Transforming growth factor β levels in rat wound chambers

Cromack, Douglas T.; Sporn, Michael B.; Roberts, Anita B.; Merino, María J.; Dart, Linda L.; Norton, Jeffrey A.

doi:10.1016/0022-4804(87)90005-9

Cited by 159 publications

(60 citation statements)

References 8 publications

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“…TGF-␤ significantly up-regulates collagen expression by dermal fibroblasts in vitro (29), by myofibroblasts (30), as well as by proliferative scar xenografts in vivo (31). Many laboratories have confirmed that TGF-␤ plays a role in the natural wound healing process and that TGF-␤ is expressed in rodent wound chambers during the early to mid phases (days 4 -7) of wound healing (32). Furthermore, in vivo gene transfer with TGF-␤1 cDNA into the skin of rats significantly enhanced the rate of wound repair (33).…”

Section: Discussionmentioning

confidence: 99%

Peripheral Blood Fibrocytes: Differentiation Pathway and Migration to Wound Sites

Abe

Donnelly

Peng

et al. 2001

The Journal of Immunology

965

1,078

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Fibrocytes are a distinct population of blood-borne cells that display a unique cell surface phenotype (collagen I+/CD11b+/CD13+/CD34+/CD45RO+/MHC class II+/CD86+) and exhibit potent immunostimulatory activities. Circulating fibrocytes rapidly enter sites of tissue injury, suggesting an important role for these cells in wound repair. However, the regulatory processes that govern the differentiation of blood-borne fibrocytes and the mechanisms that underlie the migration of these cells to wound sites are currently not known. We report herein that ex vivo cultured fibrocytes can differentiate from a CD14+-enriched mononuclear cell population and that this process requires contact with T cells. Furthermore, we demonstrate that TGF-β1 (1–10 ng/ml), an important fibrogenic and growth-regulating cytokine involved in wound healing, increases the differentiation and functional activity of cultured fibrocytes. Because fibrocytes home to sites of tissue injury, we examined the role of chemokine/chemokine receptor interactions in fibrocyte trafficking. We show that secondary lymphoid chemokine, a ligand of the CCR7 chemokine receptor, acts as a potent stimulus for fibrocyte chemotaxis in vitro and for the homing of injected fibrocytes to sites of cutaneous tissue injury in vivo. Finally, we demonstrate that differentiated, cultured fibrocytes express α smooth muscle actin and contract collagen gels in vitro, two characteristic features of wound-healing myofibroblasts. These data provide important insight into the control of fibrocyte differentiation and trafficking during tissue repair and significantly expand their potential role during wound healing.

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Section: Discussionmentioning

confidence: 99%

Peripheral Blood Fibrocytes: Differentiation Pathway and Migration to Wound Sites

Abe

Donnelly

Peng

et al. 2001

The Journal of Immunology

965

1,078

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“…There has been intense interest in the role of growth factors in the regulation of these cellular responses. Several have been found in wound fluid various times during wound healing and shown to stimulate or inhibit cell proliferation and/or migration, including platelet-derived growth factor, epidermal growth factor, macrophage-derived growth factor, transforming growth factor-beta, insulin-like growth factor-1, interleukins, an angiogenesis factor, migration stimulating factor, and fibroblast growth factor (65)(66)(67)(68)(69)(70)(71)(72)(73)(74)(75)(76)(77). Their precise mechanisms of action have not been elucidated.…”

Section: 33 34)mentioning

confidence: 99%

Shifts in the concentrations of magnesium and calcium in early porcine and rat wound fluids activate the cell migratory response.

Grzesiak¹,

Pierschbacher²

1995

J. Clin. Invest.

123

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Accruing evidence indicates that the levels of extracellular Mg2+ and Ca2+ can have a distinct impact on the adhesive and migratory activities of many cell types. The physiological relevance of these observations, however, has remained largely unexplored. In the present study, wound fluids collected throughout the early stages of cutaneous wound repair were examined for possible Mg2" and Ca2+ fluctuations. Early in the process, when cell migration into the wound site is initiated, Mg2+ is elevated and Ca2+ is reduced (Mg2+ :Ca2+ = 1). As wound healing progresses, wound fluid concentrations of Mg2+ and Ca2+ begin to return to normal plasma levels (Mg2+ :Ca2+ = 0.4). When macrophages, keratinocytes, fibroblasts, and endothelial cells were exposed to dialyzed wound fluid, the migration stimulated by undialyzed wound fluid was lost. Addition back to dialyzed wound fluid of 24 h, postinjury concentrations of Mg2+ and Ca2+ restored all migratory stimulus. This observed migration is approximately twofold greater than when normal plasma Mg2+ and Ca2+ concentrations are present. Changes in the levels of Mg2+ and Ca2+ in wound fluid occur during the same period that inflammatory cells, keratinocytes, fibroblasts, and neovasculature have been shown to migrate during wound healing in vivo. Together, these data suggest that the impact of these changes on integrins and E-cadherin may play a direct role in the activation and maintenance of the migratory phenotypes of the cells involved in the wound healing process. (J. Clin. Invest. 1995. 95:227-233.)

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“…1). Among these factors are plateletderived growth factor (PDGF), 2 transforming growth factor-␤ (TFG-␤), 3 basic fibroblast growth factor (bFGF), 4 epidermal growth factor (EGF), 5 and nerve growth factor (NGF), 6 to name but a few.…”

Section: Introductionmentioning

confidence: 99%