Your browser doesn't support javascript.
loading
Mostrar: 20 | 50 | 100
Resultados 1 - 4 de 4
Filtrar
Adicionar filtros








Intervalo de ano
1.
Chinese Journal of Trauma ; (12): 996-999, 2013.
Artigo em Chinês | WPRIM | ID: wpr-442606

RESUMO

Objective To investigate the expression of lung keratinocyte growth factor receptor (KGFR) in rats with acute spinal cord injury (ASCI) in different time points and its role in lung edema.Methods Thirty-two adult Wistar rats weighing 240 g to 260 g were assigned to experimental group (n =16) and control group (n =16) according to the random number table.Each group consisted of time points of 24 hours,3 days,1 week and 2 weeks after the modeling (4 rats per time point).A rat model of ASCI in experimental group was induced at C7 segment by dropping a weight of 10 g from the height of 2.5 cm (Allen' s method).In control group,laminas were removed only,leaving spinal cord at C7 intact.Rats were sacrificed at each time point for measurement of lung wet/dry weight ratio,Western blot analysis of expression of lung KGFR protein and RT-qPCR detection of lung KGFR mRNA expression.Results After ASCI in rats,the expressions of lung KGFR protein and mRNA began to drop at 24 hours (0.23 ±0.06,0,012 1 ±0.002 3),reached the trough at 3 days (0.17 ±0.04,0.008 5 ±0.001 7)and picked up at 1 week.Expression of lung KGFR mRNA in experiment group showed statistically significant difference from that in control group at 24 hours and 3 days (P < 0.05),whereas in each time point the difference of KGFR protein expression between experiment and control groups was statistically significant(P <0.05).Variation trend of KGFR expression was in parallel with the severity degree of pulmonary edema.Conclusion Lung KGFR presents significant down-regulation in ASCI rats and this may be associated with the development of pulmonary edema after ASCI.

2.
Chinese Journal of Emergency Medicine ; (12): 457-461, 2009.
Artigo em Chinês | WPRIM | ID: wpr-394989

RESUMO

Objective To explore the effects of keratinocyte growth factor receptor (KGFR) transgene on sodium channel in alveolar type Ⅱ cells with LPS-induced acute lung injury, to provide the evidence for gene treatment in acute lung injury. Method Totally 40 male Sprague-Dawtey rats were randomly divided into four groups, including normal control (n=8), injured control (n=10), normal transgene (n=10) and injured transgene (n=12). The models of acute lung injury were produced using LPS, and the successful criteria was the obvious enlargement in the lung tissue. The rats in normal transgene group and injured transgene group were injected with 1 mL of KGFR adenovirus vector through rats' tail vein. At 72 hours later, the rats in injured control group and injured transgene group were injected with LPS in dose of 5 mg/kg (BW). While rats in normal control group and normal transgene group were injected with equivalent saline simultaneously. Another 48 hours later, rats in the four groups were killed. The lung tissue were collected for analysis. The expression of sodium channel in rats' alveolar type Ⅱ cells were detected by immunohistochemistry and immunoeectron microscope. Difference among the experimental groups were estimated by ANOVA analysis (LSD-t-test). There was statistical signifi-cance when P<0.05. Results The levels of sodium channel expression in rats' alveolar type Ⅱ cells were differ-era, with normal control group (47.7±3.33), normal transgene group (46.9±5.21), injured tramgene group (29.19±4.11) and injured control group (5.1±2.3). The level of sodium channel expression in injured trans-gene group was lower than that in normal transgene group (t=9.134, P<0.001) and normal control group (t=10.601,P<0.001), but signifieantly higher than that in injured control group (t=16.466, P<0.001). Conclusions The transgene vector can effectively promote the expression of sodium channel in alveolar type Ⅱ cells in rats with LPS-indueed acute lung injury, and can alleviate sodium and water reteraion in alveolar.

