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Mouse platelet-derived growth factor beta polypeptide (simian sarcoma viral (v-sis) oncogene homolog) (PDGFB) ELISA kit, Species Mouse, Sample Type serum, plasma

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[#CSB-EL017709MO] Mouse platelet-derived growth factor beta polypeptide (simian sarcoma viral (v-sis) oncogene homolog) (PDGFB) ELISA kit, Species Mouse, Sample Type serum, plasma


CSB-EL017709MO | Mouse platelet-derived growth factor beta polypeptide (simian sarcoma viral (v-sis) oncogene homolog) (PDGFB) ELISA kit, Species Mouse, Sample Type serum, plasma, 96T
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(1) The Tyrosine Kinase Inhibitor TAS-115 Attenuates Bleomycin-Induced Lung Fibrosis in Mice.[TOP]

Pubmed ID :30540913
Publication Date : //
The signaling pathways of growth factors including platelet-derived growth factor (PDGF) can be considered specific targets for overcoming the poor prognosis of idiopathic pulmonary fibrosis (IPF). Nintedanib, the recently approved multiple kinase inhibitor, has shown promising anti-fibrotic effects in IPF patients; however, its efficacy is still limited, and in some cases, treatment discontinuation is necessary due to toxicities such as gastrointestinal disorders. Therefore, more effective agents with less toxicity are still needed. TAS-115 is a novel multiple tyrosine kinase inhibitor that preferably targets PDGF receptor (PDGFR), vascular endothelial growth factor receptor (VEGFR) and c-FMS in addition to other molecules. In this study, we evaluated the anti-fibrotic effect of TAS-115 on pulmonary fibrosis in vitro and in vivo. TAS-115 inhibited the phosphorylation of PDGFR on human lung fibroblast cell line MRC-5 cells and suppressed their PDGF-induced proliferation and migration. Furthermore, TAS-115 inhibited the phosphorylation of c-FMS, a receptor of macrophage colony-stimulating factor (M-CSF), in murine bone marrow-derived macrophages (BMDMs) and decreased the production of CCL2, another key molecule for inducing pulmonary fibrosis, under the stimulation of M-CSF. Importantly, the concentration of TAS-115 to exert these inhibitory effects was 10 nM, which was lower than that of nintedanib. In a mouse model of bleomycin-induced pulmonary fibrosis, TAS-115 significantly inhibited the development of pulmonary fibrosis and the collagen deposition in bleomycin-treated lungs. These data suggest that the strong inhibition of PDGFR and c-FMS by TAS-115 may be a promising strategy for overcoming the intractable pathogenesis of pulmonary fibrosis.

Authors : Koyama Kazuya, Goto Hisatsugu, Morizumi Shun, Kagawa Kozo, Nishimura Haruka, Sato Seidai, Kawano Hiroshi, Toyoda Yuko, Ogawa Hirohisa, Homma Sakae, Nishioka Yasuhiko,

(2) Enhancer of Zeste Homologue 2 Inhibition Attenuates TGF-β Dependent Hepatic Stellate Cell Activation and Liver Fibrosis.[TOP]

Pubmed ID :30539787
Publication Date : //
Transdifferentiation of hepatic stellate cells (HSCs) into myofibroblasts is a key event in the pathogenesis of liver fibrosis. Transforming growth factor β (TGF-β) and platelet-derived growth factor (PDGF) are canonical HSC activators after liver injury. The aim of this study was to analyze the epigenetic modulators that differentially control TGF-β and PDGF signaling pathways.

Authors : Martin-Mateos Rosa, De Assuncao Thiago M, Arab Juan Pablo, Jalan-Sakrikar Nidhi, Yaqoob Usman, Greuter Thomas, Verma Vikas K, Mathison Angela J, Cao Sheng, Lomberk Gwen, Mathurin Philippe, Urrutia Raul, Huebert Robert C, Shah Vijay H,

(3) Paracrine Factors Released by Osteoblasts Provide Strong Platelet Engraftment Properties.[TOP]

