The expression of transforming growth factor type beta in fetal and adult rabbit skin wounds

Nath, Rahul K.; LaRegina, Maria; Markham, Herbert; Ksander, George A.; Weeks, Paul M.

doi:10.1016/0022-3468(94)90582-7

Cited by 72 publications

(47 citation statements)

References 42 publications

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“…This idea is in line with the fetal scarless healing characterised by a lack of inflammatory response and a lack of scar formation [19][20][21][22][23][24][25][26][27][28][29][30][31]. Interestingly, in this study we have shown macroscopic and microscopic reduction of post wounding inflammatory response and post wounding scarring simulating fetal wound without completely interfering with the inflammation.…”

Section: Discussionsupporting

confidence: 85%

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Inhibition of Wound TGF Beta-1 by Celecoxib: A Possible Therapeutic Route for Scar Free Wound

El-Aleem¹,

Jude²

2017

J Cytol Histol

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Background: Wound healing is a highly ordered dynamic process associated with inflammation at early stages and with permanent scarring at late stages. Scars could be disfiguring and could advance to be hypertrophic or keloid scars, this would have a strong physical and psychological impact on the patients afterward. The role of inflammatory mediators which could be pro-or anti-inflammatory, pro-or -anti fibrotic was the focus of wound healing research for decades and the balance between them is the key factor determining the outcome of healing.

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Section: Discussionsupporting

confidence: 85%

“…This was attributed to lack of inflammatory response [20,21] and low levels of TGF Beta-1 in fetal wounds [22,23]. TGF Beta-1 is secreted by dermal cells and by inflammatory cells infiltrating the wound; it promotes collagen deposition and remodelling [24][25][26].…”

Section: Tgf Beta-1 and Postwounding Scarringmentioning

confidence: 99%

Inhibition of Wound TGF Beta-1 by Celecoxib: A Possible Therapeutic Route for Scar Free Wound

El-Aleem¹,

Jude²

2017

J Cytol Histol

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“…While some of these studies assigned no major individual role to TGF-β3, there is also evidence for distinct and specific features of TGF-β3 that even suggest potential anti-scarring properties. One of the key reports supporting this idea is the observation that cutaneous wounds heal without or only limited scarring, when TGF-β3 is present in the wound bed, either constitutively as found in the embryonic/fetal state or delivered as a therapeutic agent (Nath et al, 1994;Shah et al, 1995). Similarly, cutaneous wounds heal without or only limited scarring when TGF-β1 or -β2 is antagonized by antibodies (Shah, Foreman, & Ferguson, 1992).…”

Section: Discussionmentioning

confidence: 99%

“…In contrast, data from targeted gene knockouts and experimental models of cutaneous wound healing and chronic inflammatory bowel disease suggested distinct features of TGF-β3, when compared with TGF-β1 (Ingman & Robertson, 2002;McKaig, Hughes, Tighe, & Mahida, 2002;Shah, Foreman, & Ferguson, 1995;Van Themsche, Mathieu, Parent, & Asselin, 2007). Fetal wounds, which contain primarily TGF-β3, heal without scars, whereas adult wounds, which contain mainly TGF-β1 and -β2, always exhibit some degree of scarring (Nath, LaRegina, Markham, Ksander, & Weeks, 1994). These observations have raised considerable research efforts in the field of cutaneous wound healing, as well as debates whether TGF-β3 might even carry anti-scarring properties (Shah et al, 1995).…”

Section: Introductionmentioning

confidence: 99%

Progressive pulmonary fibrosis is mediated by TGF-β isoform 1 but not TGF-β3

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Bonniaud

Maaß

et al. 2008

The International Journal of Biochemistry & Cell Biology

154

114

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Tissue repair is a well orchestrated biological process involving numerous soluble mediators, and an imbalance between these factors may result in impaired repair and fibrosis. Transforming growth factor (TGF) β is a key profibrotic element in this process and it is thought that its three isoforms act in a similar way. Here, we report that TGF-β3 administered to rat lungs using transient overexpression initiates profibrotic effects similar to those elicited by TGF-β1, but causes less severe and progressive changes. The data suggest that TGF-β3 does not lead to inhibition of matrix degradation in the same way as TGF-β1, resulting in non-fibrotic tissue repair. Further, TGF-β3 is able to downregulate TGF-β1 induced gene expression, suggesting a regulatory role of TGF-β3. TGF-β3 overexpression results in an upregulation of Smad proteins similar to TGF-β1, but is less efficient in inducing the ALK 5 and TGF-β type II receptor (TβRII). We provide evidence that this difference may contribute to the progressive nature of TGF-β1 induced fibrotic response, in contrast to the limited fibrosis observed following TGF-β3 overexpression. TGF-β3 is important in "normal wound healing", but is outbalanced by TGF-β1 in "fibrotic wound healing" in the lung.

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“…First of all, a reduced and/or more transient expression of TGF-␤s and their receptors was observed in nonscarring fetal wounds compared with adult wounds (62,177,197,264,294). In addition, a strong and persistent expression of TGF-␤s and their receptors was detected in fibroblasts of human postburn hypertrophic scars (99,239,241,283,306), and overexpression of TGF-␤1 and -␤2 was found in keloid tissues and keloidderived fibroblasts (154,211).…”

Section: B Neutralizing Antibodies To Tgf-␤1 and -␤2 Reduce Scarringmentioning

confidence: 97%

Regulation of Wound Healing by Growth Factors and Cytokines

Werner

Grose

2003

Physiological Reviews

3,013

2,082

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Werner, Sabine, and Richard Grose. Regulation of Wound Healing by Growth Factors and Cytokines. Physiol Rev 83: 835–870, 2003; 10.1152/physrev.00032.2002.—Cutaneous wound healing is a complex process involving blood clotting, inflammation, new tissue formation, and finally tissue remodeling. It is well described at the histological level, but the genes that regulate skin repair have only partially been identified. Many experimental and clinical studies have demonstrated varied, but in most cases beneficial, effects of exogenous growth factors on the healing process. However, the roles played by endogenous growth factors have remained largely unclear. Initial approaches at addressing this question focused on the expression analysis of various growth factors, cytokines, and their receptors in different wound models, with first functional data being obtained by applying neutralizing antibodies to wounds. During the past few years, the availability of genetically modified mice has allowed elucidation of the function of various genes in the healing process, and these studies have shed light onto the role of growth factors, cytokines, and their downstream effectors in wound repair. This review summarizes the results of expression studies that have been performed in rodents, pigs, and humans to localize growth factors and their receptors in skin wounds. Most importantly, we also report on genetic studies addressing the functions of endogenous growth factors in the wound repair process.

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The expression of transforming growth factor type beta in fetal and adult rabbit skin wounds

Cited by 72 publications

References 42 publications

Inhibition of Wound TGF Beta-1 by Celecoxib: A Possible Therapeutic Route for Scar Free Wound

Inhibition of Wound TGF Beta-1 by Celecoxib: A Possible Therapeutic Route for Scar Free Wound

Progressive pulmonary fibrosis is mediated by TGF-β isoform 1 but not TGF-β3

Regulation of Wound Healing by Growth Factors and Cytokines

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