Origin of type I collagen localized within oviduct epithelium of quail hyperstimulated by progesterone

1990 ◽  
Vol 95 (1) ◽  
pp. 85-95
Author(s):  
O. Perche ◽  
M. Hayashi ◽  
K. Hayashi ◽  
D. Birk ◽  
R.L. Trelstad ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Epithelial Cells ◽  
Steroid Hormones ◽  
Basal Lamina ◽  
Type I Collagen ◽  
Sex Steroid Hormones ◽  
Collagen Fibrils ◽  
Sex Steroid ◽  
Secretory Process ◽  
Type I

Bird oviduct development is controlled by sex steroid hormones. Estrogens (E) induce cell proliferation, formation of tubular glands by epithelial cell evagination and cell differentiation. Progesterone (P) strongly increases secretory processes in E-treated quails, but inhibits cell proliferation and cell evagination. The balance between E and P is very critical for the development and morphogenesis of the oviduct. After six daily injections of low doses of E (10 micrograms day-1) and high doses of P (5 mg day-1) into ovariectomized quails, cell proliferation and secretory process are stimulated but cell evagination is totally inhibited and distribution of striated collagen is perturbed. Using antibodies against type I collagen the stroma, which is mainly composed of fibroblasts, is brightly stained, as are some regions within the epithelium. Electron microscopy shows that bundles of striated collagen fibrils appear in extracellular spaces between the lateral membranes of the epithelial cells or between the basal lamina and the epithelial basal membrane. After in situ hybridization using a 35S riboprobe specific for mRNA of the alpha 2 chain of type I collagen, mRNA was detected only in the fibroblasts of the stroma and not in epithelial cells. Furthermore electron microscope studies of collagen bundles in serial sections clearly show collagen fibrils passing through the basal lamina. It is assumed that the type I collagen between epithelial cells originates from mesenchymal cells. In the oviduct of immature birds or after physiological E + P stimulation, striated collagen is localized only in the stroma and never within the epithelium. These results indicate a modulation of extracellular matrix by sex steroid hormones in the quail oviduct.

scholarly journals Type I collagen reduces the degradation of basal lamina proteoglycan by mammary epithelial cells.

1981 ◽  
Vol 91 (1) ◽  
pp. 281-286 ◽  
Author(s):  
G David ◽  
M Bernfield
Keyword(s):  
Epithelial Cells ◽  
Heparan Sulfate ◽  
Basal Lamina ◽  
Type I Collagen ◽  
Mammary Epithelial Cells ◽  
Physiological Mechanism ◽  
Collagen Gel ◽  
Mammary Epithelial ◽  
Type I ◽  
Plastic Substratum

When mouse mammary epithelial cells are cultured on a plastic substratum, no basal lamina forms. When cultured on a type I collagen gel, the rate of glycosaminoglycan (GAG) synthesis is unchanged, but the rate of GAG degradation is markedly reduced and a GAG-rich, basal lamina-like structure accumulates. This effect of collagen was investigated by comparing the culture distribution, nature, and metabolic stability of the 35S-GAG-containing molecules produced by cells on plastic and collagen. During 48 h of labeling with 35SO4, cultures on collagen accumulate 1.4-fold more 35S-GAG per microgram of DNA. In these cultures, most of the extracellular 35S-GAG is immobilized with the lamina and collagen gel, whereas in cultures on plastic all extracellular 35S-GAG is soluble. On both substrata, the cells produce several heparan sulfate-rich 35S-proteoglycan fractions that are distinct by Sepharose CL-4B chromatography. The culture types contain similar amounts of each fraction, except that collagen cultures contain nearly four times more of a fraction that is found largely bound to the lamina and collagen gel. During a chase this proteoglycan fraction is stable in cultures on collagen, but is extensively degraded in cultures on plastic. Thus, collagen-induced formation of a basal lamina correlates with reduced degradation and enhanced accumulation of a specific heparan sulfate-rich proteoglycan fraction. Immobilization and stabilization of basal laminar proteoglycan(s) by interstitial collagen may be a physiological mechanism of basal lamina maintenance and assembly.

scholarly journals HORMONE-ASSOCIATED METABOLIC DISORDERS OF THE ORAL CAVITY ORGANS IN WOMEN OF REPRODUCTIVE AGE

2021 ◽  
Vol 78 (4) ◽  
pp. 127-134
Author(s):  
George Khodorovskyi ◽  
Lyubov Panina ◽  
Tetiana Shchurko
Keyword(s):  
Epithelial Cells ◽  
Oral Cavity ◽  
Steroid Hormones ◽  
Tight Junctions ◽  
Sex Hormones ◽  
Reproductive System ◽  
Periodontal Ligament ◽  
Sex Steroid Hormones ◽  
Sex Steroid ◽  
Periodontal Tissues

