Involvement of PDGF in pressure-induced mesangial cell proliferation through PKC and tyrosine kinase pathways

Katô, Hiroaki; Osajima, Akihiko; Uezono, Yasuhito; Okazaki, Masahiro; Tsuda, Yuki; Tanaka, Hiroshi; Oishi, Yosuke; Izumi, Fujio; Nakashima, Yasuhide

doi:10.1152/ajprenal.1999.277.1.f105

Cited by 14 publications

(18 citation statements)

References 29 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In skeletal muscle cells and osteoblast-like cells, mechanical stretch increased FGF-2 expression (7,35), but other models that generate mechanical stretch did not find an effect on FGF-2 expression in the heart, in skeletal muscle, or in mesangial cells (14,30,55). Our results are the first to demonstrate that mechanical stretch increases the expression of FGF-2 mRNA in vascular smooth muscle cells.…”

Section: Discussionmentioning

confidence: 37%

Cyclic mechanical stretch induces VEGF and FGF-2 expression in pulmonary vascular smooth muscle cells

Quinn

Schlueter

Soifer

et al. 2002

American Journal of Physiology-Lung Cellular and Molecular Phys

View full text Add to dashboard Cite

Vascular endothelial growth factor (VEGF) and basic (b) fibroblast growth factor (FGF-2/bFGF) are involved in vascular development and angiogenesis. Pulmonary artery smooth muscle cells express VEGF and FGF-2 and are subjected to mechanical forces during pulsatile blood flow. The effect of stretch on growth factor expression in these cells is not well characterized. We investigated the effect of cyclic stretch on the expression of VEGF and FGF-2 in ovine pulmonary artery smooth muscle cells. Primary confluent cells from 6-wk-old lambs were cultured on flexible silicon membranes and subjected to cyclic biaxial stretch (1 Hz; 5–25% stretch; 4–48 h). Nonstretched cells served as controls. Expression of VEGF and FGF-2 was determined by Northern blot analysis. Cyclic stretch induced expression of both VEGF and FGF-2 mRNA in a time- and amplitude-dependent manner. Maximum expression was found at 24 h and 15% stretch (VEGF: 1.8-fold; FGF-2: 1.9-fold). These results demonstrate that mechanical stretch regulates VEGF and FGF-2 gene expression, which could play a role in pulmonary vascular development or in postnatal pulmonary artery function or disease.

show abstract

Section: Discussionmentioning

confidence: 37%

Cyclic mechanical stretch induces VEGF and FGF-2 expression in pulmonary vascular smooth muscle cells

Quinn

Schlueter

Soifer

et al. 2002

American Journal of Physiology-Lung Cellular and Molecular Phys

View full text Add to dashboard Cite

show abstract

“…Slight changes of osmolarity entailed enhanced PLA 2 enzymatic activity (53), and direct mechanical stimulation of skeletal muscle cells potentiated PLA 2 but not PLC activity (94). On the contrary, PLC could be mechanically activated in mesangial cells (46). Especially in blood vessels, mechanical activation of PLC was observed (43,60,70,78).…”

Section: Potential Mechanosensors Discussed So Farmentioning

confidence: 99%

G protein-mediated stretch reception

Storch¹,

Schnitzler

Gudermann

2012

American Journal of Physiology-Heart and Circulatory Physiology

155

136

View full text Add to dashboard Cite

Mechanosensation and -transduction are important for physiological processes like the senses of touch, hearing, and balance. The mechanisms underlying the translation of mechanical stimuli into biochemical information by activating various signaling pathways play a fundamental role in physiology and pathophysiology but are only poorly understood. Recently, G protein-coupled receptors (GPCRs), which are essential for the conversion of light, olfactory and gustatory stimuli, as well as of primary messengers like hormones and neurotransmitters into cellular signals and which play distinct roles in inflammation, cell growth, and differentiation, have emerged as potential mechanosensors. The first candidate for a mechanosensitive GPCR was the angiotensin-II type-1 (AT 1) receptor. Agonist-independent mechanical receptor activation of AT 1 receptors induces an active receptor conformation that appears to differ from agonist-induced receptor conformations and entails the activation of G proteins. Mechanically induced AT 1 receptor activation plays an important role for myogenic vasoconstriction and for the initiation of cardiac hypertrophy. A growing body of evidence suggests that other GPCRs are involved in mechanosensation as well. These findings highlight physiologically relevant, ligand-independent functions of GPCRs and add yet another facet to the polymodal activation spectrum of this ubiquitous protein family. mechanosensation; G protein-coupled receptor; angiotensin-II type-1 receptor; agonist independent THIS ARTICLE is part of a collection on G Protein Kinase A Signaling in Cardiovascular Physiology and Disease. Other articles appearing in this collection, as well as a full archive of all collections, can be found online at http://ajpheart.physiology. org/.

show abstract

“…A recent study has shown that transmural pressure applied to the cells enhanced MC proliferation through activation of mitogen-activated protein kinases [5]. Quite recently, we have demonstrated that transmural pressure resulted in a pressure level dependent increase in DNA synthesis and cell proliferation through activation of protein kinase C and tyrosine kinases [6]. This study revealed that the maximal increase in DNA synthesis and cell proliferation occurred at a pressure level of 80 mm Hg which was almost identical to that transmitted to the glomerular capillary wall of five-sixths renal ablation rats, a model of advanced renal failure [7].…”

Section: Introductionmentioning

confidence: 99%

Adrenomedullin Inhibits Transmural Pressure Induced Mesangial Cell Proliferation through Activation of Protein Kinase A

Osajima¹,

Katô²,

Uezono³

et al. 1999

Nephron

Self Cite

View full text Add to dashboard Cite

Adrenomedullin (AM), a hypotensive peptide isolated from human pheochromocytoma, inhibits the proliferation of mesangial cells (MC) induced by mitogens such as platelet-derived growth factor. Quite recently, we have demonstrated that transmural pressure applied to cultured MC increased DNA synthesis and cell proliferation through protein kinase C and tyrosine kinase pathways. However, the modulatory effect of AM on pressure-induced cell proliferation is as yet unknown. In the present study, we examined the effect of AM on transmural pressure-induced DNA synthesis in cultured rat MC. Pressure was applied to cells placed in a sealed chamber using compressed helium. Application of pressure resulted in an increase in [³H]thymidine incorporation (approximately 2.0-fold). AM clearly inhibited pressure-induced DNA synthesis in a concentration-dependent manner. This inhibition was paralleled by an increase in cellular cAMP levels evoked by AM. Forskolin and dibutyryl cAMP mimicked the inhibitory effect of AM. The protein kinase A inhibitor H-89 significantly attenuated the effect of AM. Human AM(22–52)-NH₂, a putative AM receptor antagonist, reversed the inhibitory effects of AM more potently than did human CGRP(8–37), a calcitonin gene related peptide receptor antagonist. Our results suggest that AM, by acting mainly on AM-sensitive receptors, inhibits pressure-induced DNA synthesis in cultured rat MC through activation of protein kinase A. AM may play a protective role against MC proliferation in certain pathological conditions.

show abstract

Involvement of PDGF in pressure-induced mesangial cell proliferation through PKC and tyrosine kinase pathways

Cited by 14 publications

References 29 publications

Cyclic mechanical stretch induces VEGF and FGF-2 expression in pulmonary vascular smooth muscle cells

Cyclic mechanical stretch induces VEGF and FGF-2 expression in pulmonary vascular smooth muscle cells

G protein-mediated stretch reception

Adrenomedullin Inhibits Transmural Pressure Induced Mesangial Cell Proliferation through Activation of Protein Kinase A

Contact Info

Product

Resources

About