Pubmed ID :30520180
Publication Date : //
Ex vivo expansion of hematopoietic stem cells (HSC) and progenitors may one day overcome the slow platelet engraftment kinetics associated with umbilical cord blood (UCB) transplantation. Serum-free medium conditioned with osteoblasts (i.e., OCM) derived from mesenchymal stromal cells (MSC) was previously shown to increase cell growth and raise the levels of human platelets (hPLT) in mice transplanted with OCM-expanded progenitors. Herein, we characterized the cellular and molecular mechanisms responsible for these osteoblast-derived properties. Limiting dilution transplantation assays revealed that osteoblasts secrete soluble factors that synergize with exogenously-added cytokines to promote the production of progenitors with short term (ST) platelet engraftment activities, and to a lesser extent with long term (LT) platelet engraftment activities. OCM also modulated the expression repertoire of cell-surface receptors implicated in the trafficking of HSC and progenitors to the bone marrow. Furthermore, OCM contains growth factors with prosurvival and proliferation activities that synergized with stem cell factor (SCF). Insulin-like growth factor (IGF)-2 was found to be present at higher levels in OCM than in control medium conditioned with MSC. Inhibition of the IGF-1 receptor, which conveys IGF-2' intracellular signaling, largely abolished the growth-promoting activity of OCM on immature CD34 subsets and progenitors in OCM cultures. Finally, IGF-1R effects appear to be mediated in part by the coactivator beta-catenin. In summary, these results provide new insights into the paracrine regulatory activities of osteoblasts on HSC, and how these can be used to modulate the engraftment properties of human HSC and progenitors expanded in culture. SIGNIFICANCE STATEMENT: Osteoblasts are one of many different cell type implicated in the regulation of hematopoiesis through various mechanism including the release of paracrine factors such as growth factors, chemokines and extracellular matrix proteins. We show that these factors strongly modulate the growth of umbilical cord blood stem and progenitor cells through activation of insulin-like growth factor-1 receptor and subsequent activation of the transcriptional activation complex? -catenin/TCF. Osteoblasts also modulated the expression repertoire of cell-surface receptors implicated in the homing of progenitors to the bone marrow. Altogether, these properties significantly enhanced the platelet engrafting activity of progenitors produced in cultures. © AlphaMed Press 2018.

Authors : Abu-Khader Ahmad, Law Kyle W, Jahan Suria, Manesia Javed K, Pasha Roya, Hovey Owen, Pineault Nicolas,

(4) Cyclophosphamide pulse therapy normalizes vascular abnormalities in a mouse model of systemic sclerosis vasculopathy.[TOP]

Pubmed ID :30508546
Publication Date : //
Intravenous cyclophosphamide pulse, a standard treatment for systemic sclerosis (SSc)-related interstitial lung disease (ILD), elicits a disease-modifying effect on SSc vasculopathy, such as fostering microvascular de-remodeling. To investigate the molecular mechanism by which cyclophosphamide mitigates SSc vasculopathy, we employed endothelial cell-specific Fli1 knockout (Fli1 ECKO) mice that mimic the functional and structural vascular abnormalities characteristic of SSc. Biweekly cyclophosphamide injection improved vascular permeability and structural abnormalities of Fli1 ECKO mice in 2 weeks and in 3 months, respectively. In Fli1 ECKO mice, a single dose of cyclophosphamide was sufficient to normalize the decreased expression of α-smooth muscle actin in dermal blood vessels and improve the impaired neovascularization in skin-embedded Matrigel plug. Under the same condition, the decreased expression of vascular endothelial-cadherin, platelet-derived growth factor B, S1P and CCN1 (molecules associated with angiogenesis and/or vasculogenesis) was reversed along with the reversal of endothelial Fli1 expression. In SSc patients, serum CCN1 levels were significantly increased after intravenous cyclophosphamide pulse. Taken together, these results indicate that cyclophosphamide improves Fli1 deficiency-dependent vascular changes by normalizing the expression of angiogenesis- and vasculogenesis-related molecules and endothelial Fli1, which may help to explain the beneficial effect of cyclophosphamide on SSc vasculopathy.

Authors : Yamashita Takashi, Asano Yoshihide, Saigusa Ryosuke, Taniguchi Takashi, Hirabayashi Megumi, Miyagawa Takuya, Nakamura Kouki, Miura Shunsuke, Yoshizaki Ayumi, Trojanowska Maria, Sato Shinichi,

(5) Different distributions of interstitial cells of Cajal and platelet-derived growth factor receptor-α positive cells in colonic smooth muscle cell/interstitial cell of Cajal/platelet-derived growth factor receptor-α positive cell syncytium in mice.[TOP]

Pubmed ID :30510374
Publication Date : //
To investigate the distribution and function of interstitial cells of Cajal (ICCs) and platelet-derived growth factor receptor-α positive (PDGFRα) cells in the proximal and distal colon.

Authors : Lu Chen, Huang Xu, Lu Hong-Li, Liu Shao-Hua, Zang Jing-Yu, Li Yu-Jia, Chen Jie, Xu Wen-Xie,

(6) Selective deletion of hepatocyte platelet-derived growth factor receptor α and development of liver fibrosis in mice.[TOP]

Pubmed ID :30509307
Publication Date : //
Platelet-derived growth factor receptor α (PDGFRα) expression is increased in activated hepatic stellate cells (HSCs) in cirrhotic liver, while normal hepatocytes express PDGFRα at a negligible level. However, cancerous hepatocytes may show upregulation of PDGFRα, and hepatocellular carcinoma is preceded by chronic liver injury. The role of PDGFRα in non-cancerous hepatocytes and liver fibrosis is unclear. We hypothesized that upon liver injury, PDGFRα in insulted hepatocytes contributes to liver fibrosis by facilitating intercellular crosstalk between hepatocytes and HSCs.

Authors : Lim Beom Jin, Lee Woon-Kyu, Lee Hyun Woong, Lee Kwan Sik, Kim Ja Kyung, Chang Hye Young, Lee Jung Il,

(7) Different PDGF Receptor Dimers Drive Distinct Migration Modes of the Mouse Skin Fibroblast.[TOP]

Pubmed ID :30485861
Publication Date : //
The migration of mesenchymal cells is a fundamental cellular process that has been implicated in many pathophysiological conditions and is induced by chemoattractants such as platelet-derived growth factors (PDGFs). However, the regulatory mechanisms shaping this migration remain to be elucidated.

