bluuebunny/crossref_metadata_2025_split huggingface dataset:
Differential regulation of the humanCYP11A1promoter in mouse brain and adrenals
Authors: Chiang Yen‐Feng , Lin Hui‐Ting , Hu Ji‐Wei , Tai Yu‐Chen , Lin Yu‐Chi , Hu Meng‐Chun 
Published: December 2010

AbstractCYP11A1encodes the first enzyme of steroid biosynthesis, cytochrome P450scc. The expression ofCYP11A1in the nervous system allows neurosteroids to be synthesized de novo. In the classic steroidogenic tissues, adrenals and gonads, the key regulator controllingCYP11A1expression is steroidogenic factor‐1 (SF‐1), but the transcriptional regulation ofCYP11A1in the brain is unclear. We recently used the 4.4‐kb regulatory region of the humanCYP11A1gene to drive Cre recombinase expression in the diencephalon and midbrain. In this study, we characterized the regional‐specific expression of Cre reporter in the SCC‐Cre transgenic brain using a transient Cre/ROSA26R transgenic system. Mutation of either the upstream or proximal SF‐1 binding site did not affect brainCYP11A1promoter activity. The upstream SF‐1 binding site, however, is required forCYP11A1promoter function in the embryonic adrenals. The 3.8‐kb promoter, like the 4.4‐kb length promoter, directed Cre expression in the diencephalon, midbrain and olfactory epithelium, whereas Cre expression controlled by the 2.7‐kb promoter was only observed in the caudal part of midbrain. This suggests that the 5′‐flanking region between 3.8 and 2.7 kb contains a crucial element for activation ofCYP11A1promoter in the diencephalon, olfactory epithelium and the anterior part of midbrain. Thus we have identified regions of the promoter that controlCYP11A1expression in the brain and embryonic adrenals. J. Cell. Physiol. 226: 1998–2005, 2011. © 2010 Wiley‐Liss, Inc.
Activation and induction of cytosolic phospholipase A2 by TNF‐α mediated through Nox2, MAPKs, NF‐κB, and p300 in human tracheal smooth muscle cells
Authors: Lee Chiang‐Wen , Lin Chih‐Chung , Lee I‐Ta , Lee Hui‐Chun , Yang Chuen‐Mao 
Published: December 2010

AbstractCytosolic phospholipase A2 (cPLA2) plays a pivotal role in mediating agonist‐induced arachidonic acid (AA) release for prostaglandin (PG) synthesis during inflammation triggered by tumor necrosis factor‐α (TNF‐α). However, the mechanisms underlying TNF‐α‐induced cPLA2 expression and PGE2 synthesis in human tracheal smooth muscle cells (HTSMCs) remain unknown. Here, we report that TNF‐α‐induced cPLA2 protein and mRNA expression, PGE2 production, and phosphorylation of p42/p44 MAPK, p38 MAPK, and JNK1/2, which were attenuated by pretreatment with a ROS scavenger [N‐acetyl‐L‐cysteine, (NAC)] and the inhibitors of NADPH oxidase [apocynin (APO) and diphenyleneiodonium chloride (DPI)], MEK1/2 (U0126), p38 MAPK (SB202190), and JNK1/2 (SP600125) or transfection with siRNA of Nox2, p47phox, MEK1, p42, p38, or JNK2. TNF‐α‐induced cPLA2 expression was also inhibited by pretreatment with a selective NF‐κB inhibitor [helenalin (HLN)] or transfection with dominant negative mutants of NF‐κB inducing kinase (NIK) or IκB kinase (IKK)α/β. TNF‐α‐induced NF‐κB translocation was blocked by pretreatment with NAC, DPI, APO, or HLN, but not by U0126, SB202190, or SP600125. In addition, pretreatment with curcumin (a p300 inhibitor) or transfection with p300 siRNA blocked cPLA2 expression and PGE2 synthesis induced by TNF‐α. We further confirmed that p300 was associated with the cPLA2 promoter which was dynamically linked to histone H4 acetylation stimulated by TNF‐α, determined by chromatin immunoprecipitation assay. Association of p300 and histone H4 to cPLA2 promoter was inhibited by U0126, SB202190, and SP600125. These results suggested that in HTSMCs, activation of p47phox, MAPKs, NF‐κB, and p300 is essential for TNF‐α‐induced cPLA2 expression and PGE2 release. J. Cell. Physiol. 226: 2103–2114, 2011. © 2010 Wiley‐Liss, Inc.
Pulmonary microvascular endothelial cells from bleomycin‐induced rats promote the transformation and collagen synthesis of fibroblasts
Authors: Yin Qian , Nan Hai‐Yan , Zhang Wen‐Hu , Yan Lin‐Feng , Cui Guang‐Bin , Huang Xiao‐Feng , Wei Jing‐Guo 
Published: December 2010

