Somatic cell plasticity and Niemann-Pick type C2 protein: fibroblast activation.
Authors:Csepeggi C, Jiang M, Kojima F, Crofford LJ, Frolov A,
Journal:J Biol Chem
PubMed ID:21084287
A growing body of evidence points toward activated fibroblasts, also known as myofibroblasts, as one of the leading mediators in several major human pathologies including proliferative fibrotic disorders, invasive tumor growth, rheumatoid arthritis, and atherosclerosis. Niemann-Pick Type C2 (NPC2) protein has been recently identified as a product of the second ... More
Silence of TRIB3 suppresses atherosclerosis and stabilizes plaques in diabetic ApoE-/-/LDL receptor-/- mice.
Authors:Wang ZH, Shang YY, Zhang S, Zhong M, Wang XP, Deng JT, Pan J, Zhang Y, Zhang W,
Journal:Diabetes
PubMed ID:22275087
'Insulin resistance triggers the developments of diabetes mellitus and atherosclerosis. Tribbles homolog 3 (TRIB3) is involved in insulin resistance. We aimed to investigate whether TRIB3 is implicated in diabetic atherosclerosis. Sixty 3-week-old apolipoprotein E (ApoE-/-)/LDR receptor (LDLR-/-) mice were randomly divided into chow and diabetes groups. Diabetes was induced by ... More
Deficient p27 phosphorylation at serine 10 increases macrophage foam cell formation and aggravates atherosclerosis through a proliferation-independent mechanism.
Authors:Fuster JJ, González-Navarro H, Vinué A, Molina-Sànchez P, Andrés-Manzano MJ, Nakayama KI, Nakayama K, Díez-Juan A, Bernad A, Rodríguez C, Martínez-González J, Andrés V,
Journal:Arterioscler Thromb Vasc Biol
PubMed ID:21885849
Genetic ablation of the growth suppressor p27(Kip1) (p27) in the mouse aggravates atherosclerosis coinciding with enhanced arterial cell proliferation. However, it is unknown whether molecular mechanisms that limit p27's protective function contribute to atherosclerosis development and whether p27 exerts proliferation-independent activities in the arterial wall. This study aims to provide ... More
cGMP increases antioxidant function and attenuates oxidant cell death in mouse lung microvascular endothelial cells by a protein kinase G-dependent mechanism.
Authors:Stephens RS, Rentsendorj O, Servinsky LE, Moldobaeva A, Damico R, Pearse DB,
Journal:Am J Physiol Lung Cell Mol Physiol
PubMed ID:20453163
Increasing evidence suggests that endothelial cytotoxicity from reactive oxygen species (ROS) contributes to the pathogenesis of acute lung injury. Treatments designed to increase intracellular cGMP attenuate ROS-mediated apoptosis and necrosis in several cell types, but the mechanisms are not understood, and the effect of cGMP on pulmonary endothelial cell death ... More
ILK mediates LPS-induced vascular adhesion receptor expression and subsequent leucocyte trans-endothelial migration.
Authors:Hortelano S, López-Fontal R, Través PG, Villa N, Grashoff C, Boscá L, Luque A,
Journal:Cardiovasc Res
PubMed ID:20164118
The inflammatory response to injurious agents is tightly regulated to avoid adverse consequences of inappropriate leucocyte accumulation or failed resolution. Lipopolysaccharide (LPS)-activated endothelium recruits leucocytes to the inflamed tissue through controlled expression of membrane-associated adhesion molecules. LPS responses in macrophages are known to be regulated by integrin-linked kinase (ILK); in ... More