Changes in suspensions of human keratinocytes due to trypsin

Barton, S. P.; Marks, R.

doi:10.1007/bf00409453

Cited by 12 publications

(4 citation statements)

References 13 publications

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“…KGF plays an important role in lung morphogenesis and epithelial differentiation in the developing lung, and there is a growing body of evidence that KGF also plays a role in inflammation and repair of injured lung [195]. Endogenous KGF production has been shown to be up-regulated in several animal models of lung injury [196,197]. The protective effect of exogenous KGF in an animal model of acute lung injury was first reported by Panos in 1995 [198].…”

Section: Keratinocyte Growth Factormentioning

confidence: 99%

Pharmacotherapy of Acute Lung Injury and the Acute Respiratory Distress Syndrome

Cepkova

Matthay

2006

J Intensive Care Med

170

135

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Acute lung injury and the acute respiratory distress syndrome are common syndromes with a high mortality rate that affect both medical and surgical patients. Better understanding of the pathophysiology of acute lung injury and the acute respiratory distress syndrome and advances in supportive care and mechanical ventilation have led to improved clinical outcomes since the syndrome was first described in 1967. Although several promising pharmacological therapies, including surfactant, nitric oxide, glucocorticoids and lysofylline, have been studied in patients with acute lung injury and the acute respiratory distress syndrome, none of these pharmacological treatments reduced mortality. This article provides an overview of pharmacological therapies of acute lung injury and the acute respiratory distress syndrome tested in clinical trials and current recommendations for their use as well as a discussion of potential future pharmacological therapies including β 2 -adrenergic agonist therapy, keratinocyte growth factor, and activated protein C. Keywordsacute lung injury; acute respiratory distress syndrome; pulmonary edema; pharmacologic therapiesThe objective of this article is to review pharmacological therapeutic strategies for acute lung injury (ALI) and acute respiratory distress syndrome (ARDS). Following a brief overview of definitions, epidemiology, pathophysiology, and major nonpharmacological therapies of ALI/ ARDS, we will focus on pharmacological therapies. Given the large number of therapeutic agents tested or implicated for therapy of ALI/ARDS, we attempted to organize this article according to the level of available evidence. The pharmacological therapeutic strategies are divided into 3 sections. The first 2 sections, pulmonary targeted (inhaled) and systemic pharmacological therapy, review all therapeutic agents for which human, phase I, II, or III clinical trials have been conducted. The third section focuses on potential therapies for which there are plausible pathophysiological rationale and preliminary experimental data but no clinical trials. All phase II and III clinical trials are summarized in a table that includes level [1,2] and grade [2,3] of evidence and resulting current recommendations.We searched the MEDLINE database (since 1967), the Cochrane Library, and bibliographies of retrieved articles. The literature search was performed by both authors. In the first 2 sections of this article, we include all therapies for which clinical trials in patients with ALI/ARDS have NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author Manuscript been conducted and all important studies relevant to these therapies. In the third section, potential therapies, we discuss the treatments that are currently the most promising. Definitions and EpidemiologyThe acute respiratory distress syndrome is a clinical syndrome of acute inflammatory lung injury resulting from a variety of etiologies. The syndrome was first described by Ashbaugh and colleagues [4] in 1967 in a series of 12 patients, and...

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Section: Keratinocyte Growth Factormentioning

confidence: 99%

Pharmacotherapy of Acute Lung Injury and the Acute Respiratory Distress Syndrome

Cepkova

Matthay

2006

J Intensive Care Med

170

135

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“…Indeed, model 1 demonstrates that short adhesion times allow cellular suspension richer in KSC than longer adhesion times since the percentage of holoclones decreases with the time, confirming that KSC have great adhesion capacities thanks to the surrounding niche [14,15,35], making them able to adhere quicker than TA. However, holoclones being still present in the LA fraction, removed within 10 min of adhesion, show that (i) this adhesion time could be too brief for all KSC to adhere; (ii) the particularly high cellular seeding density could lead to competition between cells; (iii) there could be an integrin gradient among KSC leading to an unequal adhesion kinetic; and (iv) the enzymatic action during the keratinocyte extraction step known to be deleterious for cell surface proteins [36,37] could have a negative influence on adhesion of some KSC.…”