There is emerging evidence of a possible relationship between the oral cavity and reproductive organs. Recent studies suggest these functional relations. The aim of this review was to synthesize the available evidence on this relationship. Clinical observation established that sex hormones enhance gingival inflammation in periodontal healthy women during pregnancy and that periodontal condition is associated with variation of sex hormones in blood. Estrogen regulates DNA synthesis in human gingival epithelial cells and periodontal ligament, estrogen reduces down regulation of cytokines. Estrogen and progesterone affect the periodontium via appropriate receptors (estrogen receptor and progesterone receptor). They are localized in human periodontium, demonstrating that periodontal tissues are the target tissues for these hormones. Testosterone receptors are found in the periodontal tissues. It inhibits prostaglandin secretion and reduces interleukin production. At the same time testosterone stimulates osteoblast proliferation and differentiation, also enhances matrix synthesis by fibroblast, osteoblasts, and periodontal ligament. The role of testosterone in the formation of teeth is demonstrated in the paper. In females and males, in saliva there are sex steroid hormones. The study examined the entry mode of hormones into saliva. The results suggest that lipid soluble unconjugated steroids (estriol, testosterone, progesterone) enter saliva via intracellular route; the conjugated steroids (lipid insoluble (dehydroepiandrosterone, conjugated estrogens)) enter via the ‘tight junctions’ (infiltrations through the tight junctions between the acinar cells). Recent evidence indicates that organs of the oral cavity (salivary glands, periodontal tissues, oral epithelial cells mucus) produce ghrelin-hormone which affects organs of the reproductive system directly or indirectly via hypothalamic-pituitary-gonadal axis. In all these organs, there is an appropriate receptor. In conclusion, the organs of oral cavity and organs of reproductive system are functionally linked by sex steroid hormones and ghrelin, besides that periodont can influence ovaries by neuro-reflectory link.  

scholarly journals Associations between female lung cancer risk and sex steroid hormones: a systematic review and meta-analysis of the worldwide epidemiological evidence on endogenous and exogenous sex steroid hormones

BMC Cancer ◽  
2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Hui Zeng ◽  
Zhuoyu Yang ◽  
Jiang Li ◽  
Yan Wen ◽  
Zheng Wu ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Risk ◽  
Steroid Hormones ◽  
Lung Cancer Risk ◽  
Meta Analysis ◽  
Sex Steroid Hormones ◽  
Sex Steroid ◽  
Sex Steroid Hormone ◽  
Hormone Exposure ◽  
Female Lung Cancer

Abstract Background Published findings suggest sex differences in lung cancer risk and a potential role for sex steroid hormones. Our aim was to perform a meta-analysis to investigate the effects of sex steroid hormone exposure specifically on the risk of lung cancer in women. Methods The PubMed, MEDLINE, Web of Science, and EMBASE databases were searched. The pooled odds ratios (ORs) and 95% confidence intervals (95% CIs) for female lung cancer risk associated with sex steroid hormones were calculated overall and by study design, publication year, population, and smoking status. Sensitivity analysis, publication bias, and subgroup analysis were performed. Results Forty-eight studies published between 1987 and 2019 were included in the study with a total of 31,592 female lung cancer cases and 1,416,320 subjects without lung cancer. Overall, higher levels of sex steroid hormones, both endogenous (OR: 0.92, 95% CI: 0.87–0.98) and exogenous (OR: 0.86, 95% CI: 0.80–0.93), significantly decreased the risk of female lung cancer by 10% (OR: 0.90, 95% CI: 0.86–0.95). The risk of lung cancer decreased more significantly with a higher level of sex steroid hormones in non-smoking women (OR: 0.88, 95% CI: 0.78–0.99) than in smoking women (OR: 0.98, 95% CI: 0.77–1.03), especially in Asia women (OR: 0.84, 95% CI: 0.74–0.96). Conclusions Our meta-analysis reveals an association between higher levels of sex steroid hormone exposure and the decreased risk of female lung cancer. Surveillance of sex steroid hormones might be used for identifying populations at high risk for lung cancer, especially among non-smoking women.

Sign in / Sign up

Export Citation Format

Share Document