No abstract available.
Desmin* ; Intermediate Filament Proteins* ; Intermediate Filaments* ; Muscle, Skeletal* ; Muscular Diseases* ; Sciatic Nerve* ; Vimentin*

BACKGROUND AND OBJECTIVES: The aim of this study is to determine whether the hyperproliferative and hyperkeratotic characters of cholesteatoma are associated with differentiation of keratinocytes in cholesteatoma by examining the localization of marker proteins, such as involucrin, filaggrin, and cytokeratins. MATERIALS AND METHODS: Immunohistochemical study was carried out in 30 cholesteatoma tissues and 10 retroauricular skins to examine the expression of involucrin, filaggrin, cytokeratin 4, 10 and 16. The staining results were graded as negative, weakly positive (<10%), moderately positive (10-70%), and strongly positive (>70%). RESULTS: Involucrin was strongly expressed in upper spinous, granular, and corneal layer of cholesteatoma. Filaggrin was strongly expressed in granular and corneal layer of cholesteatoma. Cytokeratin 4 was expressed in basal layer of retroauricular skin, but occasionally expressed in suprabasal layer of cholesteatoma. Cytokeratin 10 was homogenously expressed in all suprabasal layer of retroauricular skin, whereas pattern of shift to surface layer was showed in cholesteatoma. Cytokeratin 16 was moderately expressed at suprabasal layer in cholesteatoma. CONCLUSIONS: It can be suggested that early differentiation of suprabasal layer may lead to hyperdifferentiation and hyperkeratosis. Different expression of cytokeratins possibly indicates the altered differentiation of cholesteatoma.
Cholesteatoma ; Intermediate Filament Proteins ; Keratin-16 ; Keratin-4 ; Keratinocytes ; Keratins ; Protein Precursors ; Proteins ; Skin

BACKGROUND AND OBJECTIVES: The aim of this study is to determine whether the hyperproliferative and hyperkeratotic characters of cholesteatoma are associated with differentiation of keratinocytes in cholesteatoma by examining the localization of marker proteins, such as involucrin, filaggrin, and cytokeratins. MATERIALS AND METHODS: Immunohistochemical study was carried out in 30 cholesteatoma tissues and 10 retroauricular skins to examine the expression of involucrin, filaggrin, cytokeratin 4, 10 and 16. The staining results were graded as negative, weakly positive (<10%), moderately positive (10-70%), and strongly positive (>70%). RESULTS: Involucrin was strongly expressed in upper spinous, granular, and corneal layer of cholesteatoma. Filaggrin was strongly expressed in granular and corneal layer of cholesteatoma. Cytokeratin 4 was expressed in basal layer of retroauricular skin, but occasionally expressed in suprabasal layer of cholesteatoma. Cytokeratin 10 was homogenously expressed in all suprabasal layer of retroauricular skin, whereas pattern of shift to surface layer was showed in cholesteatoma. Cytokeratin 16 was moderately expressed at suprabasal layer in cholesteatoma. CONCLUSIONS: It can be suggested that early differentiation of suprabasal layer may lead to hyperdifferentiation and hyperkeratosis. Different expression of cytokeratins possibly indicates the altered differentiation of cholesteatoma.
Cholesteatoma ; Intermediate Filament Proteins ; Keratin-16 ; Keratin-4 ; Keratinocytes ; Keratins ; Protein Precursors ; Proteins ; Skin

Atopic dermatitis (AD) is a complex disease that affects up to 20% of children and impacts the quality of patients and families in a significant manner. New insights into the pathophysiology of AD point to an important role of structural abnormalities in the epidermis combined with immune dysregulation. Filaggrin (FLG) is synthesized as a large precursor, profilaggrin, and is expressed in the upper layers of the epidermis. FLG plays a critical role in the epidermal barrier, and FLG mutations cause abnormal epidermal function. FLG mutations are strongly associated with early-onset, and persistent severe AD. In addition, FLG deficiency in the epidermis is related to allergic sensitization and asthma. The basic skin care including repair and protection of the skin barrier with proper hydration and topical anti-inflammatory therapy is important to control the severity of skin disease in patients with AD.
Asthma ; Child ; Dermatitis, Atopic ; Epidermis ; Humans ; Intermediate Filament Proteins ; Skin ; Skin Care ; Skin Diseases

