The Role of Macrophages in Wound Repair

Rf, Diegelmann; Ik, Cohen; Am, Kaplan

doi:10.1097/00006534-198107000-00025

Cited by 175 publications

(58 citation statements)

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“…These cells are discussed to be the most essential inflammatory cells involved in the normal healing response. Their presence is a marker for the nearing end of the inflammatory phase and the beginning of the proliferative phase (16). Inhibition of macrophage function results in a delay of the healing response.…”

Section: Principles Of Wound Healingmentioning

confidence: 99%

Keloids: Current concepts of pathogenesis (Review)

Bran¹

2009

Int J Mol Med

194

208

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Abstract. Excess scar formation occurs after dermal injury as a result of abnormal wound healing. Hypertrophic scars and keloids both represent fibrotic skin conditions which can be very difficult, even frustrating, to treat. Identification of differences between hypertrophic scars, keloids and normal scars are a prerequisite for finding the correct therapeutical concept. Despite the relatively high prevalence of keloids in the general population, the mechanisms underlying keloid formation are only partially understood. This fact is reflected in the multiple treatment modalities, of which no single treatment has proven to be widely effective. Advances in our understanding of the wound healing process reveal new pathophysiological concepts for keloid formation. Our article presents an overview on physiological wound healing and the pathogenesis of scar formation, differentiates keloids from hypertrophic scars and reviews current hypotheses for keloid formation. This information might assist in deciphering the complexity of keloid pathogenesis and help in the development of an efficacious therapeutical strategy.

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Section: Principles Of Wound Healingmentioning

confidence: 99%

Keloids: Current concepts of pathogenesis (Review)

Bran¹

2009

Int J Mol Med

194

208

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“…The repair ofdamaged tissue occurs through the concerted action of many specialized cell types which invade the wound in an ordered sequence (1)(2)(3)(4)(5)(6)(7)(8). Recent studies have identified some of the factors, including chemoattractants, attachment factors, and growth factors, which are required for the entry, migration, and proliferation of cells in the wound (6)(7)(8).…”

Section: Introductionmentioning

confidence: 99%

Stimulation of granulation tissue formation by platelet-derived growth factor in normal and diabetic rats.

Grotendorst¹,

Martin²,

Pencev³

et al. 1985

J. Clin. Invest.

262

128

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Subcutaneous implantation of Hunt-Schilling wound chambers in rats induces a wound repair response causing the chamber first to fill with fluid and subsequently with connective tissue. The presence of a type I collagen gel encouraged a more rapid dispersion of cells throughout the chamber but had no effect on the rate of new collagen deposition. Addition of platelet-derived growth factor (PDGF; 50 ng/chamber) to the collagen-filled chambers caused an earlier influx of connective tissue cells, a marked increase in DNA synthesis, and a greater collagen deposition in the chamber during the first 2 wk after implantation. After 3 wk, however, the levels of collagen were similar in PDGFsupplemented and control chambers. Diabetic animals exhibited a decreased rate of repair which was restored to normal by addition of PDGF to the wound chamber. Combinations of PDGF and insulin caused an even more rapid increase in collagen deposition. These results suggest that the levels of various growth factors, particularly PDGF, may be limiting at wound sites and that supplementation of wounds with these factors can accelerate the rate of new tissue formation.

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“…In that model, platelets are the initial source of TSP-1 activity. After the initial contribution by platelets, monocytes and macrophages appear to be critical sources (22)(23)(24)(25)(26). The contributions of monocytes and macrophages extend to alveolar macrophages, where TSP-1, CD36, and TGF-b localize to regulate the activity of TGF-b (27)(28)(29)(30)(31).…”

mentioning

confidence: 99%

Thrombospondin-1–Deficient Mice Are Not Protected from Bleomycin-Induced Pulmonary Fibrosis

Ezzie¹,

Piper²,

Montague³

et al. 2011

Am J Respir Cell Mol Biol

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Thrombospondin-1 (TSP-1) is an extracellular protein critical to normal lung homeostasis, and is reported to activate latent transforming growth factor-b (TGF-b). Because active TGF-b is causally involved in lung fibrosis after bleomycin challenge, alterations in TSP-1 may be relevant to pulmonary fibrosis. We sought to determine the effects of TSP-1 deficiency on the susceptibility to bleomycin-induced pulmonary fibrosis in a murine model. Agematched and sex-matched C57BL/6 wild-type (WT) and TSP-1-deficient mice were treated twice weekly for 4 weeks with intraperitoneal bleomycin (0.035 U/g) or PBS, and were allowed to rest 1 week before being killed. Their lungs were inflated with PBS, fixed in formalin, paraffin-embedded, and sectioned. A certified veterinary pathologist blindly scored each slide for inflammation and fibrosis. Lungs were homogenized to obtain RNA and protein for the real-time RT-PCR analysis of connective tissue growth factor (CTGF) and collagen I, and for Western blotting to detect phosphoSmad2, or total Smad2/3, respectively. In response to bleomycin treatment, measures of fibrosis and inflammation, along with CTGF and collagen I mRNA concentrations, were increased in TSP-1-deficient mice compared with WT mice. Notably, Smad 2/3 signaling was of equal strength in WT and TSP-1 knockout mice treated with bleomycin, suggesting that TSP-1 is not required for the activation of TGF-b. These results demonstrate that TSP-1 deficiency does not protect mice from systemic bleomycin challenge, and that TSP-1 deficiency is associated with increased expression of lung collagen and CTGF.

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The Role of Macrophages in Wound Repair

Cited by 175 publications

References 0 publications

Keloids: Current concepts of pathogenesis (Review)

Keloids: Current concepts of pathogenesis (Review)

Stimulation of granulation tissue formation by platelet-derived growth factor in normal and diabetic rats.

Thrombospondin-1–Deficient Mice Are Not Protected from Bleomycin-Induced Pulmonary Fibrosis

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