Basic Mechanisms in the Healing Cutaneous Wound

Kanzler, Matthew H.; Gorsulowsky, David C.; Swanson, Neil A.

doi:10.1111/j.1524-4725.1986.tb02099.x

Cited by 112 publications

(56 citation statements)

References 53 publications

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“…Regeneration of epidermis is a complex process that requires the proliferation of keratinocytes (Kanzler et al, 1986). The molecular mechanisms that regulate normal epidermal repair are not fully known, but protein-type growth factors -mitogens and cytokines -are central to the process of wound healing in the orchestration of tissue regeneration (McKay and Leigh, 1991;Kiritsy et al, 1993;Martin, 1997).…”

Section: Discussionmentioning

confidence: 99%

“…Keratinocytes are elemental cells forming the epidermis and are crucial for normal regeneration and healing of the epidermis. Skin healing is dependent upon several processes that comprise inflammation, protein synthesis, matrix deposition, migration and subsequent proliferation of keratinocytes (Kanzler et al, 1986;Clark, 1993). Keratinocytes are known to secrete numerous proteins that include proteolytic enzymes such as matrix metalloproteinases (Stamenkovic, 2003), interstitial collagenase (Saarialho-Kere et al, 1995) and cathepsin B (Buth et al, 2004).…”

Section: Introductionmentioning

confidence: 99%

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Procathepsin D secreted by HaCaT keratinocyte cells – A novel regulator of keratinocyte growth

Vashishta¹,

Ohri²,

Větvičková³

et al. 2007

European Journal of Cell Biology

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Procathepsin D (pCD), the precursor form of lysosomal aspartic protease, is overexpressed and secreted by various carcinomas. The fact that secreted pCD plays an essential role in progression of cancer has been established. In this study, we describe substantial secretion of pCD by the human keratinocyte cell line HaCaT, under serum-free conditions. Moreover, exogenous addition of purified pCD enhanced the proliferation of HaCaT cells. The proliferative effect of pCD was inhibited by a monoclonal antibody against the activation peptide (AP) of pCD. Treatment of HaCaT cells with pCD or AP led to the secretion of a set of cytokines that might promote the growth of cells in a paracrine manner. The role of secreted pCD and its mechanism of action were studied in a scratch wound model and the presence of pCD and AP enhanced regeneration, while this effect was reversed by the addition of anti-AP antibody. Expression and secretion of pCD was upregulated in HaCaT cells exposed to various stress conditions. Taken together, our results strongly suggest that the secretion of pCD is not only linked to cancer cells but also plays a role in normal physiological conditions like wound healing and tissue remodeling.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Procathepsin D secreted by HaCaT keratinocyte cells – A novel regulator of keratinocyte growth

Vashishta¹,

Ohri²,

Větvičková³

et al. 2007

European Journal of Cell Biology

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“…They play a central role in wound healing by secreting collagen and facilitating wound repair (3,14). They may also contribute to microbial virulence by secreting and binding fibronectin (17,18), which can facilitate the adherence of infectious organisms to themselves and other tissue cells (1,12,23).…”

mentioning

confidence: 99%

Intracellular accumulation of azithromycin by cultured human fibroblasts

Gladue

Snider

1990

Antimicrob Agents Chemother

175

105

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Azithromycin was shown to achieve high concentrations in human skin fibroblasts. IntraceUular penetration occurred rapidly (10 ig/mg of celular protein after 3 h) and then increased progressively over a 3-day period; azithromycin accumulated up to 21 times more than erythromycin (61.1 versus 2.9 ,ig/mg of protein). Uptake was dependent on the extracellular concentration, was inhibited at 4°C, did not occur in nonviable cells, and was reduced by a low pH. Intracellular accumulation was not affected by the metabolic inhibitor 2,4-dinitrophenol or sodium fluoride or by the nucleoside transport inhibitor 2-chloroadenosine. Once concentrated in cells, azithromycin remained intracellular and was released slowly in the absence of extracelular drug, compared with erythromycin (17 versus 78% released after 1 h). After 48 h of incubation in drug-free medium, 27% of the initial amount of azithromycin remained cell associated. The release of azithromycin was not affected by various monokines reported to stimulate fibroblasts (interleukin-1 or tumor necrosis factor) or by exposure to bacteria. Incubation of azithromycin-loaded fibroblasts with human polymorphonuclear leukocytes resulted in a higher intraceUlular accumulation of azithromycin in polymorphonuclear leukocytes than in cells incubated with free nonintracelular azithromycin for the same time (8.3 versus 2.2 gug/ml after 2 h), suggesting a more efficient or rapid uptake through ceUl-to-cell interaction. The widespread distribution of fibroblasts in tissues suggests a potential for these ceUls, and possibly other lysosome-containing tissue cells, to serve as a reservoir for azithromycin, slowly releasing it for activity against extracellular organisms at sites of infection and passing it to phagocytes for activity against intracellular pathogens and potential transport to sites of infection.

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“…Cutaneous wound healing is a dynamic process involving blood cells, parenchymal cells, extracellular matrix, and growth factors and occurs in three overlapping phases i.e., inflammation, re-epithelialization, and remodeling [3]. Depending upon the intensity of heat and the time the skin is exposed to this heat, burn injuries can vary in thickness from superficial to partial thickness to full thickness burns.…”

Section: Introductionmentioning

confidence: 99%