scholarly journals Pentoxifylline Inhibits Platelet-Derived Growth Factor-Stimulated Cyclin D1 Expression in Mesangial Cells by Blocking Akt Membrane Translocation

2003 ◽  
Vol 64 (4) ◽  
pp. 811-822 ◽  
Author(s):  
Shuei-Liong Lin ◽  
Ruey-Hwa Chen ◽  
Yung-Ming Chen ◽  
Wen-Chih Chiang ◽  
Tun-Jun Tsai ◽  
...  
Keyword(s):  
Growth Factor ◽  
Cyclin D1 ◽  
Mesangial Cells ◽  
Platelet Derived Growth Factor ◽  
Membrane Translocation

p38 MAP kinase negatively regulates cyclin D1 expression in airway smooth muscle cells

2001 ◽  
Vol 280 (5) ◽  
pp. L955-L964 ◽  
Author(s):  
Kristen Page ◽  
Jing Li ◽  
Marc B. Hershenson
Keyword(s):  
Growth Factor ◽  
Map Kinase ◽  
Cyclin D1 ◽  
Growth Regulation ◽  
P38 Map Kinase ◽  
Dominant Negative ◽  
Platelet Derived Growth Factor ◽  
Airway Smooth Muscle Cells ◽  
Erk Activation ◽  
Erk Phosphorylation

We have demonstrated that platelet-derived growth factor (PDGF) stimulates p38 mitogen-activated protein (MAP) kinase activation in bovine tracheal myocytes, suggesting that p38 is involved in growth regulation. We therefore examined whether p38 regulates expression of cyclin D1, a G1 cyclin required for cell cycle traversal. The chemical p38 inhibitors SB-202190 and SB-203580 each increased basal and PDGF-induced cyclin D1 promoter activity and protein abundance. Overexpression of a dominant negative allele of MAP kinase kinase-3 (MKK3), an upstream activator of p38α, had similar effects. Conversely, active MKK3 and MKK6, both of which increase p38α activity, each decreased transcription from the cyclin D1 promoter. Together, these data demonstrate that p38 negatively regulates cyclin D1 expression. We tested whether p38 regulates cyclin D1 expression via inhibition of extracellular signal-regulated kinase (ERK) activation. Chemical inhibitors of p38 induced modest ERK phosphorylation and activation. However, dominant negative MKK3 was insufficient to activate ERK, and active MKK3 and MKK6 did not attenuate platelet-derived growth factor-mediated ERK activation. These data are consistent with the notion that p38α negatively regulates cyclin D1 expression via an ERK-independent pathway.

Signaling Mechanism of Platelet-Derived Growth Factor in Cultured Rat Mesangial Cells

2015 ◽  
pp. 48-53
Author(s):  
Satoshi Ochi ◽  
Yoshihiro Fujiwara ◽  
Kenji Yokoyama ◽  
Megumu Fukunaga ◽  
SungHyo Shin ◽  
...  
Keyword(s):  
Growth Factor ◽  
Mesangial Cells ◽  
Platelet Derived Growth Factor ◽  
Signaling Mechanism

Mixed Lineage Kinase 3 Inhibits Platelet-Derived Growth Factor-Stimulated DNA Synthesis and Matrix mRNA Expression in Mesangial Cells

2002 ◽  
Vol 12 (5-6) ◽  
pp. 325-334 ◽  
Author(s):  
Narayanan Parameswaran ◽  
Carolyn Hall ◽  
Barbara Boeck ◽  
Harvey Sparks ◽  
Kathleen Gallo ◽  
...  
Keyword(s):  
Growth Factor ◽  
Dna Synthesis ◽  
Mrna Expression ◽  
Mesangial Cells ◽  
Platelet Derived Growth Factor ◽  
Mixed Lineage Kinase ◽  
Mixed Lineage Kinase 3

scholarly journals The Molecular Biology of Vestibular Schwannomas and Its Association with Hearing Loss: A Review

2012 ◽  
Vol 2012 ◽  
pp. 1-10 ◽  
Author(s):  
Erika Celis-Aguilar ◽  
Luis Lassaletta ◽  
Miguel Torres-Martín ◽  
F. Yuri Rodrigues ◽  
Manuel Nistal ◽  
...  
Keyword(s):  
Hearing Loss ◽  
Growth Factor ◽  
Molecular Biology ◽  
Cyclin D1 ◽  
Vestibular Schwannoma ◽  
Molecular Mechanisms ◽  
Platelet Derived Growth Factor ◽  
Common Symptom ◽  
The Past ◽  
New Evidence

Hearing loss is the most common symptom in patients with vestibular schwannoma (VS). In the past, compressive mechanisms caused by the tumoral mass and its growth have been regarded as the most likely causes of the hearing loss associated with VS. Interestingly, new evidence proposes molecular mechanisms as an explanation for such hearing loss. Among the molecular mechanisms proposed are methylation of TP73, negative expression of cyclin D1, expression of B7-H1, increased expression of the platelet-derived growth factor A, underexpression of PEX5L, RAD54B, and PSMAL, and overexpression of CEA. Many molecular mechanisms are involved in vestibular schwannoma development; we review some of these mechanisms with special emphasis on hearing loss associated with vestibular schwannoma.

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 ◽  
...  
Keyword(s):  
Growth Factor ◽  
Mesangial Cells ◽  
Platelet Derived Growth Factor

scholarly journals Regulation of Rat Mesangial Cell Migration by Platelet-Derived Growth Factor, Angiotensin II, and Adrenomedullin

1999 ◽  
Vol 10 (12) ◽  
pp. 2495-2502 ◽  
Author(s):  
MASAKAZU KOHNO ◽  
KENICHI YASUNARI ◽  
MIEKO MINAMI ◽  
HIROAKI KANO ◽  
KENSAKU MAEDA ◽  
...  
Keyword(s):  
Cell Migration ◽  
Angiotensin Ii ◽  
Growth Factor ◽  
Mesangial Cell ◽  
Mesangial Cells ◽  
Inhibitory Effect ◽  
Platelet Derived Growth Factor ◽  
Dependent Manner ◽  
Glomerular Mesangial Cells ◽  
Concentration Dependent Manner

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.

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