Lanthanum suppresses osteoblastic differentiation via pertussis toxin-sensitive G protein signaling in rat vascular smooth muscle cells

التفاصيل البيبلوغرافية
العنوان: Lanthanum suppresses osteoblastic differentiation via pertussis toxin-sensitive G protein signaling in rat vascular smooth muscle cells
المؤلفون: Jian Huang, Bao-Di Gou, Kui Wang, Yan-Ling Shi, Li-Wen Wang, Tian-Lan Zhang
المصدر: Journal of Cellular Biochemistry. 108:1184-1191
بيانات النشر: Wiley, 2009.
سنة النشر: 2009
مصطلحات موضوعية: Male, MAPK/ERK pathway, medicine.medical_specialty, Vascular smooth muscle, MAP Kinase Signaling System, G protein, Myocytes, Smooth Muscle, Core Binding Factor Alpha 1 Subunit, Biology, Pertussis toxin, Biochemistry, Calcification, Physiologic, GTP-Binding Proteins, Lanthanum, Internal medicine, medicine, Animals, Extracellular Signal-Regulated MAP Kinases, Molecular Biology, Cells, Cultured, Osteoblasts, Kinase, JNK Mitogen-Activated Protein Kinases, Cell Differentiation, Cell Biology, Alkaline Phosphatase, Molecular biology, Actins, Rats, Endocrinology, Pertussis Toxin, Glycerophosphates, Alkaline phosphatase, Calcium, Signal transduction, Tunica Media, Fetal bovine serum
الوصف: A major cellular event in vascular calcification is the phenotypic transformation of vascular smooth muscle cells (VSMCs) into osteoblast-like cells. After demonstrating that lanthanum chloride (LaCl3) suppresses hydrogen peroxide-enhanced calcification in rat calcifying vascular cells (CVCs), here we report its effect on the osteoblastic differentiation of rat VSMCs, a process leading to the formation of CVCs. Cells were isolated from aortic media of male SD rats, and passages between three and eight were cultured in Dulbeccol's Modified Eagle's Medium (DMEM) containing 10% fetal bovine serum (FBS) and 10 mM β-glycerophosphate (β-GP) in the presence or absence of LaCl3. Exposure of cells to LaCl3 suppressed the β-GP-induced elevations in calcium deposition, alkaline phosphatase (ALP) activity, and Cbfa1/Runx2 expression, as well as the concomitant loss of SM α-actin. Furthermore, LaCl3 activated the phosphorylation of extracellular signal-regulated kinase (ERK) and c-Jun N-terminal kinase (JNK), and the blockage of either pathway with a specific inhibitor abolished the effects of LaCl3. In addition, pretreatment of the cells with pertussis toxin (PTx), an inhibitor of G protein-mediated signaling pathway, repealed all the changes induced by LaCl3. These findings demonstrate that LaCl3 suppresses the β-GP-induced osteoblastic differentiation and calcification in rat VSMCs, and its effect is mediated by the activation of both ERK and JNK MAPK pathways via PTx-sensitive G proteins. J. Cell. Biochem. 108: 1184–1191, 2009. © 2009 Wiley-Liss, Inc.
تدمد: 1097-4644
0730-2312
الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::afd58cb3c900609117f34fc64ba3fe6eTest
https://doi.org/10.1002/jcb.22348Test
حقوق: CLOSED
رقم الانضمام: edsair.doi.dedup.....afd58cb3c900609117f34fc64ba3fe6e
قاعدة البيانات: OpenAIRE