Direct evidence for spatial and temporal regulation of transforming growth factor β1 expression during cutaneous wound healing

Kane, Cynthia J.M.; Hebda, Patricia A.; Mansbridge, Jonathan; Hanawalt, Philip C.

doi:10.1002/jcp.1041480119

Cited by 216 publications

(139 citation statements)

References 51 publications

Supporting

Mentioning

130

Contrasting

Unclassified

Order By: Relevance

“…Although TGF-, I is able to reverse many effects of corticosteroid administration and age-related phenomena, it is not clear how this reversal is mediated. Modulation ofwound repair by TGF-, 1 is complex and involves multiple levels of control (see review by Sporn and Roberts [25 ] ), and depends on the presence of other growth factors or regulatory peptides (7,26,27), the target cell, and the cell's state of differentiation (for examples, see Janat and Liau [28] or Celada and Maki [29 ]). TGF-,B1 's action on neutrophils (30) and monocytes (31 ), as well as other cell types, is presumably mediated through membrane-bound receptors that when activated stimulate cytoplasmic and nuclear responses resulting in a cascade of cellular and extracellular events (32).…”

Section: Discussionmentioning

confidence: 99%

“…The local production of growth factors such as TGF-# 1 or PDGF has been associated with various stages of tissue repair (7,8). With the recent availability of large amounts of these factors through recombinant techniques, several investigators have shown that the local application ofgrowth factors accelerates tissue repair in animal models of wound healing (9-1 1 ).…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

One systemic administration of transforming growth factor-beta 1 reverses age- or glucocorticoid-impaired wound healing.

Beck¹,

Deguzman²,

Lee³

et al. 1993

J. Clin. Invest.

226

109

View full text Add to dashboard Cite

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

One systemic administration of transforming growth factor-beta 1 reverses age- or glucocorticoid-impaired wound healing.

Beck¹,

Deguzman²,

Lee³

et al. 1993

J. Clin. Invest.

226

109

View full text Add to dashboard Cite

show abstract

“…Several publications report on the presence of TGF-␤s in wound fluid of different species (27,35,204,281). Furthermore, expression of all three isoforms was detected in many different cell types during repair, with each isoform having a characteristic distribution in the wound tissue (91,141,157,238,270,271). In most studies, a rapid induction of TGF-␤1 and -␤2 was observed, whereas an increase in TGF-␤3 expression was seen at later stages of repair.…”

Section: A Expression Of Tgf-␤ At the Wound Sitementioning

confidence: 99%

Regulation of Wound Healing by Growth Factors and Cytokines

Werner

Grose

2003

Physiological Reviews

3,017

2,082

View full text Add to dashboard Cite

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.

show abstract

“…TGFP1 has been immunologically demonstrated in the suprabasal cell layers of normal human (26) and mouse epidermis (27). In an elegant study, Kane et al (26) recently provided immunological evidence that skin expresses an inactive TGFO-precursor, which is proteolytically activated and released immediately upon injury.…”

Section: The Hierarchy Of the Epidermal Cytokine Networkmentioning

confidence: 99%

Proliferative Responses of the Skin to External Stimuli

Marks¹,

Fürstenberger²

1993

Environmental Health Perspectives

View full text Add to dashboard Cite

The skin, in particular the epidermis, offers unique opportunities to investigate the induction and control of cellular proliferation and tissue homeostasis both under in vivo and in vitro conditions. Moreover, it represents one of the most feasible model systems for experimental cancer research. As the primary border of the body, the skin has important protective and defensive functions. A general response to external injury consists of a thickening of the epithelial layer (epidermal hyperplasia) combined with an inflammatory reaction. This hyperplastic transformation of the skin is a critical condition of skin tumor development (i.e., conversion and promotion) and of the wound response. It is believed to be due to a transformation of keratinocytes into an activated state characterized by an increased rate of proliferation and the ability to release a series of growth factors and other cytokines that coordinate the defense reaction (e.g., hyperproliferation, recruitment of leukocytes, activation of the immune system) along autoand paracrine feedback loops. The initial and probably later phases of this response depend critically on a local release of eicosanoids such as prostaglandins and lipoxygenase-generated factors. A unique reaction seen upon phorbol ester treatment of mouse skin is a strong induction of the enzyme 8-lipoxygenase, which might be involved in skin tumor development by catalyzing the generation of clastogenic metabolites thought to play a role in the conversion stage.Hyperplasia may be considered to be the result of an imbalance between the rates of cell gain and cell loss. Therefore, hyperplastic transformation has to be distinguished from another response of skin to external stimuli where the homeostatic equilibrium is maintained (i.e., no hyperplasia develops in spite of strong hyperproliferation). This balanced hyperproliferation as induced by mild stimuli (pressure, phorbol ester 4-O-methyl-TPA) is neither accompanied by inflammatory reactions nor by the symptoms of keratinocyte activation. It may simply be due to an increased rate of cell-cycle traverse in the proliferative tissue compartment. In contrast, the prostaglandin-dependent activation of keratinocytes leading to hyperplastic transformation resembles in many aspects (such as, for instance, the activation of cell -cycle-related genes) the Go-S transition of cells in vitro. The control of proliferative homeostasis in normal epidermis is an unresolved problem. It is not known whether the rate of cell proliferation adapts automatically to the rate of terminal differentiation or whether this adaption is regulated by local factors such as the elusive chalones or other inhibitory signals like transforming growth factor [B.The same is true for stimulatory growth factors such as epidermal growth factor and transforming growth factor-a whose fimction may be that of wound hormones rather than of homeostatic regulators of normal tissue regeneration.

show abstract

Direct evidence for spatial and temporal regulation of transforming growth factor β1 expression during cutaneous wound healing

Cited by 216 publications

References 51 publications

One systemic administration of transforming growth factor-beta 1 reverses age- or glucocorticoid-impaired wound healing.

One systemic administration of transforming growth factor-beta 1 reverses age- or glucocorticoid-impaired wound healing.

Regulation of Wound Healing by Growth Factors and Cytokines

Proliferative Responses of the Skin to External Stimuli

Contact Info

Product

Resources

About