Expression of intercellular adhesion molecules ICAM-1 and ICAM-2 in human endometrium: regulation by interferon-gamma

Thomson, Andrew J.; Greer, Morag R.; Young, A. P.; Boswell, Fiona; Telfer, Joan F.; Cameron, Iain; Norman, JE; Campbell, Steven C.

doi:10.1093/molehr/5.1.64

Cited by 48 publications

(37 citation statements)

References 23 publications

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“…The fact that TNF produced a strong augmentation of ICAM1 protein in both endometrial cell homogenates is in accord with other studies (Rothlein et al 1988, Vigano et al 1994, Thomson et al 1999, Wu et al 2004) that demonstrate the strong ICAM1 induction mediated by proinflammatory cytokines in endometrial cultures, stimulation not observed on its mRNA suggesting posttranscriptional regulation of ICAM1 in long period of cell culture. Among the possible pathways by which TNF could mediate this increase is through the NFKB1 pathway, as it has been described in ectopic endometrial lesions in patients with endometriosis (Gonzalez-Ramos et al 2007).…”

Section: Discussionsupporting

confidence: 90%

“…Cell adhesion molecules (CAM), important mediators of these interactions, are functional receptors expressed on the cell membrane that participate actively in multiple physiological processes, such as leukocyte migration and activation, and also in pathological processes, such as tumor dissemination and metastasis (Dejana 2004, Gavert et al 2007, Fan et al 2009). Endometrial cells normally express adhesion molecules such as intercellular adhesion molecule-1 (ICAM1), a 90 kDa glycoprotein member of the immunoglobulin family, which is constitutively expressed by epithelial cells; however, it is expressed in a regulated pattern by stromal cells from endometrium during the menstrual cycle (Thomson et al 1999). ICAM1 function is related to the interaction between ICAM1 positive cells and cells from the immune system through the antigen lymphocyte function-associated antigen-1 (ITGAL) expressed on the leukocyte surface, modulating the cytotoxic activity of CD8C leucocytes and natural killer (NK) cells (Rothlein et al 1988, Tabibzadeh et al 1994, Vigano et al 1994.…”

Section: Introductionmentioning

confidence: 99%

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Association between MMP1 and MMP9 activities and ICAM1 cleavage induced by tumor necrosis factor in stromal cell cultures from eutopic endometria of women with endometriosis

Pino¹,

Galleguillos²,

Torres³

et al. 2009

Reproduction

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Endometriosis is a benign gynecological pathology in which immune system deregulation may play a role in its initiation and progression. In endometriotic lesions, intercellular adhesion molecule-1 (ICAM1) is released from the cell membrane by proteolytic cleavage of its extracellular domain, a process that coincides with increased expression and proteolytic activity of metalloproteinases such as MMP1 and MMP9. The objective of our study was to investigate the association between MMP1 and MMP9 activities and ICAM1 cleavage mediated by tumor necrosis factor (TNF) in eutopic endometrial stromal cells from women with and without (control) endometriosis during culture. The RNA was evaluated by RT-PCR, and the protein was determined by western blot (ICAM1, MMP1), casein or gelatin zymographies (secreted active MMP1 or MMP9 respectively), ELISA (soluble ICAM1 (sICAM1)), and fluorescence assay (secreted active MMP1). Under basal conditions, proMMP9 dimer and MMP9 were higher in endometriosis cell cultures. In stromal cultures derived from control women and those with endometriosis, TNF augmented the intracellular proMMP1 (1.2-fold in control stromal cells) and ICAM1 (1.4-and 1.9-fold), greatly increased MMP1 and proMMP9 levels, and the sICAM1 concentration (2.3-and 4.3-fold) in their media compared with basal levels. The combination of TNF and MMP9 increased the sICAM1 concentration 14-fold in the endometriosis cell media, whereas GM6001 inhibited the stimulatory effect of TNF in both cell cultures. The deregulation of MMP9, and the TNF participation in the MMP1 and proMMP9 secretions, in the MMP9 expression and in the expression and cleavage of ICAM1 may contribute to the pathophysiology of this disease.