3.
Korean Journal of Otolaryngology - Head and Neck Surgery ; : 374-379, 2002.
Artigo em Coreano | WPRIM | ID: wpr-644128

RESUMO

BACKGROUND AND OBJECTIVES: Epidermal-mesenchymal interactions control epidermal growth and differentiation and thus regulate tissue homeostasis in the epidermis. So the function of fibroblasts is, in addition to producing extracellular matrix as a structural framework, to act as a cellular communication bridge between epidermis and dermis by synthesizing various mediators, such as growth factors and cytokines. Although the epithelial-mesenchymal cell interaction is still not known clearly, cytokines like interleukine-1beta from keratinocyte promote Keratinocyte growth factor (KGF) which is a member of the fibroblast growth factor (FGF-7) group. IL-1beta was shown to be an important modulator of KGF expression by fibroblast cells. Like hepatocyte growth factor, KFG is best characterized as paracrine mediators of stromal-epithelial interactions produced by fibroblast cells to regulate the functions of epithelial cells and the KGF receptors (KGFR) which is a transmembrane tyrosine kinase that is a splice variant of the FGFR-2/bek gene. To study the regulation of epidermal cell proliferation and differentiation by fibroblasts via paracrine effects of oropharyngeal mucosa, an in-vitro model system has been developed to mimic epidermal-dermal interactions. Material and Method: A co-culture of fibroblasts and keratinocytes in three-dimensional collagen gels was treated with IL-1beta after carrying out the tissue culture from oropharyngeal mucosa. Immuno-histochemistry for localization of KFG and KFGR was done in these artificial tissue and in the mucosa. RESULTS: KGF and KGFR proteins were strongly expressed in cytoplasm of intermediate and superficial layers of the epithelium of the oropharyngeal mucosa. In four out of the five cases, three-dimensional oral mucosa cultures were successfully reconstructed on fibroblast-populated collagen lattice. KGF expression was found focally in the keratinocyte of epithelial layer and diffusely in fibroblast-populated collagen lattice. KGFR was only expressed focally in Keratinocyte of epithelial layer. CONCLUSION: Epidermal-mesenchymal interactions in oropharyngeal mucosa via IL-1beta, KGF and KGFR were observed in a three-dimesional culture system, showing that this system could be used as a study model of epidermal-mesenchymal interactions in oropharyngeal mucosa with some limitations.


Assuntos
Comunicação Celular , Proliferação de Células , Técnicas de Cocultura , Colágeno , Citocinas , Citoplasma , Derme , Epiderme , Células Epiteliais , Epitélio , Matriz Extracelular , Fator 7 de Crescimento de Fibroblastos , Fatores de Crescimento de Fibroblastos , Fibroblastos , Géis , Fator de Crescimento de Hepatócito , Homeostase , Peptídeos e Proteínas de Sinalização Intercelular , Interleucina-1beta , Queratinócitos , Mucosa Bucal , Mucosa , Proteínas Tirosina Quinases
4.
Medical Journal of Chinese People's Liberation Army ; (12)2001.
Artigo em Chinês | WPRIM | ID: wpr-563791

RESUMO

Objective To investigate the effects of keratinocyte growth factor(KGF) and keratinocyte growth factor receptor(KGFR) on the malignant transformation of gestational trophoblastic disease(GTD).Methods Immunolocalization of KGF/KGFR was performed on sections prepared with the samples from 26 hydatidiform mole,18 invasive mole and 12 choriocarcinoma.The in situ hybridization was used to detect the mRNA of KGF/KGFR in the tissues of hydatidiform mole and GTD.Analysis was performed according to intensity of staining and number of positive cells.Results It was revealed that specific staining for mRNA and protein of KGF/KGFR existed in hydatidiform mole and gestational trophoblastic tumor(GTT).The mRNA and protein of KGF/KGFR were allocated in cytoplasm of syncytiotrophoblasts and cytotrophoblasts of malignant hydatidiform mole,and the KGF/KGFR protein was also expressed in benign tissue,while the expression of KGFR in malignant hydatidiform mole was significantly higher than that in benign tissue(?2=12.775,P

SELEÇÃO DE REFERÊNCIAS
DETALHE DA PESQUISA