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Articles from this Volume

Hye-Soon Lee, Elaine F Remmers, Julie M Le, Daniel L Kastner, Sang-Cheol Bae, and Peter K Gregersen

A recent study in the North American White population has documented the association of a common STAT4 haplotype (tagged by rs7574865) with risk for rheumatoid arthritis (RA) and systemic lupus erythematosus. To replicate this finding in the Korean population, we performed a case-control association study. We genotyped 67 single nucleotide polymorphisms (SNPs) within the STAT1 and STAT4 regions in 1123 Korean patients with RA and 1008 ethnicity-matched controls. The most significant four risk SNPs (rs11889341, rs7574865, rs8179673, and rs10181656 located within the third intron of STAT4) among 67 SNPs are identical with those in the North American study. All four SNPs have modest risk for RA susceptibility (odds ratio 1.21–1.27). A common haplotype defined by these markers (TTCG) carries significant risk for RA in Koreans [34 percent versus 28 percent, P = 0.0027, OR (95 percent CI) = 1.33 (1.10–1.60)]. By logistic regression analysis, this haplotype is an independent risk factor in addition to the classical shared epitope alleles at the HLA-DRB1 locus. There were no significant associations with age of disease onset, radiographic progression, or serologic status using either allelic or haplotypic analysis. Unlike several other risk genes for RA such as PTPN22, PADI4, and FCRL3, a haplotype of the STAT4 gene shows consistent association with RA susceptibility across Whites and Asians, suggesting that this risk haplotype predates the divergence of the major racial groups. 

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Posted by Leah Caracappa on Oct 30, 2013 12:35 PM CDT
Pia Villa, Sara Triulzi, Barbara Cavalieri,  Rosa Di Bitondo, Riccardo Bertini, Sara Barbera, Paolo Bigini, Tiziana Mennini, Paolo Gelosa, Elena Tremoli, Luigi Sironi, and Pietro Ghezzi

Infiltration of neutrophils, or polymorphonuclear leukocytes (PMNs), contributes to the deleterious aspects of inflammation during stroke.  Interleukin-8 (IL-8/CXCL8), in conjunction with other chemokines, is induced during stroke in patients and animals models of cerebral ischemia. Blocking inflammation by inhibiting these mediators is a plausible therapy for cerebral ischemia.  Reparixin is an inhibitor of CXCR1 and CXCR2, the receptors for the CXCL8 family of chemokines implicated in the recruitment of PMNs. In this study, Villa et al. (125-133) evaluated the effects of reparixin in two cerebral ischemia models, transient and permanent middle cerebral artery occlusion, using varied treatment schedules and therapeutic windows.  Data indicate that reparixin not only reduces short-term PMN infiltration and infarct size, but also decreases long-term inflammation and improves long-term neurological outcome in transient and permanent ischemia models.  These results support the notion that CXCL8-mediated inflammation plays an important role in ischemic damage and CXCR1/2 inhibitors may represent a therapeutic strategy for the treatment of cerebral ischemia.

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Posted by Leah Caracappa on Apr 3, 2012 8:16 AM CDT
Michael Miksa, Dhruv Amin, Rongqian Wu, Weifeng Dong, Thanjavur S Ravikumar, and Ping Wang

Sepsis is a systemic inflammatory response to infection which may lead to multiple organ failure and is associated with increased rates of apoptosis. Clearance of apoptotic cells is crucial to maintaining cellular function under normal and pathological conditions. Administration of exosomes, derived from immature dendritic cells, promotes phagocytosis of apoptotic cells and improves survival in an animal model of sepsis by providing milk fat globule epidermal growth factor-factor VIII (MFG-E8). In this work, Miksa et al. (553-560) investigate whether the CX3CL1-chemokine fractalkine (CX3CL1) plays a role in apoptotic cell clearance. Their results show that CX3CL1 induces MFG-E8 in vitro and in vivo and enhances clearance of apoptotic cells in an MFG-E8 dependent manner. These findings suggest a possible novel treatment for patients with sepsis.

