Water immersion-restraint stress induces expression of immediate-early genes in gastrointestinal tract of rats

The aims of this study were to determine 1) which cells are involved in stress-induced acute gastric mucosal lesion and 2) what kinds of molecular alterations are induced by stress, using immediate-early genes (IEG) as tools for detection of cellular activation. Male Wistar rats were exposed to acute water immersion-restraint stress. Protein and mRNA for IEG were detected by immunohistochemistry and in situ hybridization, respectively. This stress induced the expression of c- fos and nerve growth factor-induced gene (NGFI-A) mRNA in gastric epithelial cells, the smooth muscle layer of small blood vessels, and the stomach wall. Stress upregulated the mRNA levels of these IEG in the duodenal epithelial cells and induced de novo expression of IEG in the smooth muscle layer of small blood vessels and the duodenal wall. These findings indicate that these cells are activated in response to stress. Expression of these IEG and/or transcriptional factors may reflect an initiation of mechanisms for repairing the lesions induced by stress as well as an adaptation to the stress.

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Cutaneous angioleiomyoma of the auricle: a painless variant of a painful tumour

BMJ Case Reports ◽

10.1136/bcr-2018-226179 ◽

2018 ◽

pp. bcr-2018-226179 ◽

Cited By ~ 1

Author(s):

Andrew J Newman ◽

Dustin Mullens ◽

Sarah Estrada ◽

Jason Barr

Keyword(s):

Smooth Muscle ◽

Head And Neck ◽

Blood Vessels ◽

Muscle Layer ◽

Smooth Muscle Layer ◽

Female Predominance ◽

Benign Tumours ◽

Sixth Decade

Cutaneous angioleiomyomas (ALMs) are uncommon benign tumours of the skin which derive from the smooth muscle layer of dermal blood vessels. They usually present as tender nodules in the fifth or sixth decade of life, predominantly in the legs of females. These tumours rarely present on the head and neck, especially the ear. Head and neck ALMs differ from their more common leg counterparts in that they are painless. Additionally, they do not manifest with a female predominance. Herein, a new case of a painless auricular ALM in a 63-year-old man is reported.

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Androgens Regulate the Immune/Inflammatory Response and Cell Survival Pathways in Rat Ventral Prostate Epithelial Cells

Endocrinology ◽

10.1210/en.2005-0942 ◽

2006 ◽

Vol 147 (1) ◽

pp. 257-271 ◽

Cited By ~ 37

Author(s):

A. J. Asirvatham ◽

M. Schmidt ◽

B. Gao ◽

J. Chaudhary

Keyword(s):

Cell Proliferation ◽

Epithelial Cells ◽

Inflammatory Response ◽

Immediate Early Genes ◽

Immediate Early ◽

Ventral Prostate ◽

Cell Renewal ◽

Early Genes ◽

Prostate Epithelial Cells ◽

Rat Ventral Prostate

A major hurdle in understanding the role of androgens is the heterogeneity of androgen receptor (AR) expression in the prostate. Because the majority of prostate cancer arises from the AR-positive secretory luminal epithelial cells, identifying the androgen-mediated pathways in the prostate epithelium is of great significance to understanding their role in prostate pathogenesis. To meet this objective, the current study was designed to identify immediate-early genes expressed in response to the synthetic androgen R1881 in cultured rat ventral prostate epithelial cells. Rat ventral prostate epithelial cells, purified from 20-d-old rats, were cultured, and the presence of AR and the response to androgen were established. The cells were then treated with R1881 for 2 and 12 h to capture immediate-early genes in an Affymetrix-based gene chip platform. A total of 66 nonredundant genes were identified that were responsive to R1881. The functional androgen response elements were identified in the proximal promoter to determine possible molecular mechanism. Cluster analysis identified five distinct signatures of R1881-induced genes. Pathway analysis suggested that R1881 primarily influences cell proliferation/differentiation and inflammatory/immune response pathways. Androgens appear to regulate cell renewal by regulating differentiation, cell proliferation, and apoptosis. Two mutually exclusive inflammatory response pathways were observed. The interferon pathway was up-regulated, and the ILs were down-regulated. The data identified novel androgen-regulated genes (e.g. Id1, Id3, IL-6, IGF-binding protein-2 and -3, and JunB). The loss of androgen regulation of these genes can have important consequences for cellular transformation and transition to androgen-independent growth and survival.

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