Human endometrial epithelial cell lines for studying steroid and cytokine actions

In the endometrium two enzymes are known to convert estradiol to its inactive metabolite estrone: microsomal 17beta-hydroxysteroid dehydrogenase type 2 (17beta-HSD2) and peroxisomal 17beta-HSD4. In order to elucidate the particular function of each of these two different enzymes, the human endometrial epithelial cell lines HEC-1-A and RL95-2 were examined with respect to the expression of 17betaHSD isozymes. They were compared with human endometrium in vivo. Non-radioactive in situ hybridization revealed both enzymes in glandular epithelial cells of human endometrium. The two cell lines were screened for mRNA expression of 17beta-HSD 1-4 by RT-PCR and Northern blot. 17beta-HSD2 and 4 could be detected by either method, 17beta-HSD1 only by RT-PCR, 17beta-HSD3 not at all. Both cell lines were proven to have no receptor for progesterone which is known as a physiological inducer of several 17beta-HSD isozymes. To study the regulation of 17beta-HSD2 and 17betaHSD4, the concentration of fetal calf serum in the cell culture media was reduced stepwise to 0.3% by dilution with a defined serum replacement. This treatment led to an inhibition of 17beta-HSD2 mRNA expression and an increase in the mRNA expression of 17beta-HSD4. Concomitantly, distinct morphological changes were observed, such as a decrease in the number and length of microvilli and a decrease in the formation of domes on top of the monolayers. The endometrial epithelial cell lines HEC-1-A and RL95-2 represent a suitable in vitro model for further studies of the differential expression of the major endometrial HSD isozymes, independent of the effect of progesterone.

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Cell surfactomes of two endometrial epithelial cell lines that differ in their adhesiveness to embryonic cells

Molecular Reproduction and Development ◽

10.1002/mrd.22301 ◽

2014 ◽

Vol 81 (4) ◽

pp. 326-340 ◽

Cited By ~ 6

Author(s):

Sonali R. Bhagwat ◽

Tejashree Redij ◽

Kruttika Phalnikar ◽

Sumeet Nayak ◽

Swati Iyer ◽

...

Keyword(s):

Epithelial Cell ◽

Cell Lines ◽

Embryonic Cells ◽

Endometrial Epithelial Cell ◽

Epithelial Cell Lines

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The effects of sex steroid hormones and interleukin-1-beta on MUC1 expression in endometrial epithelial cell lines

Reproduction ◽

10.1530/rep.1.00883 ◽

2006 ◽

Vol 131 (4) ◽

pp. 733-742 ◽

Cited By ~ 33

Author(s):

A W Horne ◽

E-N Lalani ◽

R A Margara ◽

J O White

Keyword(s):

Epithelial Cell ◽

Cell Lines ◽

Interleukin 1 ◽

Flow Cytometric Analysis ◽

Endometrial Receptivity ◽

Muc1 Expression ◽

Interleukin 1 Beta ◽

Similar Treatment ◽

Endometrial Epithelial Cell ◽

Epithelial Cell Lines

Oestrogen, progesterone and paracrine signals from the embryo have been associated with the overall control of implantation. Changes in the expression of the heavily glycosylated transmembrane glycoprotein MUC1 mucin on the endometrial epithelium are also thought to be important for embryo attachment. Increased MUC1 expression has been correlated with elevated progesterone levels in the secretory phase of the menstrual cycle. Embryonic control of endometrial receptivity through changes in MUC1 expression could be achieved through the interleukin-1 system. Four endometrial epithelial cell lines (HEC1A, HEC1B, Ishikawa and RL592) were treated with oestrogen and progesterone (with or without interleukin-1-beta) and were subjected to immunocytochemistry and flow cytometric analysis to determine MUC1 production using MUC1 antibodies. HEC1A (oestrogen receptor (ER) and progesterone receptor (PR) positive) and HEC1B (ER positive and PR negative) were transfected with theMUC1promoter, underwent similar treatment regimes and the activity of theMUC1promoter relative to their untreated controls was determined using a chloramphenicol acetyltransferase (CAT) enzyme-linked immunoassay. Using the cell lines, we determined that endometrial MUC1 expression is up-regulated by progesterone, consistent with thein vivoincreases in MUC1 related to high progesterone levels. We also revealed that neither oestrogen, nor interleukin-1-beta, appear to modulate MUC1. Progesterone-dependent regulation of MUC1 is likely to be an important factor in determining endometrial receptivity.

