Extracellular Matrix Gene Expression after Vocal Fold Injury in a Rabbit Model

Rousseau, Bernard; Ge, Ping Jiang; Ohno, Tomohisa; French, Lesley C.; Thibeault, Susan L.

doi:10.1177/000348940811700809

Cited by 41 publications

(39 citation statements)

References 24 publications

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“…It was previously demonstrated that an increase in collagen type I and type III gene expression at 72 h post-injury in rabbit vocal folds coincides with the proliferative phase of wound repair in this model (Rousseau et al 2008). In our previous work we showed decreased connective tissue fibers in the wounds of oleic acid treated mice (Cardoso et al 2004).…”

Section: Discussionsupporting

confidence: 52%

Oleic acid modulation of the immune response in wound healing: A new approach for skin repair

et al. 2011

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Section: Discussionsupporting

confidence: 52%

Oleic acid modulation of the immune response in wound healing: A new approach for skin repair

et al. 2011

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“…In addition to angiogenesis, MMP-9 has been shown to modulate inflammation and early cellular recruitment during wound healing. [62][63][64] A role of MMP-9 in scar tissue formation has also been recognized recently. 65,66 Although we cannot detect Figure 6.…”

Section: Discussionmentioning

confidence: 97%

Rescue of Impaired Fracture Healing in COX-2−/− Mice via Activation of Prostaglandin E2 Receptor Subtype 4

Xie

Liang

Xue

et al. 2009

The American Journal of Pathology

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Although the essential role of cyclooxygenase (COX)-2 in fracture healing is known, the targeted genes and molecular pathways remain unclear. Using prostaglandin E2 receptor (EP)2 and EP4 agonists, we examined the effects of EP receptor activation in compensation for the lack of COX-2 during fracture healing. In a fracturehealing model, COX-2 ؊/؊ mice showed delayed initiation and impaired endochondral bone repair, accompanied by a severe angiogenesis deficiency. The EP4 agonist markedly improved the impaired healing in COX-2 ؊/؊ mice, as evidenced by restoration of bony callus formation on day 14, a near complete reversal of bone formation, and an approximately 70% improvement of angiogenesis in the COX-2 ؊/؊ callus. In comparison, the EP2 agonist only marginally enhanced bone formation in COX-2 ؊/؊ mice. To determine the differential roles of EP2 and EP4 receptors on COX-2-mediated fracture repair, the effects of selective EP agonists on chondrogenesis were examined in E11.5 longterm limb bud micromass cultures. Only the EP4 agonist significantly increased cartilage nodule formation similar to that observed during prostaglandin E2 treatment. The prostaglandin E2/EP4 agonist also stimulated MMP-9 expression in bone marrow stromal cell cultures. The EP4 agonist further restored the reduction of MMP-9 expression in the COX-2 ؊/؊ fracture callus. Taken together, our studies demonstrate that EP2 and EP4 have differential functions during endochondral bone repair. Activation of EP4, but not EP2 rescued impaired bone fracture healing in COX-2 ؊/؊ mice. Fracture healing is a complex process orchestrated by precise presentation of growth factors and cytokines that control activation, proliferation, and differentiation of the local mesenchymal stem/progenitor cells. Fracture healing begins with hematoma formation and an inflammatory response. The activated stem/progenitor cells proliferate and further differentiate into osteoblasts and chondrocytes. Endochondral bone formation takes place toward the most central avascular region of the callus. Chondrogenesis initiates directly adjacent to the surface of the cortical bone and is surrounded by less-differentiated mesenchymal progenitor cells. The subsequent expansion of the callus involves the conversion of the lingering mesenchymal progenitor cells into chondrocytes and further proliferation and differentiation of chondrocytes into a calcified cartilage template that permits vascular invasion and bone formation. Areas of intramembranous bone formation flank the area of endochondral ossification, particularly along the bone surface furthest from the central fracture site where the blood supply is typically better preserved. The coordinated endochondral and intramembranous bone formation pathways eventually result in a bridging mineralized callus that re-establishes the integrity of the skeletal element.

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“…Type 1 collagen produced during vocal fold healing differs in molecular and macroscopic structure from the native collagen, which is largely type 3. Type 3 fibers are of finer caliber than type 1 fibers and well-organized in the normal vocal fold [20].…”

Section: Vocal Fold Wound Healingmentioning

confidence: 96%

Perspectives on Adipose-Derived Stem/Stromal Cells as Potential Treatment for Scarred Vocal Folds: Opportunity and Challenges

Kumai¹,

Kobler²,

Herrera³

et al. 2010

CSCR

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Regenerative therapy using stem cells for the treatment of vocal fold wound healing and fibrosis is a very active area of research in Otolaryngology. Although modern phonosurgical methods can deal with many types of vocal fold pathology, vocal fold scar remains a clinical challenge. Trauma (e.g. vocal abuse, phonosurgery) and inflammation (e.g. laryngitis) are the two main causes of the vocal fold scarring. Several recent reviews detail the problem of vocal fold scarring and the array of possible solutions under investigation. The search for solutions includes autologous tissues, biomaterial implants, growth factors, anti-fibrotic agents and stem cells. This review focuses on emerging research on stem cells for vocal fold regeneration and our own studies of interactions between adipose-derived stem/stromal cells and vocal fold fibroblasts using an in vitro model. While clearly an opportunity, the challenging approach of treating vocal scarring using ASCs has just started. For future in vivo studies, improvements in cell viability and markers of stem-cell differentiation into normal fibroblasts are needed. The roles of stem cell-derived cytokines in paracrine signaling need to be further explored at a cellular level in vitro, and then extended to in vivo experiments.

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Extracellular Matrix Gene Expression after Vocal Fold Injury in a Rabbit Model

Cited by 41 publications

References 24 publications

Oleic acid modulation of the immune response in wound healing: A new approach for skin repair

Oleic acid modulation of the immune response in wound healing: A new approach for skin repair

Rescue of Impaired Fracture Healing in COX-2−/− Mice via Activation of Prostaglandin E2 Receptor Subtype 4

Perspectives on Adipose-Derived Stem/Stromal Cells as Potential Treatment for Scarred Vocal Folds: Opportunity and Challenges

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