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Posted by Leah Caracappa on Apr 2, 2012 5:05 PM CDT
Chia-Chen Kuo and Shih-Chang Lin

The members of the forkhead box class O (FOXO) transcription factors (FOXO1, FOXO3a, and FOXO4) play an important role in controlling lymphocyte activation and proliferation.  Kuo and Lin (561-566) evaluated the possibility that FOXO transcriptional expression is dysregulated in systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA), two autoimmune diseases with tissue damage mediated by overactivation of autoreactive lymphocytes.  Kuo and Lin determined quantities of FOXO forkhead transcription factors in peripheral blood mononuclear cells from control, SLE and RA patients.  Their results show differential regulation of FOXO1 in SLE and RA patients when compared with control subjects. The data suggest transcriptional dysregulation in FOXO1 may be linked with the pathogenesis of autoimmune disease and that FOXO1 transcript levels in peripheral blood may serve as a biomarker for disease activity.

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Posted by Leah Caracappa on Apr 2, 2012 5:04 PM CDT
Rui Wang, Ke Dong, Fang Lin, Xi Wang, Ping Gao, San-Hua Wei, Shi-Yin Cheng, and Hui-Zhong Zhang

Osteosarcomas, the most frequently occurring type of bone tumor, are malignant tumors derived from bone tissues.  Osteosarcomas are characterized by aggressive invasion, early metastasis and resistance to existing chemotherapeutic agents.  Novel diagnostic and treatment approaches are needed to improve the poor prognosis of osteosarcoma.  The stathmin family of proteins is important in signal transduction and is highly expressed in human osteosarcoma.  Here, Wang et al. (567-575) investigate stathmin as a therapeutic target by using osteosarcoma RNA interference to reduce stathmin expression in human osteosarcoma cell lines.  Downregulation of stathmin expression significantly inhibited osteosarcoma cell proliferation in vitro, tumorgenicity in vivo, enhanced apoptosis and enhanced chemosensitivity to taxanes in human osteosarcoma cell lines.  These data indicate that RNA interference-mediated stathmin downregulation exerts potent anti-proliferative and chemosensitizing effects in human osteosarcomas.

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Posted by Leah Caracappa on Apr 2, 2012 5:03 PM CDT
By Guest Editors Stefano L Sensi, Lorella MT Canzoniero and Susan Benoff
     
      In this special issue of Molecular Medicine we report on the 6th Zinc Signals conference held last year at the Abbey of Monte Oliveto in Italy. At the meeting, more than 130 researchers from around the globe gathered to discuss the latest advances in the field of Zn2+ biology. Zinc is the second most abundant heavy metal in the human body, essential for proper development and function of brain, skin, reproductive, and digestive systems. Although eukaryotic cells contain as much as 200μM of this ion, the vast majority is tightly bound to intracellular proteins, serving in a functional and/or structural role or catalyzing the activity of more than 300 enzymes and proteins. Participants in the Zinc Signals meeting study the free ionic form (i.e., free or chelatable) Zn2+, whose concentration is considered to be in the picomolar range. This “free-Zn2+ constitutes a highly dynamic pool that mediates cell signaling.

 

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Posted by Leah Caracappa on Mar 28, 2012 10:24 AM CDT
Posted by Leah Caracappa on Mar 28, 2012 9:06 AM CDT
Posted by Leah Caracappa on Mar 28, 2012 9:05 AM CDT
Posted by Leah Caracappa on Mar 28, 2012 9:05 AM CDT
Hidenori Koyama, Hiroshi Yamamoto, and Yoshiki Nishizawa

Receptor for advanced gylcation end-products (RAGE) is associated with macrovascular diabetic complications through regulation of atherogenesis, angiogenic response, vascular injury and inflammatory response.  The significance of RAGE in cardiovascular disease pathogenesis is not confined to diabetic conditions but also plays a role in non-diabetic conditions.  In this review Koyama et al. (625-635) summarize recent findings regarding pathophysiological roles of RAGE and soluble RAGE in cardiovascular disease and discuss their potential usefulness as therapeutic targets and biomarkers for the disease.

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Posted by Leah Caracappa on Dec 5, 2007 12:00 AM CST
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