Authors : Yamada Kohta, Hamashima Takeru, Ishii Yoko, Yamamoto Seiji, Okuno Noriko, Yoshida Naofumi, Yamada Moe, Huang Ting Ting, Shioda Norifumi, Tomihara Kei, Fujimori Toshihiko, Mori Hisashi, Fukunaga Kohji, Noguchi Makoto, Sasahara Masakiyo,

(8) Effects of VEGFR1 hematopoietic progenitor cells on pre-metastatic niche formation and in vivo metastasis of breast cancer cells.[TOP]

Pubmed ID :30483898
Publication Date : //
The pre-metastatic niche has been shown to play a critical role in tumor metastasis, and its formation is closely related to the tumor microenvironment. However, the underlying molecular mechanisms remain unclear. In the present study, we successfully established a mouse model of lung metastasis using luciferase-expressing MDA-MB-435s cells. In this model, recruitment of vascular endothelial growth factor receptor-1 (VEGFR1)CD133 hematopoietic progenitor cells (HPCs) was gradually increased in lung but gradually decreased after the formation of tumor colonies in lung. We also established a highly metastatic MDA-MB-435s (MDA-MB-435s-HM) cell line from the mouse model. Changes in protein profiles in different culture conditions were investigated by protein microarray analysis. The levels of CXC chemokine ligand 16, interleukin (IL)-2Rα, IL-2Rγ, matrix metalloproteinase (MMP)-1, MMP-9, platelet-derived growth factor receptor (PDGFR)-α, stromal cell-derived factor (SDF)-1α, transforming growth factor (TGF)-β, platelet endothelial cell adhesion molecule (PECAM)-1 and vascular endothelial (VE)-cadherin were significantly greater (> fivefold) in the culture medium from MDA-MB-435s-HM cells than in that from MDA-MB-435s cells. Moreover, the levels of MMP-9, PDGFR-α, and PECAM-1 were significantly greater in the co-culture medium of MDA-MB-435s-HM cells and CD133 HPCs than in that from MDA-MB-435s-HM cells. Differentially expressed proteins were validated by enzyme-linked immunosorbent assay, and expression of their transcripts was confirmed by quantitative real-time polymerase chain reaction. Moreover, inhibition of MMP-9, PDGFR-α, and PECAM-1 by their specific inhibitors or antibodies significantly decreased cell migration, delayed lung metastasis, and decreased recruitment of VEGFR1CD133 HPCs into lung. Intra-hepatic growth of HPCs enhanced the invasive growth of MDA-MB-435s-HM cells in the liver. Our data indicate that VEGFR1CD133 HPCs contribute to lung metastasis.

Authors : Meng Du, Meng Min, Luo Anqi, Jing Xin, Wang Guanying, Huang Shangke, Luo Minna, Shao Shan, Zhao Xinhan, Liu Rui,

(9) Myofibroblast proliferation and heterogeneity are supported by macrophages during skin repair.[TOP]

Pubmed ID :30467144
Publication Date : //
During tissue repair, myofibroblasts produce extracellular matrix (ECM) molecules for tissue resilience and strength. Altered ECM deposition can lead to tissue dysfunction and disease. Identification of distinct myofibroblast subsets is necessary to develop treatments for these disorders. We analyzed profibrotic cells during mouse skin wound healing, fibrosis, and aging and identified distinct subpopulations of myofibroblasts, including adipocyte precursors (APs). Multiple mouse models and transplantation assays demonstrate that proliferation of APs but not other myofibroblasts is activated by CD301b-expressing macrophages through insulin-like growth factor 1 and platelet-derived growth factor C. With age, wound bed APs and differential gene expression between myofibroblast subsets are reduced. Our findings identify multiple fibrotic cell populations and suggest that the environment dictates functional myofibroblast heterogeneity, which is driven by fibroblast-immune interactions after wounding.

Authors : Shook Brett A, Wasko Renee R, Rivera-Gonzalez Guillermo C, Salazar-Gatzimas Emilio, López-Giráldez Francesc, Dash Biraja C, Muñoz-Rojas Andrés R, Aultman Krystal D, Zwick Rachel K, Lei Vivian, Arbiser Jack L, Miller-Jensen Kathryn, Clark Damon A, Hsia Henry C, Horsley Valerie,

(10) Positive effects of α-asarone on transplanted neural progenitor cells in a murine model of ischemic stroke.[TOP]

Pubmed ID :30466612
Publication Date : //
Some traditional Oriental herbal medicines, such as Acorus tatarinowii and Acorus gramineus, produce beneficial effects for cognition enhancement. An active compound in rhizomes and the bark of these plants is α-asarone.

Authors : Lee Hong Ju, Ahn Sung Min, Pak Malk Eun, Jung Da Hee, Lee Seo-Yeon, Shin Hwa Kyoung, Choi Byung Tae,