Modulation of wound contracture α‐smooth muscle actin and multispecific vitronectin receptor integrin αvβ3 in the rabbit's experimental model

Kahi, Cynthia G El; Atiyeh, Bishara S.; Hussein, Inaya Abdallah Hajj; Jurjus, Rosalyne; Dibo, Saad; Jurjus, A

doi:10.1111/j.1742-481x.2009.00597.x

Cited by 25 publications

(19 citation statements)

References 44 publications

(99 reference statements)

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“…The persistent presence of myofibroblasts is a distinctive feature of HTS and contributes to excessive matrix production [21], [34]. Differentiation of fibroblasts into myofibroblasts is closely associated with α-SMA [17], [35]. Our results indicate down-regulation of α-SMA expression by bFGF in the HSF and rabbit model (Figure 5 and 6J).…”

Section: Discussionmentioning

confidence: 58%

The Anti-Scar Effects of Basic Fibroblast Growth Factor on the Wound Repair In Vitro and In Vivo

et al. 2013

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Hypertrophic scars (HTS) and keloids are challenging problems. Their pathogenesis results from an overproduction of fibroblasts and excessive deposition of collagen. Studies suggest a possible anti-scarring effect of basic fibroblast growth factor (bFGF) during wound healing, but the precise mechanisms of bFGF are still unclear. In view of this, we investigated the therapeutic effects of bFGF on HTS animal model as well as human scar fibroblasts (HSF) model. We show that bFGF promoted wound healing and reduced the area of flattened non-pathological scars in rat skin wounds and HTS in the rabbit ear. We provide evidence of a new therapeutic strategy: bFGF administration for the treatment of HTS. The scar elevation index (SEI) and epidermal thickness index (ETI) was also significantly reduced. Histological reveal that bFGF exhibited significant amelioration of the collagen tissue. bFGF regulated extracellular matrix (ECM) synthesis and degradation via interference in the collagen distribution, the α-smooth muscle actin (α-SMA) and transforming growth factor-1 (TGF-β1) expression. In addition, bFGF reduced scarring and promoted wound healing by inhibiting TGFβ1/SMAD-dependent pathway. The levels of fibronectin (FN), tissue inhibitor of metalloproteinase-1 (TIMP-1) collagen I, and collagen III were evidently decreased, and matrix metalloproteinase-1 (MMP-1) and apoptosis cells were markedly increased. These results suggest that bFGF possesses favorable therapeutic effects on hypertrophic scars in vitro and in vivo, which may be an effective cure for human hypertrophic scars.

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Section: Discussionmentioning

confidence: 58%

The Anti-Scar Effects of Basic Fibroblast Growth Factor on the Wound Repair In Vitro and In Vivo

et al. 2013

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“…Notably, MEBO enhanced the protein expression of VEGF and bFGF and also elevated their mRNA expression. A previous study reported that MEBO enhanced α-smooth muscle actin in fibroblasts, indicating that MEBO activates fibroblasts (43). It is hypothesized that leukocytes, including fibroblasts and endothelial cells are the primary origin of VEGF and bFGF (41).…”

Section: Discussionmentioning

confidence: 99%

“…In addition, increasing evidence indicates that MEBO promotes wound contraction and improves scar quality of wounds (43,46). Therefore, MEBO is hypothesized to be an ideal therapy for cutaneous wounds.…”

Section: Discussionmentioning

confidence: 99%

Moist exposed burn ointment promotes cutaneous excisional wound healing in rats involving VEGF and bFGF