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Brucella suis vaccine strain S2-infected immortalized caprine endometrial epithelial cell lines induce non-apoptotic ER-stress

Cell Stress and Chaperones ◽

10.1007/s12192-014-0564-x ◽

2015 ◽

Vol 20 (3) ◽

pp. 399-409 ◽

Cited By ~ 10

Author(s):

Xiangguo Wang ◽

Pengfei Lin ◽

Yanlong Yin ◽

Jinhua Zhou ◽

Lanjie Lei ◽

...

Keyword(s):

Epithelial Cell ◽

Er Stress ◽

Cell Lines ◽

Vaccine Strain ◽

Endometrial Epithelial Cell ◽

Epithelial Cell Lines ◽

Brucella Suis

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Regulation of hTERT Expression and Function in Newly Immortalized p53 (+) Human Mammary Epithelial Cell Lines

10.21236/ada440296 ◽

2005 ◽

Author(s):

Martha R. Stampfer

Keyword(s):

Epithelial Cell ◽

Cell Lines ◽

Mammary Epithelial Cell ◽

Human Mammary Epithelial Cell ◽

Mammary Epithelial ◽

Htert Expression ◽

Epithelial Cell Lines ◽

Human Mammary Epithelial ◽

And Function

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Cationic amino acid transport by two renal epithelial cell lines: LLC-PK1and MDCK cells

Journal of Cellular Physiology ◽

10.1002/jcp.1041230121 ◽

1985 ◽

Vol 123 (1) ◽

pp. 144-150 ◽

Cited By ~ 20

Author(s):

Francisco V. Sepúlveda ◽

Jeremy D. Pearson

Keyword(s):

Amino Acid ◽

Epithelial Cell ◽

Cell Lines ◽

Amino Acid Transport ◽

Mdck Cells ◽

Acid Transport ◽

Renal Epithelial Cell ◽

Cationic Amino Acid ◽

Epithelial Cell Lines

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Essential Role of Visfatin in Lipopolysaccharide and Colon Ascendens Stent Peritonitis-Induced Acute Lung Injury

International Journal of Molecular Sciences ◽

10.3390/ijms20071678 ◽

2019 ◽

Vol 20 (7) ◽

pp. 1678 ◽

Cited By ~ 1

Author(s):

Yi-Chen Lee ◽

Chun-Yu Lin ◽

Yen-Hsu Chen ◽

Wen-Chin Chiu ◽

Yen-Yun Wang ◽

...

Keyword(s):

Acute Lung Injury ◽

Epithelial Cell ◽

Lung Injury ◽

Cell Lines ◽

Inflammatory Cytokines ◽

Bronchial Epithelial Cell ◽

Bronchial Epithelial ◽

Epithelial Cell Lines ◽

Nfκb Pathway ◽

Pro Inflammatory Cytokines

Acute lung injury (ALI) is a life-threatening syndrome characterized by acute and severe hypoxemic respiratory failure. Visfatin, which is known as an obesity-related cytokine with pro-inflammatory activities, plays a role in regulation of inflammatory cytokines. The mechanisms of ALI remain unclear in critically ill patients. Survival in ALI patients appear to be influenced by the stress generated by mechanical ventilation and by ALI-associated factors that initiate the inflammatory response. The objective for this study was to understand the mechanisms of how visfatin regulates inflammatory cytokines and promotes ALI. The expression of visfatin was evaluated in ALI patients and mouse sepsis models. Moreover, the underlying mechanisms were investigated using human bronchial epithelial cell lines, BEAS-2B and NL-20. An increase of serum visfatin was discovered in ALI patients compared to normal controls. Results from hematoxylin and eosin (H&E) and immunohistochemistry staining also showed that visfatin protein was upregulated in mouse sepsis models. Moreover, lipopolysaccharide (LPS) induced visfatin expression, activated the STAT3/NFκB pathway, and increased the expression of pro-inflammatory cytokines, including IL1-β, IL-6, and TNF-α in human bronchial epithelial cell lines NL-20 and BEAS-2B. Co-treatment of visfatin inhibitor FK866 reversed the activation of the STAT3/NFκB pathway and the increase of pro-inflammatory cytokines induced by LPS. Our study provides new evidence for the involvement of visfatin and down-stream events in acute lung injury. Further studies are required to confirm whether the anti-visfatin approaches can improve ALI patient survival by alleviating the pro-inflammatory process.

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