Soluble in Chloroform,Dichloromethane,Ethyl Acetate,DMSO,Acetone,etc.
356.2±30.0 °C at 760 mmHg
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provides coniferyl ferulate(CAS#:74635-61-3) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate
Leukocyte migration is critical for the infiltration of monocytes and accumulation of monocyte derived macrophages in inflammation. Considering that Hck and Fgr are instrumental in this process, their impact on atherosclerosis and on lesion inflammation and stability was evaluated.
Methods and Results
Hematopoietic Hck/Fgr-deficient, LDLr?/? chimeras, obtained by bone marrow transplantation, had smaller but, paradoxically, less stable lesions with reduced macrophage content, overt cap thinning, and necrotic core expansion as most prominent features. Despite a Ly6Chigh skewed proinflammatory monocyte phenotype, Hck/Fgr deficiency led to disrupted adhesion of myeloid cells to and transmigration across endothelial monolayers in-vitro and atherosclerotic plaques in-vivo, as assessed by intravital microscopy, flow cytometry and histological examination of atherosclerotic arteries. Moreover, Hck/Fgr deficient macrophages showed blunted podosome formation and mesenchymal migration capacity. In consequence transmigrated dKO macrophages were seen to accumulate in the fibrous cap, potentially promoting its focal erosion, as observed for dKO chimeras.
Hematopoietic deficiency of Hck and Fgr led to attenuated atherosclerotic plaque formation by abrogating endothelial adhesion and transmigration; paradoxically it also promoted plaque instability by causing monocyte subset imbalance and subendothelial accumulation, raising a note of caution regarding src kinase targeted intervention in plaque inflammation.
kinases, mobility, atherosclerosis, immunology, leukocyte, migration, plaque progression
Hck/Fgr Kinase Deficiency Reduces Plaque Growth and Stability by Blunting Monocyte Recruitment and Intraplaque Motility
Indira Medina, PhD,1,2 Celine Cougoule, PhD,#3,4 Maik Drechsler, PhD,#5 Beatriz Bermudez, PhD,1,6 Rory R. Koenen, PhD,5 Judith Sluimer, PhD,1 Ine Wolfs, PhD,1 Yvonne Doring, PhD,5 Veronica Herias, PhD,1 Marjon Gijbels, PhD,1 Ilze Bot, PhD,2 Saskia de Jager, PhD,2 Christian Weber, MD,5 Jack Cleutjens, PhD,1 Theo J.C. van Berkel, PhD,2 Kees-Jan Sikkink, PhD, MD,7 Atilla Mocsai, PhD,8 Isabelle Maridonneau-Parini, PhD,3,4,** Oliver Soehnlein, PhD, MD,5,9,10,** and Erik A.L. Biessen, PhD1
2016 Feb 11
Physical exercise (PE) is recommended for Rheumatoid Arthritis (RA), but the molecular and biological mechanisms that impact the inflammatory process and joint destruction in RA remain unknown. The objective of this study was to evaluate the effect of PE on the histological and transcriptional changes in the joints of adjuvant-induced arthritis (AIA) rat model. AIA rats were subjected to PE on a treadmill for eight weeks. The joints were subjected to histological and microarray analysis. The differentially expressed genes (DEGs) by PE in the arthritic rats were obtained from the microarray. The bioinformatic analysis allowed the association of these genes in biological processes and signaling pathways. PE induced the differential expression of 719 genes. The DEGs were significantly associated with pathogenic mechanisms in RA, including HIF-1, VEGF, PI3-Akt, and Jak-STAT signaling pathways, as well as response to oxidative stress and inflammatory response. At a histological level, PE exacerbated joint inflammatory infiltrate and tissue destruction. The PE exacerbated the stressed joint environment aggravating the inflammatory process, the hypoxia, and the oxidative stress, conditions described as detrimental in the RA joints. Research on the effect of PE on the pathogenesis process of RA is still necessary for animal models and human.
running, exercise, physical activity, rheumatoid arthritis, adjuvant-induced arthritis
Exercise Exacerbates the Transcriptional Profile of Hypoxia, Oxidative Stress and Inflammation in Rats with Adjuvant-Induced Arthritis
Susana Aidee Gonzalez-Chavez,1,2 Celia Maria QuiNonez-Flores,1,2,* Gerardo Pavel Espino-Solis,1 Jose angel Vazquez-Contreras,3 and Cesar Pacheco-Tena1
The asymmetric unit of the title compound, C47H58N6O6, comprises three independent molecules, in one of which one tert-butyl group is disordered in a 1:1 ratio. The molecule is a di(aryl)methane having two aliphatic and one N-heterocyclic substituent in each aryl ring. For the molecule having the disordered tert-butyl group, the aryl rings make an angle of 115.3?(2)° at the methylene carbon; one aryl ring is aligned at 42.0?(1)° with respect to the N-heterocyclic substituent and the other at 48.7?(1)° with respect to its substituent. The two ordered molecules are disposed about a pseudo center of inversion. The pairs of twist angles in these two molecules differ [52.7?(1) and 61.7?(1)°, and 29.1?(1) and 58.5?(1)°].
Tahir Qadri,a Itrat Anis,a M. R. Shah,a and Seik Weng Ngb,*
2011 Mar 1;