Altered Procollagen Gene Expression in Mid-Gestational Mouse Excisional Wounds

Goldberg, Stephanie R.; Quirk, Gerald L.; Sykes, Virginia W.; Kordula, Tomasz; Lanning, David A.

doi:10.1016/j.jss.2007.05.013

Cited by 20 publications

(19 citation statements)

References 15 publications

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“…These data suggest that p1158/59 stimulated collagen III deposition, resulting in a decreased ratio of collagen I/collagen III, which would generate a less stiff scar and may explain the better LV geometry (Figure 4C). Fetal tissues show increased expression of collagen III compared to adult tissue, which has led some to hypothesize that collagen III is a main contributor to the scarless phenotype observed in the early stages of gestation (30). We further looked at the expression of MMPs and tissue inhibitors of metalloproteinases (TIMP), since MMP activity and MMP/TIMP ratios can determine ECM turnover and remodeling (31).…”

Section: Resultsmentioning

confidence: 99%

A Novel Collagen Matricryptin Reduces Left Ventricular Dilation Post-Myocardial Infarction by Promoting Scar Formation and Angiogenesis

Lindsey

Iyer

Zamilpa

et al. 2015

Journal of the American College of Cardiology

136

118

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Background Proteolytically-released extracellular matrix (ECM) fragments, matricryptins, are biologically active and play important roles in wound healing. Following myocardial infarction (MI), collagen I, a major component of cardiac ECM, is cleaved by matrix metalloproteinases (MMPs). Objectives We identified novel collagen-derived matricryptins generated post-MI that mediate remodeling of the left ventricle (LV). Results In situ, MMP-2 and -9 generate a collagen Iα1 C-1158/59 fragment, and MMP-9 can further degrade it. The C-1158/59 fragment was identified post-MI both in human plasma and mouse LV at levels that inversely correlated to MMP-9 levels. We synthesized a peptide beginning at the cleavage site (p1158/59, amino acids 1159 to 1173) to investigate its biological functions. In vitro, p1158/59 stimulated fibroblast wound healing and robustly promoted angiogenesis. In vivo, early post-MI treatment with p1158/59 reduced LV dilation at day 7 post-MI by preserving LV structure (p < 0.05 versus control). The p1158/59 stimulated both in vitro and in vivo wound healing by enhancing basement membrane proteins, granulation tissue components, and angiogenic factors. Conclusions Collagen Iα1 matricryptin p1158/59 facilitates LV remodeling post-MI by regulating scar formation through targeted ECM generation and stimulation of angiogenesis.

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Section: Resultsmentioning

confidence: 99%

A Novel Collagen Matricryptin Reduces Left Ventricular Dilation Post-Myocardial Infarction by Promoting Scar Formation and Angiogenesis

Lindsey

Iyer

Zamilpa

et al. 2015

Journal of the American College of Cardiology

136

118

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“…Fetal bioscaffold leads to a decreased Cola1/Cola3 ratio characteristic of the developing heart and that has been suggested to contribute to the scarless phenotype seen in early stages of gestation [69]. Moreover, a decreased ratio of these two collagen forms has been shown to improve tissue remodeling in response to myocardial infarction [70].…”

Section: A C C E P T E D Accepted Manuscriptmentioning

confidence: 99%

Three-dimensional scaffolds of fetal decellularized hearts exhibit enhanced potential to support cardiac cells in comparison to the adult

et al. 2016

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“…This expression pattern suggests Col3 is a key mediator of tissue regeneration and may provide a target for therapeutic intervention for impaired wound healing. Increased expression of Col3 in fetal tissues relative to adult tissues has led some to hypothesize that Col3 may contribute to the scarless phenotype of midgestational cutaneous wounds [Cuttle et al, 2005;Goldberg et al, 2007]. Further supporting a role for Col3 in modulating scar formation is the fact that humans with Col3 mutations have impaired healing which may be associated with excessive scar formation [Burk et al, 2006;Germain, 2007;Sharma et al, 2009].…”

Section: Introductionmentioning

confidence: 99%

Diminished Type III Collagen Promotes Myofibroblast Differentiation and Increases Scar Deposition in Cutaneous Wound Healing

Volk

Wang²,

Mauldin³

et al. 2011

Cells Tissues Organs

197

153

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The repair of cutaneous wounds in the postnatal animal is associated with the development of scar tissue. Directing cell activities to efficiently heal wounds while minimizing the development of scar tissue is a major goal of wound management and the focus of intensive research efforts. Type III collagen (Col3), expressed in early granulation tissue, has been proposed to play a prominent role in cutaneous wound repair, although little is known about its role in this process. To establish the role of Col3 in cutaneous wound repair, we examined the healing of excisional wounds in a previously described murine model of Col3 deficiency. Col3 deficiency (Col3+/–) in aged mice resulted in accelerated wound closure with increased wound contraction. In addition, Col3-deficient mice had increased myofibroblast density in the wound granulation tissue as evidenced by an increased expression of the myofibroblast marker, α-smooth muscle actin. In vitro, dermal fibroblasts obtained from Col3-deficient embryos (Col3+/– and –/–) were more efficient at collagen gel contraction and also displayed increased myofibroblast differentiation compared to those harvested from wild-type (Col3+/+) embryos. Finally, wounds from Col3-deficient mice also had significantly more scar tissue area on day 21 postwounding compared to wild-type mice. The effect of Col3 expression on myofibroblast differentiation and scar formation in this model suggests a previously undefined role for this ECM protein in tissue regeneration and repair.

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Altered Procollagen Gene Expression in Mid-Gestational Mouse Excisional Wounds

Cited by 20 publications

References 15 publications

A Novel Collagen Matricryptin Reduces Left Ventricular Dilation Post-Myocardial Infarction by Promoting Scar Formation and Angiogenesis

A Novel Collagen Matricryptin Reduces Left Ventricular Dilation Post-Myocardial Infarction by Promoting Scar Formation and Angiogenesis

Three-dimensional scaffolds of fetal decellularized hearts exhibit enhanced potential to support cardiac cells in comparison to the adult

Diminished Type III Collagen Promotes Myofibroblast Differentiation and Increases Scar Deposition in Cutaneous Wound Healing

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