Abrogation of the fibrotic effect of transforming growth factor‐β in dermal wound healing

Parrelli, Jo M.; Meisler, Natalie T.; Cutroneo, Kenneth R.

doi:10.1046/j.1524-475x.1997.50204.x

Cited by 5 publications

(3 citation statements)

References 12 publications

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“…33 There have been numerous studies on the possible role of TGF-β in scarring, including attempts to reduce scar formation by blocking or countering the biological effects of TGF-β. 34 The antiTGF-β1 antibody may show therapeutic potential for treating scars by blocking TGF-β1 or accelerating the degeneration of type 1 and 3 collagens, which are abundant in scar tissue. 35 Here, we provide an additional candidate for molecular-based therapies that upregulate TGF-β3.…”

Section: Discussionmentioning

confidence: 99%

“…Understanding the mechanisms of TGF-β mediated scar formation would provide novel opportunities for a therapeutic approach 33. There have been numerous studies on the possible role of TGF-β in scarring, including attempts to reduce scar formation by blocking or countering the biological effects of TGF-β 34. The antiTGF-β1 antibody may show therapeutic potential for treating scars by blocking TGF-β1 or accelerating the degeneration of type 1 and 3 collagens, which are abundant in scar tissue 35.…”

Section: Discussionmentioning

confidence: 99%

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Influence of Transforming Growth Factors beta 1 and beta 3 in the Scar Formation Process

Lee¹,

Cho²,

Lee³

et al. 2022

Journal of Craniofacial Surgery

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Background: Transforming growth factor-beta (TGF-β) plays an instrumental role in forming scars and keloids. TGF-β isoforms exhibit differential expression, indicating distinct wound healing and scar formation functions. However, the role of TGF-β1 and TGF-β3 in wound healing and scar formation remains unclear. This study aimed to compare the specific roles of TGF-β1 and TGF-β3 in wound healing and scar formation by biomolecular analysis. Materials and Methods: The study was conducted by cell isolation and culture cells from a total of 20 human samples. Normal human fibroblasts (NHF) were isolated from normal human samples and myofibroblasts from the different scar types, namely hypertrophic (HT) and keloid (K) scars. NHF and cells from the HT, and K scar, each of which were divided into 3 sample groups: the untreated control, TGF-β1 (10 µg/ mL)-treated group, and TGF-β3 (10 µg/mL)-treated group. The results of confocal microscopy and fluorescence-activated cell sorting experiments were compared. Results: Both the HT and K groups had higher α-smooth muscle actin (α-SMA) expression than the NHF group in the untreated control group. In comparison with the untreated group, NHFs showed a significant increase in α-SMA expression in the TGF-β1-treated group. HT showed a high α-SMA level, which was statistically significant compared with the normal fibroblasts. In the TGF-β3-treated group, α-SMA expression was slightly increased in NHF as compared with the untreated group. TGF-β3 treated HT exhibited a greater reduction in α-SMA expression than in the TGF-β1 treated HT. K, on the other hand, had only a minimal effect on the treatment of TGF-β1 and TGF-β3. Conclusions: The findings suggest that TGF-β3 may play a regulatory role in the wound repair process, which could be useful in the development of scar-reducing therapies for patients with scar-related cosmetic concerns.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Influence of Transforming Growth Factors beta 1 and beta 3 in the Scar Formation Process

Lee¹,

Cho²,

Lee³

et al. 2022

Journal of Craniofacial Surgery

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“…Dexamethasone has the opposite effects on collagen synthesis, both in low passage human dermal fibroblasts in culture [Slavin et al, 1994] and in granuloma and granulation tissue fibroblasts [Meisler et al, 1997]. When used in conjunction with TGF‐β1, glucocorticoids may normalize the effect of TGFβ‐1 on collagen synthesis thereby reducing excessive collagen deposition and fibrosis [Parrelli et al, 1997]. TGF‐β is the crossroad for glucocorticoid and bleomycin regulation of collagen synthesis [Shukla et al, 1999].…”

Section: Cytokines Which Influence Collagen Synthesismentioning

confidence: 99%

How do glucocorticoids compare to oligo decoys as inhibitors of collagen synthesis and potential toxicity of these therapeutics?

Cutroneo

Sterling

2004

J of Cellular Biochemistry

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This article demonstrates how glucocorticoids decrease collagen synthesis. The parameters used to assess procollagen synthesis in our laboratory will be compared to those used by others. This article will note all the pertinent literature on the molecular mechanisms of this down regulation of procollagen synthesis. For example, what are the effects of glucocorticoids at the levels of transcription and translation of collagen mRNAs? Finally, we will define a molecular mechanism to inhibit Type I collagen synthesis by decreasing the binding of the TGF-beta activator protein complex to the TGF-beta element in the distal promoter of the proalpha1 Type I collagen gene, preventing the 2:1 ratio of alpha1 to alpha2 chains in the processed Type I collagen molecule. We will next ask "How do sense oligo decoys decrease Type I collagen synthesis at the in vivo and at the cell levels?" In primary fibrotic cell culture, the double-stranded phosphorothioate oligodeoxynucleotide decoys were more effective than their sense single-stranded counterparts. The molecular mechanism for the decrease in Type I collagen synthesis is the same as glucocorticoids, that is by decreasing the binding of the TGF-beta activator protein complex to the TGF-beta element in the distal promoter of the proalpha1 Type I collagen gene for the transcription of the proalpha1 mRNAs. The reason for using sense oligo decoys as anti-fibrotic agents as compared to the anti-fibrotic glucocorticoids, is that presently marketed and FDA approved glucocorticoids have many untoward side effects which the sense oligo decoys do not have.

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Peroxisome proliferator-activated receptor-γ (PPAR-γ) agonist inhibits transforming growth factor-beta1 and matrix production in human dermal fibroblasts

Zhang

Cheng

Zheng

et al. 2010

Journal of Plastic, Reconstructive & Aesthetic Surgery

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Abrogation of the fibrotic effect of transforming growth factor‐β in dermal wound healing

Cited by 5 publications

References 12 publications

Influence of Transforming Growth Factors beta 1 and beta 3 in the Scar Formation Process

Influence of Transforming Growth Factors beta 1 and beta 3 in the Scar Formation Process

How do glucocorticoids compare to oligo decoys as inhibitors of collagen synthesis and potential toxicity of these therapeutics?

Peroxisome proliferator-activated receptor-γ (PPAR-γ) agonist inhibits transforming growth factor-beta1 and matrix production in human dermal fibroblasts

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