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Daniel S. Greenspan - One of the best experts on this subject based on the ideXlab platform.

  • procollagen c proteinase enhancer 1 pcpe 1 functions as an anti angiogenic factor and enhances epithelial recovery in injured Cornea
    Cell and Tissue Research, 2017
    Co-Authors: Dawiyat Massoudi, Colin J Germer, Jeffrey M Glisch, Daniel S. Greenspan
    Abstract:

    Procollagen C-proteinase enhancer 1 (PCPE-1) has been characterized as a protein capable of enhancing the activity of bone morphogenetic protein 1/tolloid-like proteinases in the biosynthetic processing of C-propeptides from procollagens I–III. This processing step is thought necessary to the formation of collagen I–III monomers capable of forming fibrils. Thus, PCPE-1 is predicted to play an important role in scarring, as scar tissue is predominantly composed of fibrillar collagen. Corneal scarring is of great clinical importance, as it leads to loss of visual acuity and, in severe cases, blindness. Here, we investigate a possible role for PCPE-1 in Corneal scarring. Although differences in Corneal opacity associated with scarring following Injury of Pcolce −/− and wild-type (WT) mice using full-thickness excision or alkali burn models of Corneal Injury were not grossly apparent, differences in procollagen I processing levels between Pcolce −/− and WT primary Corneal keratocytes were consistent with a role for PCPE-1 in Corneal collagen deposition. An unexpected finding was that neoangiogenesis, which follows alkali burn Cornea Injury, was strikingly increased in Pcolce −/− Cornea, compared to WT. A series of aortic ring assays confirmed the anti-angiogenic effects of PCPE-1. Another unexpected finding was of abnormalities of epithelial basement membrane and of re-epithelialization following Pcolce −/− Corneal Injury. Thus, PCPE-1 appears to be of importance as an anti-angiogenic factor and in re-epithelialization following Injury in Cornea and perhaps in other tissues as well.

Dawiyat Massoudi - One of the best experts on this subject based on the ideXlab platform.

  • procollagen c proteinase enhancer 1 pcpe 1 functions as an anti angiogenic factor and enhances epithelial recovery in injured Cornea
    Cell and Tissue Research, 2017
    Co-Authors: Dawiyat Massoudi, Colin J Germer, Jeffrey M Glisch, Daniel S. Greenspan
    Abstract:

    Procollagen C-proteinase enhancer 1 (PCPE-1) has been characterized as a protein capable of enhancing the activity of bone morphogenetic protein 1/tolloid-like proteinases in the biosynthetic processing of C-propeptides from procollagens I–III. This processing step is thought necessary to the formation of collagen I–III monomers capable of forming fibrils. Thus, PCPE-1 is predicted to play an important role in scarring, as scar tissue is predominantly composed of fibrillar collagen. Corneal scarring is of great clinical importance, as it leads to loss of visual acuity and, in severe cases, blindness. Here, we investigate a possible role for PCPE-1 in Corneal scarring. Although differences in Corneal opacity associated with scarring following Injury of Pcolce −/− and wild-type (WT) mice using full-thickness excision or alkali burn models of Corneal Injury were not grossly apparent, differences in procollagen I processing levels between Pcolce −/− and WT primary Corneal keratocytes were consistent with a role for PCPE-1 in Corneal collagen deposition. An unexpected finding was that neoangiogenesis, which follows alkali burn Cornea Injury, was strikingly increased in Pcolce −/− Cornea, compared to WT. A series of aortic ring assays confirmed the anti-angiogenic effects of PCPE-1. Another unexpected finding was of abnormalities of epithelial basement membrane and of re-epithelialization following Pcolce −/− Corneal Injury. Thus, PCPE-1 appears to be of importance as an anti-angiogenic factor and in re-epithelialization following Injury in Cornea and perhaps in other tissues as well.

Colin J Germer - One of the best experts on this subject based on the ideXlab platform.

  • procollagen c proteinase enhancer 1 pcpe 1 functions as an anti angiogenic factor and enhances epithelial recovery in injured Cornea
    Cell and Tissue Research, 2017
    Co-Authors: Dawiyat Massoudi, Colin J Germer, Jeffrey M Glisch, Daniel S. Greenspan
    Abstract:

    Procollagen C-proteinase enhancer 1 (PCPE-1) has been characterized as a protein capable of enhancing the activity of bone morphogenetic protein 1/tolloid-like proteinases in the biosynthetic processing of C-propeptides from procollagens I–III. This processing step is thought necessary to the formation of collagen I–III monomers capable of forming fibrils. Thus, PCPE-1 is predicted to play an important role in scarring, as scar tissue is predominantly composed of fibrillar collagen. Corneal scarring is of great clinical importance, as it leads to loss of visual acuity and, in severe cases, blindness. Here, we investigate a possible role for PCPE-1 in Corneal scarring. Although differences in Corneal opacity associated with scarring following Injury of Pcolce −/− and wild-type (WT) mice using full-thickness excision or alkali burn models of Corneal Injury were not grossly apparent, differences in procollagen I processing levels between Pcolce −/− and WT primary Corneal keratocytes were consistent with a role for PCPE-1 in Corneal collagen deposition. An unexpected finding was that neoangiogenesis, which follows alkali burn Cornea Injury, was strikingly increased in Pcolce −/− Cornea, compared to WT. A series of aortic ring assays confirmed the anti-angiogenic effects of PCPE-1. Another unexpected finding was of abnormalities of epithelial basement membrane and of re-epithelialization following Pcolce −/− Corneal Injury. Thus, PCPE-1 appears to be of importance as an anti-angiogenic factor and in re-epithelialization following Injury in Cornea and perhaps in other tissues as well.

Jeffrey M Glisch - One of the best experts on this subject based on the ideXlab platform.

  • procollagen c proteinase enhancer 1 pcpe 1 functions as an anti angiogenic factor and enhances epithelial recovery in injured Cornea
    Cell and Tissue Research, 2017
    Co-Authors: Dawiyat Massoudi, Colin J Germer, Jeffrey M Glisch, Daniel S. Greenspan
    Abstract:

    Procollagen C-proteinase enhancer 1 (PCPE-1) has been characterized as a protein capable of enhancing the activity of bone morphogenetic protein 1/tolloid-like proteinases in the biosynthetic processing of C-propeptides from procollagens I–III. This processing step is thought necessary to the formation of collagen I–III monomers capable of forming fibrils. Thus, PCPE-1 is predicted to play an important role in scarring, as scar tissue is predominantly composed of fibrillar collagen. Corneal scarring is of great clinical importance, as it leads to loss of visual acuity and, in severe cases, blindness. Here, we investigate a possible role for PCPE-1 in Corneal scarring. Although differences in Corneal opacity associated with scarring following Injury of Pcolce −/− and wild-type (WT) mice using full-thickness excision or alkali burn models of Corneal Injury were not grossly apparent, differences in procollagen I processing levels between Pcolce −/− and WT primary Corneal keratocytes were consistent with a role for PCPE-1 in Corneal collagen deposition. An unexpected finding was that neoangiogenesis, which follows alkali burn Cornea Injury, was strikingly increased in Pcolce −/− Cornea, compared to WT. A series of aortic ring assays confirmed the anti-angiogenic effects of PCPE-1. Another unexpected finding was of abnormalities of epithelial basement membrane and of re-epithelialization following Pcolce −/− Corneal Injury. Thus, PCPE-1 appears to be of importance as an anti-angiogenic factor and in re-epithelialization following Injury in Cornea and perhaps in other tissues as well.

Shizuya Saika - One of the best experts on this subject based on the ideXlab platform.

  • trpa1 is required for tgf β signaling and its loss blocks inflammatory fibrosis in mouse Corneal stroma
    Laboratory Investigation, 2014
    Co-Authors: Yuka Okada, Kumi Shirai, Peter S Reinach, Ai Kitanoizutani, Masayasu Miyajima, Kathleen C Flanders, James V Jester, Makoto Tominaga, Shizuya Saika
    Abstract:

    We examined whether the loss of transient receptor potential ankyrin 1 (TRPA1), an irritant-sensing ion channel, or TRPA1 antagonist treatment affects the severity inflammation and scarring during tissue wound healing in a mouse Cornea Injury model. In addition, the effects of the absence of TRPA1 on transforming growth factor β1 (TGF-β1)-signaling activation were studied in cell culture. The lack of TRPA1 in cultured ocular fibroblasts attenuated expression of TGF-β1, interleukin-6, and α-smooth muscle actin, a myofibroblast the marker, but suppressed the activation of Smad3, p38 MAPK, ERK, and JNK. Stroma of the healing Corneas of TRPA1(-/-) knockout (KO) mice appeared more transparent compared with those of wild-type mice post-alkali burn. Eye globe diameters were measured from photographs. An examination of the Corneal surface and eye globes suggested the loss of TRPA1 suppressed post-alkali burn inflammation and fibrosis/scarring, which was confirmed by histology, immunohistochemistry, and gene expression analysis. Reciprocal bone marrow transplantation between mice showed that KO Corneal tissue resident cells, but not KO bone marrow-derived cells, are responsible for KO mouse wound healing with reduced inflammation and fibrosis. Systemic TRPA1 antagonists reproduced the KO phenotype of healing. In conclusion, a loss or blocking of TRPA1 in mice reduces inflammation and fibrosis/scarring in the Corneal stroma during wound healing following an alkali burn. The responsible mechanism may include the inhibition of TGF-β1-signaling cascades in fibroblasts by attenuated TRPA1 signaling. Inflammatory cells are considered to have a minimum involvement in the exhibition of the KO phenotype after Injury.