PURPOSE: Filaggrin (FLG) is a key protein that facilitates the terminal differentiation of the epidermis and the formation of the skin barrier. Recent studies showed that atopic dermatitis (AD) associates closely with loss-of-function mutations in the FLG gene. Asian and European populations differ in the frequencies of FLG mutations. Several FLG mutations, including 3321delA, E2422X, K4671X, S2554X, and R501X, occur frequently in Chinese and Japanese populations. The association between three FLG null mutations and AD in Korean children was investigated. METHODS: The FLG mutations in 1,430 children (aged 0-18 years) with AD and 862 control subjects were genotyped by using the TaqMan assay. RESULTS: The FLG null mutation E2422X was not detected in any patients with AD or control subjects. The R501X null mutation was detected in only one child with AD (0.1%). Children with AD had the 3321delA deletion significantly more frequently (2.4%) than the control subjects (0.0%, P<0.001). Children with AD also had a significantly higher combined allele frequency of the three FLG null mutations (2.6%) than the controls (0.0%, P<0.001). The 3321delA null mutation did not associate significantly with AD severity (P=0.842). When the patients with AD were divided into allergic AD and non-allergic AD patient groups, these two groups did not differ in terms of the frequency of 3321delA. CONCLUSIONS: The Korean children had a lower frequency of FLG mutations than European populations. FLG null mutations may be associated with the development of AD in Korean children.
Asian Continental Ancestry Group ; Child ; Dermatitis, Atopic ; Epidermis ; Gene Frequency ; Humans ; Intermediate Filament Proteins ; Skin

OBJECTIVETo investigate the role of microtubule-associated protein 2 (MAP-2) and nestin in gastric development in human embryos and fetuses.

METHODSImmunohistochemistry was used to detect the expressions of MAP-2 and nestin proteins in the gastric cardia, pyloric and gastric tissues of human embryos and fetuses during the second, third and fourth month of development.

RESULTSIn the second to fourth months of gestation, MAP-2 and nestin expressions were detected in the neural cells and neural fibers of the intermuscular nerve plexus and submucosal plexus in the gastric cardia, pyloric and gastric tissues. As the gestational age increased, the number of MAP-2- and nestin-positive cells and the expression intensity all increased in the myenteric plexus, but MAP-2 and nestin expressions were negative in the glandular and mucosal tissues of human embryonic and fetal gastric cardia, pylorus or gastric walls.

CONCLUSIONMAP-2 and nestin participate in the regulation of the development of gastric tissues in human embryos.

Fetus ; metabolism ; Humans ; Intermediate Filament Proteins ; metabolism ; Microtubule-Associated Proteins ; metabolism ; Nerve Tissue Proteins ; metabolism ; Nestin ; Stomach ; embryology ; metabolism

Recent studies have suggested that nestin facilitates cellular structural remodeling in vasculature-associated cells in response to ischemic injury. The current study was designed to investigate the potential role of post-ischemic nestin expression in parenchymal astrocytes. With this aim, we characterized ischemia-induced nestin expression in the CA1 hippocampal region, an area that undergoes a delayed neuronal death, followed by a lack of neuronal generation after transient forebrain ischemia. Virtually all of the nestin-positive cells in the ischemic CA1 hippocampus were reactive astrocytes. However, induction of nestin expression did not correlate simply with astrogliosis, but rather showed characteristic time- and strata-dependent expression patterns. Nestin induction in astrocytes of the pyramidal cell layer was rapid and transient, while a long-lasting induction of nestin was observed in astrocytes located in the CA1 dendritic subfields, such as the stratum oriens and radiatum, until at least day 28 after ischemia. There was no detectable expression in the stratum lacunosum moleculare despite the evident astroglial reaction. Almost all of the nestin-positive cells also expressed a transcription factor for neural/glial progenitors, i.e., Sox-2 or Sox-9, and some cells were also positive for Ki-67. However, all of the nestin-positive astrocytes expressed the calcium-binding protein S100beta, which is known to be expressed in a distinct, post-mitotic astrocyte population. Thus, our data indicate that in the ischemic CA1 hippocampus, nestin expression was induced in astroglia that were becoming reactive, but not in a progenitor/stem cell population, suggesting that nestin may allow for the structural remodeling of these cells in response to ischemic injury.
Animals ; Astrocytes ; CA1 Region, Hippocampal ; Hippocampus ; Intermediate Filament Proteins ; Ischemia ; Nerve Tissue Proteins ; Neurons ; Prosencephalon ; Pyramidal Cells ; Rats ; Transcription Factors

