Differential Expression of Procollagen Genes Between Mid- and Late-Gestational Fetal Fibroblasts

Carter, Richard; Jain, Kunoor; Sykes, Virginia W.; Lanning, David A.

doi:10.1016/j.jss.2009.03.056

Cited by 32 publications

(21 citation statements)

References 13 publications

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“…62 This correlates with the observation that scarless fetal wound healing is associated with a higher ratio of collagen III to collagen I in multiple small and large mammal models. [63][64][65][66] Likewise, collagen type V has been shown to regulate collagen I fiber assembly, with mice deficient in collagen V demonstrating large structurally abnormal collagen fibrils. 67,68 However its presence has been associated with decreased dermal fibroblast apoptosis, increased Earliest demonstrable histologic appearance and regular histologic appearance of ECM components in human wounds is indicated.…”

Section: Fibrillar Collagensmentioning

confidence: 99%

Extracellular Matrix and Dermal Fibroblast Function in the Healing Wound

Tracy

Minasian

Caterson

2016

Advances in Wound Care

674

584

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Section: Fibrillar Collagensmentioning

confidence: 99%

Extracellular Matrix and Dermal Fibroblast Function in the Healing Wound

Tracy

Minasian

Caterson

2016

Advances in Wound Care

674

584

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“…Collagens I and III, the major fibrillar collagens in connective tissues, play important roles in tissue repair [1]. In particular, collagen III is suggested to regulate collagen I synthesis [2], as a higher ratio of collagen III to collagen I is associated with scarless wound healing in mammal models [3, 4], and collagen III-deficient mice exhibit more pronounced wound contracture than those with collagen III [5]. However, the expression of collagen III is regulated by the activity of local fibroblasts [6].…”

Section: Introductionmentioning

confidence: 99%

Cathepsin B Regulates Collagen Expression by Fibroblasts via Prolonging TLR2/NF-κB Activation

et al. 2016

Oxidative Medicine and Cellular Longevity

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Fibroblasts are essential for tissue repair due to producing collagens, and lysosomal proteinase cathepsin B (CatB) is involved in promoting chronic inflammation. We herein report that CatB regulates the expression of collagens III and IV by fibroblasts in response to a TLR2 agonist, lipopolysaccharide from Porphyromonas gingivalis (P.g. LPS). In cultured human BJ fibroblasts, mRNA expression of CatB was significantly increased, while that of collagens III and IV was significantly decreased at 24 h after challenge with P.g. LPS (1 μg/mL). The P.g. LPS-decreased collagen expression was completely inhibited by CA-074Me, the specific inhibitor of CatB. Surprisingly, expression of collagens III and IV was significantly increased in the primary fibroblasts from CatB-deficient mice after challenge with P.g. LPS. The increase of CatB was accompanied with an increase of 8-hydroxy-2′-deoxyguanosine (8-OHdG) and a decrease of IκBα. Furthermore, the P.g. LPS-increased 8-OHdG and decreased IκBα were restored by CA-074Me. Moreover, 87% of CatB and 86% of 8-OHdG were colocalized with gingival fibroblasts of chronic periodontitis patients. The findings indicate the critical role of CatB in regulating the expression of collagens III and IV by fibroblasts via prolonging TLR2/NF-κB activation and oxidative stress. CatB-specific inhibitors may therefore improve chronic inflammation-delayed tissue repair.

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“…16 Fibroblasts from mid-gestation (E15) fetal mice also demonstrate decreased expression of pro-collagen 1α1, indicating lower rates of type I collagen synthesis. In contrast, fibroblasts from late gestation (E18) showed increased pro-collagen 1α1 expression with decreased pro-collagen 3 expression, 23 demonstrating upregulation of type I collagen synthesis and decreased type III collagen synthesis with advancing gestational age.…”

Section: Fetal Vs Adult Wound Healingmentioning

confidence: 96%

Tissue Engineering and Regenerative Repair in Wound Healing

et al. 2014

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Wound healing is a highly evolved defense mechanism against infection and further injury. It is a complex process involving multiple cell types and biological pathways. Mammalian adult cutaneous wound healing is mediated by a fibroproliferative response leading to scar formation. In contrast, early to mid-gestational fetal cutaneous wound healing is more akin to regeneration and occurs without scar formation. This early observation has led to extensive research seeking to unlock the mechanism underlying fetal scarless regenerative repair. Building upon recent advances in biomaterials and stem cell applications, tissue engineering approaches are working towards a recapitulation of this phenomenon. In this review, we describe the elements that distinguish fetal scarless and adult scarring wound healing, and discuss current trends in tissue engineering aimed at achieving scarless tissue regeneration.

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Differential Expression of Procollagen Genes Between Mid- and Late-Gestational Fetal Fibroblasts

Cited by 32 publications

References 13 publications

Extracellular Matrix and Dermal Fibroblast Function in the Healing Wound

Extracellular Matrix and Dermal Fibroblast Function in the Healing Wound

Cathepsin B Regulates Collagen Expression by Fibroblasts via Prolonging TLR2/NF-κB Activation

Tissue Engineering and Regenerative Repair in Wound Healing

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