Tang

Han

Feng

et al. 2014

Molecular Medicine Reports

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Abstract. Cutaneous delayed wounds are a challenging clinical problem, and vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF) exhibit key roles in wound healing. Moist exposed burn ointment (MEBO), a Chinese burn ointment with a USA patented formulation, has been reported to promote chronic ischemic and neurogenic ulcer healing in patients; however, the underlying mechanisms remain unclear. In the present study, MEBO significantly promoted the formation of granulation tissue in cutaneous excisional wounds, shortened the time of wound healing, and increased neovascularization and the number of fibroblasts. Furthermore, as well as enhancing the protein expression, MEBO application also increased the gene expression of VEGF and bFGF. The results indicate that MEBO promotes cutaneous excisional wound healing by at least partially enhancing VEGF and bFGF production, implicating the potential uses of MEBO for delayed cutaneous wound healing. IntroductionCutaneous wounds, known as ulcers, are an extremely common clinical problem and often arise following acute or chronic mechanical causes, physical or chemical burns, frostbite, infections, and disorders, including rheumatism, diabetes, peripheral vascular disease, lipodermatosclerosis and malignant tumors (1,2). Furthermore, cutaneous wound healing may be significantly delayed due to the aforementioned factors. At present, delayed cutaneous wounds are one of major burdens for health care, and lead to a reduced quality of life in patients who suffer from this type of wound (3,4).Wound healing is a complicated biological process involving a series of dynamic events, including hemostasia, inflammation, cell proliferation and differentiation, neovascularization, granulation tissue formation, collagen synthesis, epithelialization, and wound contraction. Increasing evidence has established the hypothesis that growth factors, including vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF), are key regulators of normal and abnormal angiogenesis, and tissue repair in animals and humans (5-8). VEGF promotes angiogenesis/vasculogenesis and vascular permeability, and enhances endothelial cell proliferation and migration as well as the adhesion of leukocytes (5,9). Further research revealed that VEGF stimulates hydrogen sulfide synthesis and release from endothelial cells, thus leading to subsequent endothelial cell growth, migration and permeability, microvessel formation, and wound healing (10). In addition, VEGF promotes epithelialization and collagen deposition in the wound (11). FGF-2, known as bFGF, is a member of a large FGF family and induces angiogenesis, endothelial cell and fibroblast proliferation, and wound healing (12)(13)(14). Recent data indicated that bFGF-mediated angiogenesis refers to endothelial cell proliferation, migration and tube formation by activating c-Jun N-terminal kinase/stress-activated protein kinase signaling (15). Notably, the expression of VEGF and bFGF was increased following skin in...

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“…Initially type III collagen is produced and then replaced by type I collagen [18]–[20]. Myofibroblasts can contract by using a smooth muscle type actin-myosin complex, rich in α-smooth muscle actin (αSMA) and are involved in the contraction and closure of wounds [21], [22]. αSMA is commonly used as a marker for the detection of myofibroblasts, but it is also present in pericytes located at the wall of blood vessels.…”

Section: Introductionmentioning

confidence: 99%

Immunohistochemical Monitoring of Wound Healing in Antibiotic Treated Buruli Ulcer Patients

Andreoli

Ruf

Sopoh³

et al. 2014

PLoS Negl Trop Dis

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BackgroundWhile traditionally surgery has dominated the clinical management of Buruli ulcer (BU), the introduction of the combination chemotherapy with oral rifampicin and intramuscular streptomycin greatly improved treatment and reduced recurrence rates. However management of the often extensive lesions after successful specific therapy has remained a challenge, in particular in rural areas of the African countries which carry the highest burden of disease. For reasons not fully understood, wound healing is delayed in a proportion of antibiotic treated BU patients. Therefore, we have performed immunohistochemical investigations to identify markers which may be suitable to monitor wound healing progression.Methodology/Principal findingsTissue specimens from eight BU patients with plaque lesions collected before, during and after chemotherapy were analyzed by immunohistochemistry for the presence of a set of markers associated with connective tissue neo-formation, tissue remodeling and epidermal activation. Several target proteins turned out to be suitable to monitor wound healing. While α-smooth muscle actin positive myofibroblasts were not found in untreated lesions, they emerged during the healing process. These cells produced abundant extracellular matrix proteins, such as pro-collagen 1 and tenascin and were found in fibronectin rich areas. After antibiotic treatment many cells, including myofibroblasts, revealed an activated phenotype as they showed ribosomal protein S6 phosphorylation, a marker for translation initiation. In addition, healing wounds revealed dermal tissue remodeling by apoptosis, and showed increased cytokeratin 16 expression in the epidermis.Conclusion/SignificanceWe have identified a set of markers that allow monitoring wound healing in antibiotic treated BU lesions by immunohistochemistry. Studies with this marker panel may help to better understand disturbances responsible for wound healing delays observed in some BU patients.

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Modulation of wound contracture α‐smooth muscle actin and multispecific vitronectin receptor integrin αvβ3 in the rabbit's experimental model

Cited by 25 publications

References 44 publications

The Anti-Scar Effects of Basic Fibroblast Growth Factor on the Wound Repair In Vitro and In Vivo

The Anti-Scar Effects of Basic Fibroblast Growth Factor on the Wound Repair In Vitro and In Vivo

Moist exposed burn ointment promotes cutaneous excisional wound healing in rats involving VEGF and bFGF

Immunohistochemical Monitoring of Wound Healing in Antibiotic Treated Buruli Ulcer Patients

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