Dental pulp is innervated mostly by unmyelinated axons and small myelinated axons. These axons are implicated pain transmission and contain various neurotransmitters and receptors. However, little information, so far, is available on the distribution pattern and characterization of axons involved in the dental pain. In this study, to enhance understanding of dental pain processing, we observed distribution of axons expressing peripherin, an unmyelinated and small myelinated axonal marker, the in rat maxillary molar pulp. Peripherin-immunopositive (+) axons are mostly distributed in the peripheral pulp, and a few peripherin+ axons ascend into the odontoblast layer. Peripherin+ axons expressing NF200 are more frequently observed in the odontoblast layer (86.3+/-3.0%) than in the pulpal core region (79.3+/-2.8%) and nerve plexus region (78.6+/-1.9%). In contrast, peripherin+ axons expressing CGRP are less frequently observed in the odontoblast layer (17.7+/-5.0%) than in the pulpal core (37.7+/-10.1%) and nerve plexus regions (40.0+/-5.7%). These findings indicate that small myelinated axons are implicated in the transmission of dental pain arising from the odontoblast layer while peptidergic unmyelinated axons are implicated in the transmission of dental pain arising from central core and nerve plexus regions of the dental pulp.
Animals ; Axons ; Dental Pulp ; Intermediate Filament Proteins ; Membrane Glycoproteins ; Molar ; Myelin Sheath ; Nerve Tissue Proteins ; Neurotransmitter Agents ; Odontoblasts ; Rats

PURPOSE: The aim of this experiment was to observe the phenotypic changes of intermediate filaments in skeletal muscle fibers during the degeneration and regeneration of the physical injury. MATERIALS AND METHODS: The gastrocnemius muscles of rats were physically damaged by needles and serial cryosections of the damaged muscles were prepared at 2, 4, 6, 9, 15, 21 and 35 days after injury. The cryosections were immunolabelled with desmin, vimentin and histochemically reacted with NADH-TR (nicotinamide adenine dinucleotide tetrazolium reductase). RESULTS: Myotubes, asvisualized by desmin and vimentin, appeared at 9 days after injury. The regenerative myofibers were similar to normal muscles 35 days after injury. Degeneration and regeneration occurred simultaneously and positive reactions for desmin disappeared earlier than those of vimentin. CONCLUSION: Both desmin and vimentin are strong staining tools for the evaluation of myopathy. The phenotypic patterns of intermediate filaments showed various degrees of regeneration in the early stages after physical injury.
Adenine ; Animals ; Desmin ; Intermediate Filament Proteins* ; Intermediate Filaments* ; Leg* ; Muscle Fibers, Skeletal ; Muscle, Skeletal ; Muscles* ; Muscular Diseases ; Needles ; Rats* ; Regeneration* ; Vimentin

BACKGROUND: Through differentiation processes, keratinocytes provide a physical barrier to our bodies and control skin features such as moisturization, wrinkles and pigmentation. Keratinocyte differentiation is disturbed in several skin diseases such as psoriasis and atopic dermatitis. OBJECTIVE: The aim of this study is to evaluate the keratinocyte differentiation-enhancing effect of rose absolute oil (RAO). METHODS: Primary cultured human normal keratinocytes were treated with RAO, and differentiation then checked by the expression of marker genes. RESULTS: RAO did not induce cytotoxicity on cultured keratinocytes at a dose of 10microM. The level of involucrin, an early marker for keratinocyte differentiation, was significantly increased by RAO. Concomitantly, RAO increased involucrin promoter activity, indicating that RAO increased involucrin gene expression at the mRNA level. Furthermore, RAO increased the level of filaggrin in cultured keratinocytes, and in the granular layer of mouse skin. In line with these results, RAO decreased the proliferation of keratinocytes cultured in vitro. When RAO was applied topically on the tape-stripped mouse skins, it accelerated the recovery of disturbed barrier function. CONCLUSION: These results suggest that RAO may be applicable for the control of skin texture and keratinocyte differentiation-related skin diseases.
Animals ; Dermatitis, Atopic ; Gene Expression ; Humans ; Intermediate Filament Proteins ; Keratinocytes ; Mice ; Pigmentation ; Protein Precursors ; Psoriasis ; RNA, Messenger ; Skin ; Skin Diseases