Keratinocyte Proliferation and Intermittent Pressure

NewsBot · Sep 14, 2007

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Intermittent Pressure Decreases Human Keratinocyte Proliferation in vitro.
Nasca MR, Shih AT, West DP, Martinez WM, Micali G, Landsman AS.
Skin Pharmacol Physiol. 2007 Sep 12;20(6):305-312

Background: The aim of this study was to investigate the correlation between pressure changes and keratinocyte proliferation by determining whether keratinocytes exposed to altered mechanical pressures would proliferate at different rates compared to control cells not subjected to pressure changes.

Methods: Tissue culture flasks of human keratinocytes plated at an approximate density of 15,000 cells/cm(2) undergoing an intermittent cyclic pressure of 362 mm Hg at a frequency of 2.28 or 5.16 cycles/min (0.038 or 0.086 Hz) for 8 h were compared to control flasks grown at ambient room pressure. An in-line pressure transducer was used to monitor and adjust pressure within the cell chambers, using a solenoid valve. A thymidine incorporation assay assessed the amount of cell proliferation in each set of experiments.

Results: Differences in proliferation between keratinocytes subjected to cyclic pressure changes and control cells were found to be statistically significant (p < 0.05) in 4 out of 5 proliferation assays. Also, a higher frequency of pressure changes consistently generated a reduced proliferation rate compared to that seen in cells exposed to a lower frequency of pressure changes.

Conclusion: These data indicate that keratinocytes undergoing intermittent pressure changes exhibit decreased proliferation rates compared to controls. Furthermore, an increased frequency rate seems to have a greater effect on proliferation than low-frequency rate pressure changes, suggesting that the stress caused by frequently changed pressure may play a greater role in reducing keratinocyte proliferation than the actual magnitude of load applied to the cells. Our results support the current treatment protocol of reducing speed and duration of walking on the site of the wound to promote healing of foot ulcers.
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Admin2 · Sep 15, 2007

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NewsBot · May 12, 2010

Callus formation is associated with hyperproliferation, incomplete differentiation of keratinocytes, and increased expression of adhesion molecules.
Kim SH, Kim S, Choi HI, Choi YJ, Lee YS, Sohn KC, Lee Y, Kim CD, Yoon TJ, Lee JH, Lee YH.
Br J Dermatol. 2010 Apr 30. [Epub ahead of print]

Background A callus is a local thickening of skin, characterised by accelerated keratinisation and a reduced rate of desquamation. However, the mechanism of callus formation is not fully understood.

Objectives The aim of this study was to evaluate the expression patterns, in callused skin, of genes that are implicated in keratinisation and adhesion/desquamation.

Methods Samples of skin from the dorsum of the foot (DF), centre of the plantar arch (CP), and anterior aspect of the heel (AH) were obtained from fresh cadavers, and protein and gene expression were determined by immunohistochemistry and RT-PCR, respectively.

Results The stratum corneum in the DF showed a splitting phenotype by conventional H&E staining, while the stratum corneum was normal in the AH. Cells of the stratum corneum in the AH were non-squamous. Expression of cornification-related molecules including involucrin, filaggrin, caspase 14, and calcium-sensing receptor (CaSR) was higher in the AH. Similarly, expression of adhesive proteins, such as corneodesmosin (CDSN), desmoglein 1 (DSG1), and desmocollin 1 (DSC1), was increased in the AH. However, protease-activated receptor 2 (PAR2) expression was reduced in the stratum granulosum in the AH. The number of proliferating cells in the stratum basale was significantly increased in the AH, compared with the DF and CP.

Conclusions Our data suggest that calluses form as a result of hyperproliferation and incomplete differentiation of epidermal keratinocytes, and increased expression of adhesion molecules.
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