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Section: Discussionsupporting

confidence: 90%

Section: Introductionmentioning

confidence: 99%

Association between MMP1 and MMP9 activities and ICAM1 cleavage induced by tumor necrosis factor in stromal cell cultures from eutopic endometria of women with endometriosis

Pino¹,

Galleguillos²,

Torres³

et al. 2009

Reproduction

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“…(2) Tf culture: cell monolayers were cultured for 48 h in medium supplemented with the major iron transport protein, transferrin (Tf; 4 mg/ml; Sigma, St. Louis, Mo., USA), as a source of iron. (3) IFN-␥ culture: cell monolayers were cultured for 48 h in medium supplemented with interferon-␥ (IFN-␥ ; 100 ng/ml; Sigma), an inducer of ICAM-1 expression in endometrial cells [27,28] .…”

Section: Experimental Designmentioning

confidence: 99%

“…However, little information is available on the expression of ICAM-1 and VCAM-1, or its regulation in the endometrium. It has been localized in vivo in endometrial biopsies, mainly by immunohistochemical staining on paraffin sections or on cryosections of normal endometrium [9][10][11][12] and Northern blotting [12] .…”

Section: Introductionmentioning

confidence: 99%

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Expression of Intercellular Adhesion Molecule-1 and Vascular Cell Adhesion Molecule-1 in Human Endometrial Stromal and Epithelial Cells Is Regulated by Interferon-Gamma but Not Iron

Defrère

Donnez²,

Moulin³

et al. 2007

Gynecol Obstet Invest

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Background/Aims: Endometrial cells are chronically exposed to iron due to cyclic menstrual bleeding. Iron induces expression of adhesion molecules in endothelial cells. The purpose of this study was to investigate iron incorporation by human endometrial cells and to test whether iron may stimulate expression of intercellular adhesion molecule (ICAM)-1 and vascular cell adhesion molecule (VCAM)-1. Methods: Endometrial stromal and epithelial cells were cultured in medium alone or supplemented with INF-γ or transferrin (Tf). Iron incorporation by cells was quantified by densitometry of ferritin immunostaining. ICAM-1 and VCAM-1 expression were evaluated at the transcriptional level by real-time RT-PCR. Membrane-bound and soluble protein levels of ICAM-1 were measured by quantitative immunohistochemistry and ELISA, respectively. Results: Tf induced a significant increase in ferritin immunostaining in both endometrial cell types. Endometrial cells treated with INF-γ expressed more ICAM-1 and VCAM-1 than untreated cells. By contrast, Tf treatment did not alter ICAM-1 and VCAM-1 expression in cultured endometrial cells. Conclusions: Endometrial cells are able to incorporate iron from Tf and to metabolize it to ferritin. Iron, unlike interferon-γ, does not appear to be involved in the regulation of ICAM-1 and VCAM-1 expression in cultured endometrial cells.

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ICAM1 and fibrinogen‐γ are increased in uterine epithelial cells at the time of implantation in rats

Lecce

Kaneko

Madawala

et al. 2011

Molecular Reproduction Devel

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Uterine epithelial cells transform into a receptive state to adhere to an implanting blastocyst. Part of this transformation includes the apical concentration of cell adhesion molecules at the time of implantation. This study, for the first time, investigates the expression of ICAM1 and fibrinogen-γ (FGG) in uterine epithelial cells during normal pregnancy, pseudopregnancy and in hormone-treated rats. An increase (P < 0.05) in ICAM1 was seen at the apical membrane of uterine epithelial cells at the time of implantation compared with day 1 of pregnancy. ICAM1 was also increased (P < 0.05) on day 6 of pseudopregnancy as well as in ovariectomized rats treated with progesterone plus oestrogen. These results show that ICAM1 up-regulation at the time of implantation is under the control of progesterone, and is not dependent on cytokine release from the blastocyst or in semen. FGG dimerization increased (P < 0.05) on day 6 of pregnancy compared with day 1, and was not up-regulated in day 6 pseudopregnant animals, suggesting this increase is dependent on a developing blastocyst. The presence of ICAM1 and FGG in the uterine epithelium at the time of implantation in the rat is similar to that seen in lymphocyte-endothelium adhesion, and we suggest a similar mechanism in embryo-uterine epithelium adhesion is utilized.

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Expression of intercellular adhesion molecules ICAM-1 and ICAM-2 in human endometrium: regulation by interferon-gamma

Cited by 48 publications

References 23 publications

Association between MMP1 and MMP9 activities and ICAM1 cleavage induced by tumor necrosis factor in stromal cell cultures from eutopic endometria of women with endometriosis

Association between MMP1 and MMP9 activities and ICAM1 cleavage induced by tumor necrosis factor in stromal cell cultures from eutopic endometria of women with endometriosis

Expression of Intercellular Adhesion Molecule-1 and Vascular Cell Adhesion Molecule-1 in Human Endometrial Stromal and Epithelial Cells Is Regulated by Interferon-Gamma but Not Iron

ICAM1 and fibrinogen‐γ are increased in uterine epithelial cells at the time of implantation in rats

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