Section: Discussionmentioning

confidence: 99%

α6 Integrin (α6high)/Transferrin Receptor (CD71)low Keratinocyte Stem Cells Are More Potent for Generating Reconstructed Skin Epidermis Than Rapid Adherent Cells

Metral

Bêchetoille²,

Demarne³

et al. 2017

IJMS

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The epidermis basal layer is composed of two keratinocyte populations: Keratinocyte Stem cells (KSC) and Transitory Amplifying (TA) cells that arise from KSC division. Unfortunately, no specific marker exists to differ between KSC and TA cells. Here, we aimed at comparing two different methods that pretended to isolate these two populations: (i) the rapid adhesion method on coated substrate and (ii) the flow cytometry method, which is based on the difference in cell surface expressions of the α6 integrin and transferrin receptor (CD71). Then, we compared different parameters that are known to discriminate KSC and TA populations. Interestingly, we showed that both methods allow enrichment in stem cells. However, cell sorting by flow cytometry (α6high/CD71low) phenotype leads to a better enrichment of KSC since the colony forming efficiency is five times increased versus total cell suspension, whereas it is only 1.4 times for the adhesion method. Moreover, α6high/CD71low cells give rise to a thicker pluristratified epithelium with lower seeding density and display a low Ki67 positive cells number, showing that they have reached the balance between proliferation and differentiation. We clearly demonstrated that cells isolated by a rapid adherent method are not the same population as KSC isolated by flow cytometry following α6high/CD71low phenotype.

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“…It is difficult to evaluate these results because of the heterogeneity of the epidermal tissues used for the fractionation and the crudeness of the epidermal proteins for SDS-PAGE analysis. Although keratin proteins may not be free from influences by trypsin [as Barton (19) reported], the evidence that identical major components of keratin proteins were present in both the whole epidermis and in trypsin treated epidermal cells made it possible to consider the presence of the abnormal proteins in the psoriatic involved epidermis.…”

Section: Discussionmentioning

confidence: 99%

Sds‐page Analysis of Whole and Fractionated Psoriatic Epidermis

Kato

Umeda

Iizuka

et al. 1983

The Journal of Dermatology

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The SDS‐PAGE patterns of keratinous proteins extracted from whole epidermis and fractionated epidermal cells were studied. Those from the whole and fractionated epidermal cells of psoriatic involved skin showed an extra 58,000 dalton polypeptide in addition to the four major polypeptides (M.W.: 67,000, 63,000, 59,000 and 55,000) which were demonstrated to be common to normal epidermis and psoriatic‐uninvolved epidermis. The stratum corneum of psoriatic involved skin did not contain a 67,000 dalton polypeptide which was present in the stratum corneum of normal and psoriatic uninvolved skin. The presence of the additional 58,000 dalton polypeptide may be due to abnormal synthesis of keratin proteins in the psoriatic epidermis, since this additional polypeptide was present in the lower living layers of the psoriatic epidermis as well. On the other hand, the absence of the 67,000 dalton polypeptide in the psoriatic stratum corneum may be due to enzymatic modifications during the transition from the living cell layers to the horny layer.

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Changes in suspensions of human keratinocytes due to trypsin

Cited by 12 publications

References 13 publications

Pharmacotherapy of Acute Lung Injury and the Acute Respiratory Distress Syndrome

Pharmacotherapy of Acute Lung Injury and the Acute Respiratory Distress Syndrome

α6 Integrin (α6high)/Transferrin Receptor (CD71)low Keratinocyte Stem Cells Are More Potent for Generating Reconstructed Skin Epidermis Than Rapid Adherent Cells

Sds‐page Analysis of Whole and Fractionated Psoriatic Epidermis

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