metaplasia/proline

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A small proline-rich protein, SPRR1, is upregulated early during tobacco smoke-induced squamous metaplasia in rat nasal epithelia.

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Small proline-rich proteins, believed to be precursor proteins for the crosslinked envelope formation in cells undergoing squamous differentiation, are encoded by the SPRR genes. To further investigate the role of these proteins, the time course of increased synthesis of SPRR1 mRNA in nasal

Small proline-rich protein 1B (SPRR1B) is a biomarker for squamous metaplasia in dry eye disease.

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OBJECTIVE Squamous metaplasia occurs in ocular surface diseases like Sjögren's syndrome (SS). It is a phenotypic change whereby epithelial cells initiate synthesis of squamous cell-specific proteins such as small proline-rich protein 1B (SPRR1B) that result in pathologic keratin formation on the

Molecular mechanism of proinflammatory cytokine-mediated squamous metaplasia in human corneal epithelial cells.

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OBJECTIVE The cornified envelope protein small proline-rich protein 1B (SPRR1B) is a biomarker for squamous metaplasia. Proinflammatory cytokines IL-1beta and IFN-gamma are potent inducers of ocular surface keratinization and SPRR1B expression. Here the molecular mechanisms controlling SPRR1B gene

Small proline-rich proteins 2 are noncoordinately upregulated by IL-6/STAT3 signaling after bile duct ligation.

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Small proline-rich proteins 2 (SPRR2) are coordinately expressed with other epidermal differential complex (EDC) genes in the skin. They function as crosslinking proteins that form bridges between other proteins that comprise the cornified cell envelope, which is the major barrier against the

MicroRNA-196a is a potential marker of progression during Barrett's metaplasia-dysplasia-invasive adenocarcinoma sequence in esophagus.

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Barrett's esophagus (BE)/Barrett's metaplasia (BM) is a recognized precursor of esophageal adenocarcinoma (EA) with an intermediary stage of dysplasia. The low yield and high cost of endoscopic screening of patients with BE underscores the need for novel biomarkers, such as microRNA (miRNA), which

Immune profile of squamous metaplasia development in autoimmune regulator-deficient dry eye.

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OBJECTIVE Squamous metaplasia of the ocular surface epithelium in severe Sjögren syndrome (SS) dry eye has been implicated to be associated with chronic engagement of immune-mediated inflammation. While the detailed immunopathological mechanism underlying keratinization of the ocular muco-epithelium

Epidermal differentiation and squamous metaplasia: from stem cell to cell death.

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Epidermal differentiation is a multi-step process defined by a cascade of interrelated changes in the expression of growth-regulatory and differentiation-specific genes (Fig. 1). Irreversible growth arrest is an early event in epidermal differentiation which occurs when cells transit from the basal

Interleukin-1 as a phenotypic immunomodulator in keratinizing squamous metaplasia of the ocular surface in Sjögren's syndrome.

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Chronic inflammation of the ocular surface in Sjögren's syndrome (SS) is associated with a vision-threatening, phenotypic change of the ocular surface, which converts from a nonkeratinized, stratified squamous epithelium to a nonsecretory, keratinized epithelium. This pathological process is known

Dry eye-induced conjunctival epithelial squamous metaplasia is modulated by interferon-gamma.

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OBJECTIVE To investigate the role of interferon (IFN)-gamma in the pathogenesis of conjunctival squamous metaplasia in dry eye. METHODS Experimental dry eye was created by subjecting C57BL/6 and IFN-gamma-knockout mice to desiccating environmental stress for 5 or 10 days. T-cell antigens and

Developmental diethylstilbestrol exposure alters genetic pathways of uterine cytodifferentiation.

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The formation of a simple columnar epithelium in the uterus is essential for implantation. Perturbation of this developmental process by exogenous estrogen, such as diethylstilbestrol (DES), results in uterine metaplasia that contributes to infertility. The cellular and molecular mechanism

Whole-exome sequencing of lobular endocervical glandular hyperplasia.

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Lobular endocervical glandular hyperplasia (LEGH) was first reported as a benign proliferative disorder of the uterine cervix. However, it currently remains unclear whether it has the biological characteristics of pyloric metaplasia or precursor of minimal deviation adenocarcinoma (MDA)/gastric-type

Organ culture study of effect of vitamin-A-deficiency on rat third molar development.

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A culture procedure for rat third molars suitable for nutritional-developmental studies is described. Unerupted third molars from 12-day-old rats were cultured in BGJb media containing 20 per cent rat serum and supplemented with 25 mM HEPES buffer, 25 mg ascorbic acid, 20 mg L-glutamine, 12 mg

Experimental chronic obstructive lung disease. I. Bronchopulmonary changes induced in rabbits by prolonged exposure to formaldehyde.

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The prolonged exposure to formaldehyde induces in the rabbit lung reactional and dystrophic changes involving the intrapulmonary bronchi, the bronchioli and the lung tissue. These changes are represented by bronchial cell hyperplasia with hypermucigenesis, extrusion of bronchial cells, bronchiolar

Isolation of a sulfated glycopeptidic antigen from human gastric tumors: its localization in normal and cancerous gastrointestinal tissues.

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A sulfated glycopeptidic antigen (SGA) was purified from papain-digested cancerous human gastric mucosa. The amino acid composition of this antigen was characterized by a high percentage of threonine and proline. Serine was present in small quantities and aromatic amino acids were absent. The amount

Expression of a squamous cell marker, the spr1 gene, is posttranscriptionally down-regulated by retinol in airway epithelium.

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Vitamin A (retinol) is required for the normal mucociliary differentiation of respiratory epithelium. A depletion of vitamin A promotes squamous cell metaplasia. To understand how vitamin A suppresses squamous cell differentiation, the expression of a squamous cell differentiation marker, the small

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