Regulation of Collagen Gene Expression in Keloids and Hypertrophic Scars

Friedman, David; Boyd, Charles D.; Mackenzie, James W.; Norton, Peggy; Olson, R M; Deak, Susan B.

doi:10.1006/jsre.1993.1132

Cited by 149 publications

(103 citation statements)

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“…All cultures (palmar and nonpalmar) showed upregulation of collagen I ( Figure 4A) and a-SMA ( Figure 4C), when TGFb1 was present in the media (lanes 2, 4,6,8). At the same time little effect was seen on the vimentin levels.…”

Section: Protein Expression In Fibroblasts From Keloid Formers and Nomentioning

confidence: 93%

Myofibroblast phenotype and apoptosis in keloid and palmar fibroblasts in vitro

Chipev¹,

Simman²,

Hatch³

et al. 2000

Cell Death Differ

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Keloid formation is a wound healing response, which fails to resolve and leads to formation of a raised collagen mass extending beyond the original wound margins. Keloids are typically excluded from palms and soles. Therefore we compared keloid and palmar fibroblasts in vitro using fibroblasts from nonaffected individuals as controls. Collagen I, a-smooth muscle actin and thrombospondin-1 were found at higher levels in keloid than in palmar fibroblasts. These differences were ameliorated by addition of TGFb1. The potential for resolution of the wound healing response was estimated analyzing apoptosis during serum starvation. Annexin V and TUNEL assays showed that palmar fibroblasts underwent faster apoptosis, than did the keloid fibroblasts, and started detaching. Addition of TGFb1 counteracted this effect. The weak expression of the myofibroblast phenotype and the advanced apoptosis of palmar fibroblasts suggest mechanisms for the exclusion of keloids from palmar sites.

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Section: Protein Expression In Fibroblasts From Keloid Formers and Nomentioning

confidence: 93%

Myofibroblast phenotype and apoptosis in keloid and palmar fibroblasts in vitro

Chipev¹,

Simman²,

Hatch³

et al. 2000

Cell Death Differ

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“…This is due to both excessive collagen synthesis 33,34 and abnormal collagen turnover by matrix degrading enzymes such as MMP-1 and MMP-2. 22 Cells from the active margin of keloid scars have been shown to have increased expression of collagen I and III mRNA.…”

Section: Collagen Nanotopography Reduces Matrix Synthesismentioning

confidence: 99%

Effect of Collagen Nanotopography on Keloid Fibroblast Proliferation and Matrix Synthesis: Implications for Dermal Wound Healing

Muthusubramaniam

Zaitseva

Paukshto

et al. 2014

Tissue Engineering Part A

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Keloids are locally exuberant dermal scars characterized by excessive fibroblast proliferation and matrix accumulation. Although treatment strategies include surgical removal and intralesional steroid injections, an effective regimen is yet to be established due to a high rate of recurrence. The regressing center and growing margin of the keloid have different collagen architecture and also differ in the rate of proliferation. To investigate whether proliferation is responsive to collagen topography, keloid, scar, and dermal fibroblasts were cultured on nanopatterned scaffolds varying in collagen fibril diameter and alignment-small and large diameter, aligned and random fibrils, and compared to cells grown on flat collagen-coated substrates, respectively. Cell morphology, proliferation, and expression of six genes related to proliferation (cyclin D1), phenotype (asmooth muscle actin), and matrix synthesis (collagens I and III, and matrix metalloproteinase-1 and -2) were measured to evaluate cell response. Fibril alignment was shown to reduce proliferation and matrix synthesis in all three types of fibroblasts. Further, keloid cells were found to be most responsive to nanotopography.

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“…Dans une étude pilote menée sur 15 patients (14 femmes et un homme phototype I à IV), une différence significative a été observée à 12 mois à la dose 80-130 J/cm², basée sur une comparaison de cicatrices traitées et non traitées par laser. Aucune complica- Ces observations sont en accord avec différents travaux qui montrent bien que la valeur du rapport entre les collagènes de type I et de type III joue un rôle déter-minant dans le processus de formation de la cicatrice [37][38][39][40]. Les processus cicatriciels pathologiques sont systématiquement associés à une valeur élevée du rapport type I-type III alors qu'une valeur faible conduit à un processus de régénération (scarless healing dans la littérature anglo-saxonne) [41,42].…”

Section: La Cicatrisation Cutanée Assistée Par Lasersunclassified