Angiotensin II and Epidermal Growth Factor Induce Cyclooxygenase-2 Expression in Intestinal Epithelial Cells through Small GTPases Using Distinct Signaling Pathways

Slice, Lee W.; Chiu, Terence; Rozengurt, Enrique

doi:10.1074/jbc.m408172200

Cited by 51 publications

(68 citation statements)

References 89 publications

(89 reference statements)

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“…However, its expression level did not differ between the 'sparse' and 'dense' culture conditions. In DLD-1 cells, in addition to amphiregulin, epidermal growth factor (EGF), interferon g (IFN-g), transforming growth factor bII (TGF-bII) and insulin-like growth factor II (IGF-II), which have been reported to enhance COX-2 expression (Han et al, 2004;Kim and Kim, 2004;Sheares et al, 2004;Slice et al, 2005;Vila-del Sol and Fresno, 2005), were upregulated in the 'dense' condition ( Figure 3b). On the other hand, 30 and 34 genes in Intestine-407 and DLD-1 cells, respectively, were decreased in the 'dense' condition, but there were no genes that are known to regulate COX-2 expression.…”

Section: Resultsmentioning

confidence: 99%

Hypoxia induced by benign intestinal epithelial cells is associated with cyclooxygenase-2 expression in stromal cells through AP-1-dependent pathway

et al. 2006

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Cyclooxygenase-2 (COX-2) plays important roles in tumor development. Especially in the early-stage colorectal tumors, COX-2 expression is often observed in the tumor stroma. However, the mechanism regulating such stromal expression of COX-2 remains unknown. In the present study, we simulated the indirect interaction between epithelial cells and stromal cells in the process of colorectal tumor development using an in vitro co-culture model in which NIH3T3 fibroblasts were co-cultured with 'sparsely' or 'densely' populated intestinal epithelial cells, Intestine-407 as a model of premalignant or benign intestinal epithelial cells, and DLD-1 and Caco-2 as models of malignant epithelial cells. COX-2 expression in NIH3T3 fibroblasts was upregulated when co-cultured with the 'dense' epithelial cells regardless of their character. Interestingly, there was pericellular hypoxia in the vicinity of NIH3T3 fibroblasts when cocultured with 'dense' epithelial cells, and the recovery of the partial pressure of oxygen level resulted in the reduction of enhanced COX-2 expression only in NIH3T3 fibroblasts co-cultured with 'dense' Intestine-407 cells. Furthermore, COX-2 expression was also reduced by the inhibition of transcription factor AP-1. Thus, pericellular hypoxia of the stromal cells caused by densely populated epithelial cells may be one of the potent COX-2 enhancers before completion of malignant transformation during intestinal tumor development.

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Section: Resultsmentioning

confidence: 99%

Hypoxia induced by benign intestinal epithelial cells is associated with cyclooxygenase-2 expression in stromal cells through AP-1-dependent pathway

et al. 2006

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“…In addition, in the CGC assay CADASIL VSMCs possessed altered spontaneous contractility compared with control VSMCs. These findings are intriguing, because angiotensin II stimulates smooth muscle cell contraction by a Rho family GTPase-dependent pathway (72)(73)(74)(75). Because angiotensin II downregulates Notch3 expression in VSMCs (76), the accumulation of N3ECD on the surface of CADASIL VSMCs could activate a feedback loop and enhance the ability of the VSMCs to respond to angiotensin II stimulus, and as a "side effect" lead to accentuated contraction of VSMCs demonstrated in CADASIL patients (26,27).…”

Section: Interrelationship Of Our Findingsmentioning

confidence: 99%

Proteome Analysis of Cultivated Vascular Smooth Muscle Cells from a CADASIL Patient

Ihalainen

Soliymani

Iivanainen

et al. 2007

Mol Med

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Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is a vascular dementing disease caused by mutations in the NOTCH3 gene, most which are missense mutations leading to an uneven number of cysteine residues in epidermal growth factor-like repeats in the extracellular domain of Notch3 receptor (N3ECD). CADASIL is characterized by degeneration of vascular smooth muscle cells (VSMC) and accumulation of N3ECD on the VSMCs of small and middle-sized arteries. Recent studies have demonstrated that impairment of Notch3 signaling is not the primary cause of the disease. In the present study we used proteomic analysis to characterize the protein expression pattern of a unique material of genetically genuine cultured human CADASIL VSMCs. We identified 11 differentially expressed proteins, which are involved in protein degradation and folding, contraction of VSMCs, and cellular stress. Our findings indicate that misfolding of Notch3 may cause endoplasmic reticulum stress and activation of unfolded protein response, leading to increased reactive oxygen species and inhibition of cell proliferation. In addition, upregulation of contractile proteins suggests an alteration in the signaling system of VSMC contraction. The accumulation of N3ECD on the cell surface possibly upregulates the angiotensin II regulatory feedback loop and thereby enhances the readiness of the cells to respond to angiotensin II stimulation.

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“…These cells endogenously express G␣ q/11 -coupled receptors for angiotensin II (ANG II) and vasopressin (23,39,40,(43)(44)(45)(46) and have been extensively used as a model system to examine signal transduction pathways in response to GPCR activation (23,36,38,39,(43)(44)(45)47). ANG II and vasopressin act as potent growth factors for IEC-18 and IEC-6 cells (23,39,(43)(44)(45)47). Because the levels of YAP/TAZ influence their association with transcriptional cofactors especially when expressed at elevated levels, we studied the localization, phosphorylation, and activity of the endogenous YAP protein.…”

Section: Identification Of a Novel Pattern Of Yap Nuclear-cytoplasmicmentioning

confidence: 99%

Biphasic Regulation of Yes-associated Protein (YAP) Cellular Localization, Phosphorylation, and Activity by G Protein-coupled Receptor Agonists in Intestinal Epithelial Cells

Wang¹,

Sinnett‐Smith

Stevens³

et al. 2016

Journal of Biological Chemistry

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Angiotensin II and Epidermal Growth Factor Induce Cyclooxygenase-2 Expression in Intestinal Epithelial Cells through Small GTPases Using Distinct Signaling Pathways

Cited by 51 publications

References 89 publications

Hypoxia induced by benign intestinal epithelial cells is associated with cyclooxygenase-2 expression in stromal cells through AP-1-dependent pathway

Hypoxia induced by benign intestinal epithelial cells is associated with cyclooxygenase-2 expression in stromal cells through AP-1-dependent pathway

Proteome Analysis of Cultivated Vascular Smooth Muscle Cells from a CADASIL Patient

Biphasic Regulation of Yes-associated Protein (YAP) Cellular Localization, Phosphorylation, and Activity by G Protein-coupled Receptor Agonists in Intestinal Epithelial Cells

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