GP130 Is Involved in Stretch-Induced MAP Kinase Activation in Cardiac Myocytes

Nyui, Nobuo; Tamura, Kouichi; Mizuno, Keiko; Ishigami, Tomoaki; Kihara, Minoru; Ochiai, Hisao; Kimura, Kazuo; Umemura, Satoshi; Ohno, Shigeo; Taga, Tetsuya; Ishii, Masao

doi:10.1006/bbrc.1998.8548

Cited by 17 publications

(11 citation statements)

References 25 publications

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“…Indeed, a high-affinity STAT binding element is present within the c-fos promoter, and the presence of AP-1 motifs in many MMP promoters has been well documented (62,63). Apart from the JAK/STAT pathway (64), OSM has been shown to signal through the mitogen-activated protein kinase (MAPK) cascade (65,66), including the involvement of tyrosine kinases (67). This activity has been suggested to be essential for maximal transcriptional activation of MMP-1 (59).…”

Section: Discussionmentioning

confidence: 99%

Synergistic effects of glycoprotein 130 binding cytokines in combination with interleukin-1 on cartilage collagen breakdown

Rowan

Koshy

Shingleton

et al. 2001

Arthritis & Rheumatism

132

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Section: Discussionmentioning

confidence: 99%

Synergistic effects of glycoprotein 130 binding cytokines in combination with interleukin-1 on cartilage collagen breakdown

Rowan

Koshy

Shingleton

et al. 2001

Arthritis & Rheumatism

132

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“…Typically, 10 ng/ml murine IL-3, 15 ng/ml murine IL-6, 50 ng/ml murine TPO, and 4 g/ml GST or GST-PLP-E were included in the treatments. In some experiments, a mixture of monoclonal antibodies (RX187 and RX435) against gp130 (18), provided by Dr. Tetsuya Taga, was added to the cultures at a concentration of 5 g/ml. Colonies were dried and stained for AchE activity before processing for microscopy and colony scoring.…”

Section: Methodsmentioning

confidence: 99%

Induction of Megakaryocyte Differentiation by a Novel Pregnancy-specific Hormone

Lin

Linzer

1999

Journal of Biological Chemistry

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Maturation of megakaryocytes and subsequent platelet release are normally regulated by a network of cytokines, including thrombopoietin and various interleukins. Because abnormal platelet production and activation have been implicated in gestational pathologies, additional pregnancy-specific cytokines may play important roles in the regulation of megakaryocytopoiesis. Consistent with this hypothesis, we have found that the hormone prolactin-like protein E, a placental hormone that we have recently characterized, targets megakaryocytes through a specific cell surface receptor and induces megakaryocyte differentiation through a gp130-dependent signal transduction pathway.Coordinated physiological changes during pregnancy are critical for mammalian reproduction. Many pregnancy-associated diseases such as pregnancy-induced hypertension, preeclampsia, and diabetes are the consequences of aberrant modulation of maternal physiology. Higher rates of platelet activation in plasma have been clinically linked to pre-eclampsia, and antiplatelet treatment has been widely used to treat patients with this disorder (1-3). The development of megakaryocytes (MK), 1 release of platelets into the circulation, and activation of platelets are tightly regulated processes (4), and in rodents megakaryocytopoiesis and platelet levels are elevated throughout gestation (5, 6). Although the platelet count has been found to decrease slightly in human pregnancy in some studies (7), the actual rates of platelet production apparently increase to compensate for the dramatic increase in blood volume during pregnancy (8).An accelerated production of platelets in gestation presumably depends on higher levels of thrombopoietic factors present in the maternal plasma. Many cytokines, including thrombopoietin (TPO), interleukin-6 (IL-6), IL-11, leukemia inhibitory factor, and kit ligand, have been demonstrated to enhance MK maturation to different extents under normal physiological conditions (4, 9). It is unclear, however, what factors are responsible for the pregnancy-associated thrombopoietic activity. In mammalian pregnancy, the placenta functions as a transient endocrine organ that secretes a number of factors and modulates numerous physiological processes to accommodate the needs of the developing fetus.Among the factors synthesized by the placenta are numerous proteins in the prolactin (PRL)/growth hormone family (10, 11). These proteins target distinct maternal tissues and exert various biological effects, such as the remodeling of the vascular network in the mouse by proliferin and proliferin-related protein (12), the regulation of steroid hormone production and metabolism by the placental lactogens (11), and the control of immune response by PRL-like protein A (13). As members of the cytokine superfamily, these placental hormones may act on a variety of hematopoietic cell types. We have therefore begun to search for the targets and physiological effects of these proteins with the expectation that some of these hormones will be found to be res...

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“…For example, we previously showed that treatment with Ang II or stimulation with stretch significantly upregulates expression of the angiotensinogen gene in cardiomyocytes and increases the expression of angiotensin-converting enzyme and AT1 receptor genes with induction of extracellular matrix genes, including fibronectin and collagen type I genes [8][9][10]. These changes are followed by activation of downstream signaling pathways and cellular hypertrophic and proliferative responses; these responses are inhibited by AT1 receptor antagonists, indicating that AT1 receptor signaling plays an important role in the pathological remodeling responses of cardiovascular cells [8][9][10][11][12].…”

Section: Introductionmentioning

confidence: 99%

The role of angiotensin AT1 receptor-associated protein in renin-angiotensin system regulation and function

Tamura

Tanaka²,

Tsurumi³

et al. 2007

Current Science Inc

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We cloned a novel molecule, AT1 receptor-associated protein (ATRAP), which is expressed in many tissues but specifically interacts with the AT1 receptor carboxyl-terminal. In the kidney, ATRAP was broadly distributed along the renal tubules; salt intake modulated its expression. In cardiovascular cells, angiotensin II (Ang II) stimulation made ATRAP co-localized with AT1 receptor in cytoplasm; ATRAP overexpression decreased cell surface AT1 receptor. In downstream signaling pathways, ATRAP suppressed Ang II-induced phosphorylation of mitogen-activated protein kinase, activation of c-fos gene transcription, and enhancement of amino acid or bromodeoxyuridine incorporation in cardiovascular cells. Thus, cardiovascular ATRAP may promote AT1 receptor internalization and attenuate Ang II-mediated cardiovascular remodeling. We would expect ATRAP to become a new therapeutic target molecule to treat and prevent cardiovascular remodeling in hypertension.

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GP130 Is Involved in Stretch-Induced MAP Kinase Activation in Cardiac Myocytes

Cited by 17 publications

References 25 publications

Synergistic effects of glycoprotein 130 binding cytokines in combination with interleukin-1 on cartilage collagen breakdown

Synergistic effects of glycoprotein 130 binding cytokines in combination with interleukin-1 on cartilage collagen breakdown

Induction of Megakaryocyte Differentiation by a Novel Pregnancy-specific Hormone

The role of angiotensin AT1 receptor-associated protein in renin-angiotensin system regulation and function

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