Eicosanoids, Mesangial Contraction, and Intracellular Signal Transduction.

Menè, Paolo; Simonson, Michael S.; Dünn, Michael J.

doi:10.1620/tjem.166.57

Cited by 10 publications

(6 citation statements)

References 61 publications

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“…In adrenergic receptors, the seventh transmembrane domain has been suggested to regulate receptor-ligand binding (43,44). In this seventh transmembrane region of rTX receptor, the amino acid residues of Arg-292 and Trp-296 which are considered to be crucial for specific ligand binding (14,39) (17,18). In the present study, we also confirmed the presence of functional receptor in rat mesangial cells (Fig.…”

Section: Resultssupporting

confidence: 84%

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Rat kidney thromboxane receptor: molecular cloning, signal transduction, and intrarenal expression localization.

et al. 1995

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Section: Resultssupporting

confidence: 84%

“…The receptor mRNA is expressed mainly in the brain, thymus, heart, liver, spleen, uterus, and in the kidney. In isolated renal glomeruli (3,17), cultured renal glomerular mesangial cells (18,19), and epithelial cells of urinary bladder (20) (14,15,28).…”

Section: Introductionmentioning

confidence: 99%

Rat kidney thromboxane receptor: molecular cloning, signal transduction, and intrarenal expression localization.

et al. 1995

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“…In other cell types such as mesangial cells, PGF,, has been shown to increase [Ca2+li while PGE, has been shown to stimulate adenylate cyclase activity (Mene et al, 1992). We have also previously shown that PGE, can stimulate an increase in cellular cAMP and tCa2+li in osteoblast-like cells while PGF,, stimulates only an increase in [Ca2+li (Yamaguchi et al, 1988(Yamaguchi et al, ,1989.…”

Section: Discussionmentioning

confidence: 92%

Prostaglandin‐stimulated second messenger signaling in bone‐derived endothelial cells is dependent on confluency in culture

Lee

Huang

et al. 1994

Journal Cellular Physiology

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New bone formation is associated with an increase in blood flow by the invasion of capillaries. Endothelial cells that line the capillaries can produce paracrine factors that affect bone growth and development, and in turn, could be affected by products produced by bone cells, in particular the osteoblasts. Since osteoblasts produce prostaglandins E2 and F2 alpha (PGE2, PGF2 alpha), it was investigated if these PGs were agonists to bone-derived endothelial cells (BBE) by assessing changes in cAMP and free cytosolic calcium concentration ([Ca2+]i) second messenger generation. We found that confluent cultures of BBE cells, a clonal endothelial cell line derived from bovine sternal bone, responded to 1 microM PGE2 by an increase in cAMP. PGF2 alpha at the same concentration was less potent in stimulating an increase in cAMP production in confluent BBE cells. Subconfluent cells with a morphology similar to that of fibroblastic cells were not as sensitive to PGE2-stimulated cAMP generation. PGF2 alpha failed to elicit any cAMP production in subconfluent cultures. PGE2 and PGF2 alpha both stimulated an increase in [Ca2+]i concentration in a dose-dependent manner. The potency of PGE2 was similar to that of PGF2 alpha in stimulating an increase in [Ca2+]i. The Ca2+ response was mostly independent of extracellular Ca+, was unchanged even with prior indomethacin treatment, was unaffected by caffeine pretreatment, but was abolished subsequent to thapsigargin pretreatment. The PG-induced increase in [Ca2+]i was also dependent on the confluency of the cells. In a subconfluent state, the responses to PGE2, or PGF2 alpha were either negligible, or only small increases in [Ca2+]i were noted with high concentrations of these two PGs. Consistent, dose-dependent increases in [Ca2+]i were stimulated by these PGs only when the cells were confluent and had a cobblestoned appearance. Since it was previously demonstrated that BBE cells respond to parathyroid hormone (PTH) by the production of cAMP, we tested if bovine PTH(1-34) amide ]bPTH(1-34) also increased [Ca2+]i in these cells. No change in [Ca2+]i was found in response to bPTH (1-34), although bPTH (1-34) stimulated a nine to tenfold increase in cAMP. We conclude that BBE cells respond to PGE2 and PGF2 alpha but not to bPTH(1-34) by an increase in [Ca2+]i probably secondary to stimulation of phospholipase C and that the cAMP and [Ca2+]i second messenger responses in BBE cells are dependent on the state of confluency of the cells.

