scholarly journals Epithelial protein lost in neoplasm modulates platelet-derived growth factor–mediated adhesion and motility of mesangial cells

2014 ◽  
Vol 86 (3) ◽  
pp. 548-557 ◽  
Author(s):  
Haruko Tsurumi ◽  
Yutaka Harita ◽  
Hidetake Kurihara ◽  
Hidetaka Kosako ◽  
Kenji Hayashi ◽  
...  
Author(s):  
Satoshi Ochi ◽  
Yoshihiro Fujiwara ◽  
Kenji Yokoyama ◽  
Megumu Fukunaga ◽  
SungHyo Shin ◽  
...  

2002 ◽  
Vol 12 (5-6) ◽  
pp. 325-334 ◽  
Author(s):  
Narayanan Parameswaran ◽  
Carolyn Hall ◽  
Barbara Boeck ◽  
Harvey Sparks ◽  
Kathleen Gallo ◽  
...  

1999 ◽  
Vol 10 (12) ◽  
pp. 2495-2502 ◽  
Author(s):  
MASAKAZU KOHNO ◽  
KENICHI YASUNARI ◽  
MIEKO MINAMI ◽  
HIROAKI KANO ◽  
KENSAKU MAEDA ◽  
...  

Abstract. This study sought to determine whether platelet-derived growth factor (PDGF) and angiotensin II (AngII) stimulate migration of cultured rat glomerular mesangial cells. After finding that this was so, the effects of adrenomedullin (ADM) and cAMP-elevating agents on basal and stimulated mesangial cell migration were examined. Two isoforms of PDGF, AB and BB, stimulated migration in a concentration-dependent manner between 1 and 50 ng/ml, while the AA isoform lacked significant effect. AngII modestly but significantly stimulated migration in a concentration-dependent manner between 10-7 and 10-6 mol/L. Rat ADM significantly inhibited the PDGF BB- and AngII-stimulated migration in a concentration-dependent manner between 10-8 and 10-7 mol/L. Inhibition by rat ADM was accompanied by an increase in cellular cAMP. cAMP agonists or inducers such as 8-bromo cAMP, forskolin, and prostaglandin I2 also significantly reduced the stimulated migration. H 89, a protein kinase A (PKA) inhibitor, attenuated the inhibitory effect of ADM, and a calcitonin gene-related peptide (CGRP) receptor antagonist, human CGRP (8-37), abolished the inhibitory effects of rat ADM. These results suggest that PDGF AB and BB as well as AngII stimulate rat mesangial cell migration and that ADM can inhibit PDGF BB- and AngII-stimulated migration, at least in part through cAMP-dependent mechanisms likely to involve specific ADM receptors with which CGRP interacts. The adenylate cyclase/cAMP/PKA system may be involved in the migration-inhibitory effect of ADM in these cells.


1994 ◽  
Vol 267 (2) ◽  
pp. C456-C465 ◽  
Author(s):  
H. Matsunaga ◽  
B. N. Ling ◽  
D. C. Eaton

We used patch-clamp methods to study the effect of platelet-derived growth factor (PDGF) on Ca2+ entry in cultured rat glomerular mesangial cells. In cell-attached patches, application of 50 ng/ml PDGF-BB inside, but not outside, the pipette frequently induced channel openings. The unitary conductance was 0.67 +/- 0.09 pS (n = 8) with 110 mM Mn2+ and 1.03 +/- 0.19 pS (n = 11) with 110 mM Ca2+ as the charge carrier. Number of channels times open probability was 0.515 +/- 0.144 (n = 14) with intrapipette PDGF and 0.037 +/- 0.022 (n = 12) without. Channel kinetics were only slightly voltage dependent. There was no effect of replacing chloride with gluconate in excised inside-out patches, showing that the channel was cation selective. The permeability (P) ratio for PMn/PNa was 1.65 and for PCa/PNa was 1.24. With the use of amphotericin B " perforated" whole cell patches, PDGF induced a small inward current (-16.1 +/- 4.33 pA; n = 11, membrane potential = -70 mV) consistent with 3,000-4,000 channels/cell. In summary, we have described a very-low-conductance Ca(2+)-permeable channel in rat mesangial cells with the following properties. 1) Activation by PDGF-BB occurs only when applied in close proximity to the channel. 2) Once activated, open probability is only slightly voltage dependent. 3) Under normal circumstances, the channel would probably appear to be cation nonselective, but with a permeability to divalent more than monovalent cations. 4) This PDGF-induced channel could provide a ligand-gated pathway for Ca2+ entry into mesangial cells that does not require membrane depolarization.


2001 ◽  
Vol 101 (1) ◽  
pp. 11-19 ◽  
Author(s):  
Chiyoko N. INOUE ◽  
Isao NAGANO ◽  
Ryo ICHINOHASAMA ◽  
Natsumi ASATO ◽  
Yoshiaki KONDO ◽  
...  

Although mesangial cell death has been shown to be correlated with mesangial cell mitosis in vivo, little is known about how these two apparently opposite events are regulated. We show that the addition of platelet-derived growth factor (PDGF; 10–50 ng/ml) to primary cultured rat mesangial cells for 24 h caused continuous proliferation along with simultaneous cell death. This process was accompanied by the fragmentation of DNA into nucleosomal oligomers, the development of apoptotic morphological changes in the nucleus, and increased expression of p53. Accumulation of lactate dehydrogenase (LDH) was also observed in the culture medium, suggesting that both apoptosis and necrosis are involved in the cell death mechanisms observed. We also observed that addition of 30 µM lysophosphatidic acid (LPA) to the culture medium greatly suppressed PDGF-induced cell death, leading to synergistically enhanced mesangial cell proliferation. DNA fragmentation, p53 expression and LDH release were all suppressed by LPA. We suggest that PDGF is a bifunctional molecule in mesangial cells that evokes both cell proliferation and cell death simultaneously, whereas LPA is a survival factor. We speculate that PDGF and LPA may play important roles in the progression or exacerbation of proliferative glomerulonephritis.


1994 ◽  
Vol 158 (1) ◽  
pp. 140-150 ◽  
Author(s):  
Hanna E. Abboud ◽  
Giuseppe Grandaliano ◽  
Massimo Pinzani ◽  
Thomas Knauss ◽  
Glenn F. Pierce ◽  
...  

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