by the procedure. Recent findings of the expression of a contractile muscle actin isoform, a-smooth muscle actin (SMA), in musculoskeletal connective tissue cells prompted this immunohistochemical study of the expression of SMA in cells participating in distraction osteogenesis in a rat model. The tissues within and adjacent to the distraction site could be distinguished histologically on the basis of cell morphology, density, and extracellular matrix make-up. The percentage of SMA-containing cells within each tissue zone was graded from 0 to 4. The majority of the cells in each of the zones stained positive for SMA within five days of the distraction period. The SMA-containing cells included those with elongated morphology in the center of the distraction site and the active osteoblasts on the surfaces of the newly forming bone.These finding warrant further investigation of the role of this contractile actin isoform in distraction osteogenesis and investigation of the effects of modulation of this actin isoform on the procedure.

Vascular development during distraction osteogenesis proceeds by sequential intramuscular arteriogenesis followed by intraosteal angiogenesis

“…Specifically, many SMA-positive, fibrous cells were observed within the distraction gap at POD 10, which is consistent with the peak in mRNA expression of Ephrin 2b (a gene associated with smooth muscle cells that would be concurrently expressed with SMA) found in the gap tissues at this time-point in our recent study on DO [20]. Prior studies have indicated that SMA expression is associated with movement of mesenchymal stem cells into the fracture callus [30] and the DO regenerate [31], and have speculated that SMA is a marker of stem cells that give rise to tissues in the fracture callus [32]. Collectively, these findings raise interesting questions about the sources of the cell populations that contribute to vascular tissue development.…”

Combination of stromal cell‐derived factor‐1 and collagen–glycosaminoglycan scaffold delays contraction and accelerates reepithelialization of dermal wounds in wild‐type mice

“…Digital images of the stained sections were obtained at 4× magnification to measure the relative percentage of the α-SMA-positive cell area in the wound area using NIH ImageJ software. 16 H&E stain was performed to visualize and compare the infiltration of inflammatory cells into the wound area among the animal groups at an early time point (Day 3). The inflammatory cell density was evaluated among the control and the GCSF+SDF-1 animal groups by assessing three fields per histological stained slide (one in the middle of the wound scaffold area and two on either lateral aspect) at ×40 magnification.…”

Calcification on cultured human dental pulp cells exposed to high glucose level

“…There is an indication that NG2 and calponin are more suitable markers for odontoblast progenitors than α-SMA, which is a marker suitable for osteogenesis. It has been reported that α-SMA can be expressed by osteoblasts (22). In the rat pulp cavity after tooth replantation, α-SMA positive cells are localized around newly-formed bone-like tissue, whereas they are not found around newly-formed dentin-like tissue (23).…”