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“…The addition of TXA 2 analogs, PGE 2 or leukotrienes (LTC4 and LTD4), stimulated the contraction of cultured mesangial cells, and PGE 2 and PGI 2 antagonized mesangial contraction induced by TXA 2 analogs [106]. Several studies have highlighted an upregulation of COX-2, the inducible form of COX, in renal chronic inflammation [102][103][104]106]. In cultured mesangial cells, enhanced COX-2 protein levels were induced by ET-1, PDGF, LPS, TNFα, and IL-1 [96,102,107,108].…”

Section: Cyclooxygenasementioning

confidence: 99%

“…Prostanoids may have variable effects on mesangial cells, ranging from mitogenic (PGE 2α ) to growth inhibitory (PGI 2 , PGF 2 , TXA 2 ) [45,105]. The addition of TXA 2 analogs, PGE 2 or leukotrienes (LTC4 and LTD4), stimulated the contraction of cultured mesangial cells, and PGE 2 and PGI 2 antagonized mesangial contraction induced by TXA 2 analogs [106]. Several studies have highlighted an upregulation of COX-2, the inducible form of COX, in renal chronic inflammation [102][103][104]106].…”

Section: Cyclooxygenasementioning

confidence: 99%

Mesangial Cells and Glomerular Inflammation: From the Pathogenesis to Novel Therapeutic Approaches

Gómez-Guerrero¹,

Hernández-Vargas²,

López-Franco³

et al. 2005

CDTIA

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The mesangium occupies a central anatomical position in the glomerulus, and also plays an important regulatory role in immune-mediated glomerular diseases, with an active participation in the response to local inflammation. In general, the mesangial cell responses to the pathological stimuli are associated with the main events of glomerular injury: leukocyte infiltration, cell proliferation and fibrosis. Leukocyte migration and infiltration into the glomerulus is responsible for the initiation and amplification of glomerular injury, and is mediated by adhesion molecules and chemokines, which can be locally synthesized by mesangial cells. The increase in mesangial cell number is also due to proliferation of intrinsic mesangial cell population. Regulatory mechanisms of mesangial cell replication include a complex array of factors which control cell proliferation, survival and apoptosis. Mesangial matrix accumulation leading to glomerulosclerosis, is a consequence of an imbalance between matrix production and degradation, and is controlled by growth factors and pro-inflammatory cytokines. The initial phase of immune-mediated glomerular inflammation depends on the interaction of immune complexes with specific Fc receptors in infiltrating leukocytes and resident mesangial cells, the ability of immune complexes to activate complement system, and on local inflammatory processes. Activated mesangial cells then produce many inflammatory mediators leading to amplification of the injury. This review will focus on the biological functions of mesangial cells that contribute to glomerular injury, with special attention to immune-mediated glomerulonephritis. Furthermore, new therapies based on the pathophysiology of the mesangial cell that are being developed in experimental models are also proposed.

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Eicosanoids, Mesangial Contraction, and Intracellular Signal Transduction.

Cited by 10 publications

References 61 publications

Rat kidney thromboxane receptor: molecular cloning, signal transduction, and intrarenal expression localization.

Rat kidney thromboxane receptor: molecular cloning, signal transduction, and intrarenal expression localization.

Prostaglandin‐stimulated second messenger signaling in bone‐derived endothelial cells is dependent on confluency in culture

Mesangial Cells and Glomerular Inflammation: From the Pathogenesis to Novel Therapeutic Approaches

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