An Examination of Skin from Patients with Collagen Disease Utilizing the Combined Alcian Blue-Periodic Acid Schiff Stain

Cawley, Edward P.; McManus, J. F. A.; Lupton, Charles H.; Wheeler, Clayton E.

doi:10.1038/jid.1956.113

Cited by 24 publications

(4 citation statements)

References 7 publications

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“…To test whether phenytoin treatment could induce an increased extracellular matrix accumulation in HGFs, we used alcian blue staining (Cawley et al 1956) of cultured HGFs following prolonged treatment with phenytoin. Phenytoin produced a substantial increment in extracellular matrix accumulation after 10 d of treatment.…”

Section: Phenytoin Treatment Induces Extracellular Matrix Accumulation and Collagen Deposit In Hgfs By A Trpa1-dependent Mechanismsmentioning

confidence: 99%

TRPA1 Channels Mediate Human Gingival Fibroblast Response to Phenytoin

et al. 2017

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Drug-induced gingival enlargement (GE) is a frequent adverse effect observed in patients treated with anticonvulsant, immunosuppressant, and some antihypertensive medications-the antiepileptic phenytoin being the main drug associated with GE due to its high incidence (around 50%). The molecular mechanisms behind drug-induced gingival overgrowth are still unknown. By reverse transcription polymerase chain reaction, we demonstrate that the calcium-permeable ion channels TRPA1, TRPV1, and its capsaicin-insensitive isoform TRPV1b are expressed in human gingival fibroblasts (HGFs), the most abundant cellular type in periodontal tissue. Cultured HGFs responded with intracellular calcium elevations to phenytoin and to the canonical TRPA1 agonist allyl isothiocyanate. Application of phenytoin activated a nonselective cationic current in HGFs with a typical signature for TRPA1 channels. Moreover, this activation was blocked by HC030031, a specific TRPA1 blocker. Similarly, the use of shRNAs against hTRPA1 in HGFs reduced TRPA1 expression and activation by phenytoin. In addition, we show that phenytoin increased intracellular calcium levels in cells transfected with mouse or human TRPA1 channels. Responses to phenytoin were not observed in untransfected cells or cells expressing TRPM8 or TRPV1. The activation of HGFs by phenytoin was markedly reduced in the presence of antioxidant vitamins: ascorbic acid, folic acid, and α-tocopherol. By performing cell proliferation assays, we found that phenytoin did not augment the proliferation rate of HGFs. In contrast, alcian blue and picrosirius red staining of long-term HGFs cultures indicated that phenytoin induces extracellular matrix accumulation of collagen. Collectively, these findings support an important role of TRPA1 channels in phenytoin-induced GE, provide insight into the pathophysiologic mechanism, and offer novel therapeutic opportunities for its treatment.

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Section: Phenytoin Treatment Induces Extracellular Matrix Accumulation and Collagen Deposit In Hgfs By A Trpa1-dependent Mechanismsmentioning

confidence: 99%

TRPA1 Channels Mediate Human Gingival Fibroblast Response to Phenytoin

et al. 2017

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“…After being deparaffinized, jejunum sections were processed according to Cawley et al (1956). They were washed in running water for 5 min, then the sections were dipped in the equilibrium solution (3 % acetic acid) for 3 min; afterwards they were immersed in 1 % Alcian blue (pH 2.5), and finally washed with equilibration solution and distilled water.…”

Section: Methodsmentioning

confidence: 99%

Evaluation of mucositis induced by irinotecan after microbial colonization in germ-free mice

et al. 2015

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Mucositis is one of the most debilitating side effects of chemotherapy and some previous studies suggest a role for indigenous microbiota in the course of this pathology. Therefore, the aim of our study was to evaluate the differences in phenotype between germ-free (GF) and conventional (CV) mice, and the role of b-glucuronidase-producing bacteria in the development of irinotecan treatment in a murine model. After mucositis induction, CV mice showed a significant increase in all inflammatory parameters when compared to GF mice. CV animals also showed more lesions of the intestinal epithelium, coherent with their higher intestinal permeability. The conventionalization of GF animals reversed their phenotype to that found in CV mice. In addition, gnotobiotic mice monoassociated with an Escherichia coli strain producing b-glucuronidase showed an increased permeability when compared to gnotobiotic mice monoassociated with an E. coli strain deleted for the gene encoding b-glucuronidase, but these did not show any differences in the influx of neutrophils, eosinophils or histological characteristics. Our data confirmed that components of the gut microbiota are involved in the signs of mucositis. Nevertheless, other mechanisms than this enzyme are involved in the irinotecan treatment, since the monoassociation was not able to restore the entire phenotype observed in the CV animals with irinotecan treatment in our murine model.

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“…Papillary dermal edema is often conspicuous, accompanied by telangiectatic superficial blood vessels and focal erythrocyte extravasation 1 . The reticular dermis shows pronounced mucin deposition between the collagen fibers, consisting of glycosaminoglycans and acid mucopolysaccharides and highlighted with Alcian blue or colloidal iron stains 3,40,41 . In early lesions the basement membrane is often only slightly thickened, although this thickening becomes progressively more developed as highlighted by staining with the Periodic acid‐Schiff (PAS) reaction 40 .…”

Section: Discoid Lupus Erythematosusmentioning

confidence: 99%