Disease relevance of Cicatrix, Hypertrophic

• Surprisingly, the level of the crosslinking enzyme lysyl oxidase is normal or elevated in hypertrophic scar and keloid despite the relative lack of crosslinking [1].
• In this study we examined the expression of dermatopontin mRNA and protein in skin fibroblast cultures from patients with hypertrophic scar and patients with systemic sclerosis [2].
• We examined by immunofluorescence the distribution of vimentin, desmin, alpha-smooth muscle actin and alpha-sarcomeric actin in normal human soft tissues and in pathologic tissues containing myofibroblasts, including normally healing granulation tissue, hypertrophic scar, and fibromatosis [3].
• Fibronectin. Localization in normal human skin, granulation tissue, hypertrophic scar, mature scar, progressive systemic sclerotic skin, and other fibrosing dermatoses [4].
• Steroid-induced 'granulomas' in hypertrophic scar [5].

High impact information on Cicatrix, Hypertrophic

• Letter: Polyglycolic-acid sutures and hypertrophic scars [6].
• Our results show that, in hypertrophic scars, pressure therapy restores in part the extracellular matrix organization observed in normal scar and induces the disappearance of alpha-smooth muscle actin-expressing myofibroblasts, probably by apoptosis [7].
• In hypertrophic scars the mRNA distribution corroborated the abnormal K16 protein distribution [8].
• In this study, the expression of keratin intermediate filament proteins and filaggrin has been investigated in the epidermis of hypertrophic scars and site-matched controls from the same patients [8].
• Hypertrophic scar epidermis was found to express the hyperproliferative keratins K6 and K16 in interfollicular epidermis in association with K17 and precocious expression of filaggrin [8].

Chemical compound and disease context of Cicatrix, Hypertrophic

• Tranilast (n-[3,4-dimethoxycinnamoyl] anthranilic acid), an antifibrotic agent that is used to treat hypertrophic scars and scleroderma, has also been shown to inhibit TGF-beta-induced extracellular matrix synthesis in a range of cell types, including those of renal origin [9].
• Free radicals, reported to be associated with the formation of pyridinoline crosslinks, and free iron content, were also found to have higher concentration in hypertrophic scar than in normal skin [10].
• We thus provide a molecular explanation to the observed clinical benefits of 5-FU in the treatment of keloids and hypertrophic scars [11].
• The proteoglycans (PGs) in pooled normal scars and pooled hypertrophic scars were extracted with 4 M guanidinium chloride and isolated by DEAE-cellulose chromatography [12].
• In this study we examined integrin expression in keloids (n = 11), hypertrophic scars (n = 5), radiation ulcers (n = 2), and normal skin specimens (n = 8) [13].

Biological context of Cicatrix, Hypertrophic

• Gene expression profiles from hypertrophic scar fibroblasts before and after IL-6 stimulation [14].
• As it has been suggested that MMP-28 may restructure the skin basal membrane (Saarialho-Kere et al., 2002), our data indicate that mechanical compression directly acts to modulate the remodeling phase of wound healing, altering release and activity of MMP-28 in hypertrophic scars [15].
• There is no evidence for any association between C3 alleles or phenotypes and the formation of hypertrophic scars [16].
• Therefore, cellular signal pathways are induced by EGFR, which might play a role in hypertrophic scar pathogenesis [17].
• CONCLUSIONS: Hypertrophic scar fibroblasts have both intrinsic up-regulation of CTGF transcription and an exaggerated capacity for CTGF transcription in response to TGF-beta stimulation [18].

Anatomical context of Cicatrix, Hypertrophic

• Exogenous hyaluronan induced a decline in measurable CD44 expression for normal skin fibroblasts but not for hypertrophic scar fibroblasts [19].
• PDGF was significantly increased in the dermis of normal scars after 3 months and in both the epidermis and the dermis of hypertrophic scars after 12 months [20].
• In this study, hypertrophic scar formation was significantly associated with an increased number of epidermal Langerhans cells (p=0.0001) and significantly (p<0.05) increased expression of epidermal IL-4 [21].
• A TGF-beta1-dependent autocrine loop regulates the structure of focal adhesions in hypertrophic scar fibroblasts [22].
• Keloids, but not hypertrophic scars or normal dermis, also exhibited intensive immunoreactivity for the CXCR2 receptor in endothelial cells and inflammatory infiltrates with occasional staining of myofibroblasts [23].

Gene context of Cicatrix, Hypertrophic

• Expression and role of IL-15 in post-burn hypertrophic scars [24].
• In this study, NOS expression and NO production were compared in human fibroblasts derived from hypertrophic scar (HSc) and site-matched normal dermis [25].
• The percentage of TNF alpha- and beta-positive cells was analyzed in hypertrophic scar (N = 13), normotrophic scar (N = 7), and normal skin (N = 6) biopsies using monoclonal antibodies and immunoperoxidase staining of cryostat tissue sections [26].
• This study was conducted to monitor the time-course of expression of decorin in healing burn wounds by in-situ hybridization to determine whether its absence from hypertrophic scars could result from reduced synthesis [27].
• Biglycan and versican were virtually undetectable in normal dermis but readily seen in hypertrophic scars [28].

Analytical, diagnostic and therapeutic context of Cicatrix, Hypertrophic

• CONCLUSIONS: Clinical improvement of keloidal and hypertrophic scars after treatment with intralesional corticosteroid alone or combined with 5-FU, 5-FU alone, and PDL seemed comparable, with the exceptions of the incidence of adverse reactions, which were most common with intralesional corticosteroid [29].
• Analysis of MMP-28 protein secretion, assessed by Western blot and beta-casein zymography in scar conditioned media, revealed that normotrophic scar did not release MMP-28 in any condition while hypertrophic scar released active MMP-28 both in control conditions and after compression [15].
• The histologic localization of fibronectin (FN) in normal human skin, granulation tissue, hypertrophic scar, mature scar, progressive systemic sclerotic skin, and tissue of other fibrotic disorders was investigated by an indirect immunofluorescence technique using specific antiserum prepared in rabbits against purified human plasma FN [4].
• CONCLUSION: Concomitant use of the high-energy, pulsed CO2 and PDL laser systems was superior to CO2 laser vaporization alone for revision of nonerythematous hypertrophic scars [30].
• Three additional hypertrophic scar samples were quantitatively analyzed on Northern blots and showed increases of 246%, 102%, and 250% of the specific messages for pro-alpha 1(I), pro-alpha 1(III), and TGF-beta 1 relative to a normal skin control [31].

References