AbstractAccumulation and activation of myofibroblasts are the hallmark of progressive pulmonary fibrosis, and the resident fibroblasts are the major source of myofibroblasts. However, the key factors involved in the transformation of fibroblasts are unknown. Pulmonary microvascular endothelial cells (PMVECs), major effector cells against pathogenesis in early stages of the disease, can secrete cytokines to induce the differentiation of mesenchymal cells. We speculated that PMVECs could secrete pro‐fibrotic cytokines and promote the transformation of fibroblasts into myofibroblasts. Accordingly, we established a co‐culture system with PMVECs and fibroblasts to examine the specific transformation and collagen synthesis of the co‐cultured fibroblasts by FACS and Western blot, prior to and after treatment with neutralizing antibodies against transforming growth factor‐beta1 (TGF‐β1) and connective tissue growth factor (CTGF). We also analyzed expression of TGF‐β1 and CTGF in PMVECs. The synthesis and secretion of TGF‐β1 and CTGF protein were up‐regulated in PMVECs isolated from bleomycin (BLM)‐treated rats, most prominently at 7 days post‐instillation. We showed that the PMVECs isolated from BLM‐induced rats could induce the transformation of normal fibroblasts and their secretion of collagen I, which was inhibited by both neutralizing anti‐TGF‐β1 and anti‐CTGF antibodies. Therefore, up‐regulation of TGF‐β1 and CTGF in PMVECs plays an important role in activation, transformation, and collagen synthesis of fibroblasts; in particular, these effects in PMVECs are likely to be the key factors for activation and stimulation of static fibroblasts in lung interstitium in early stages of pulmonary fibrosis disease. J. Cell. Physiol. 226: 2091–2102, 2011. © 2010 Wiley‐Liss, Inc.
Leptin up‐regulates pro‐inflammatory cytokines in discrete cells within mouse colon
Authors: Padidar Sara , Farquharson Andrew J. , Williams Lynda M. , Kelaiditi Eirini , Hoggard Nigel , Arthur John R. , Drew Janice E. 
Published: December 2010

AbstractDysregulation of leptin associated with obesity is implicated in obesity‐related colon cancer, but mechanisms are elusive. Increased adiposity and elevated plasma leptin are associated with perturbed metabolism in colon and leptin receptors are expressed on colon epithelium. We hypothesise that obesity increases the sensitivity of the colon to cancer by disrupting leptin‐regulated gene targets within colon tissues. PCR arrays were used to firstly identify leptin responsive genes and secondly to identify responses to leptin challenge in wild‐type mice, or those lacking leptin (ob/ob). Leptin‐regulated genes were localised in the colon using in situ hybridisation. IL6, IL1β and CXCL1 were up‐regulated by leptin and localised to discrete cells in gut epithelium, lamina propria, muscularis and at the peritoneal serosal surface. Leptin regulates pro‐inflammatory genes such as IL6, IL1β and CXCL1, and might increase the risk of colon cancer among obese individuals. J. Cell. Physiol. 226: 2123–2130, 2011. © 2010 Wiley‐Liss, Inc.
Resistin induces monocyte–endothelial cell adhesion by increasing ICAM‐1 and VCAM‐1 expression in endothelial cells via p38MAPK‐dependent pathway
Authors: Hsu Wei‐Yen , Chao Yu‐Wen , Tsai Ying‐Lan , Lien Chih‐Chan , Chang Chao‐Fu , Deng Ming‐Chung , Ho Low‐Tone , Kwok Ching Fai , Juan Chi‐Chang 
Published: December 2010

AbstractResistin, firstly reported as an adipocyte‐specific hormone, is suggested to be an important link between obesity and diabetes. Recent studies have suggested an association between resistin and atherogenic processes. The adhesion of circulating monocytes to endothelial cells is a critical step in the early stages of atherosclerosis. The purpose of the present study was to investigate the effect of resistin on the adhesion of THP‐1 monocytes to human umbilical vein endothelial cells (HUVECs) and the underlying mechanism. Our results showed that resistin caused a significant increase in monocyte adhesion. In exploring the underlying mechanisms of resistin action, we found that resistin‐induced monocyte adhesion was blocked by inhibition of p38MAPK activation using SB203580 and SB202190. Furthermore, resistin increased the expression of intercellular adhesion molecule‐1 (ICAM‐1) and vascular cell adhesion molecule‐1 (VCAM‐1) by HUVECs and these effects were also p38MAPK‐dependent. Resistin‐induced monocyte adhesion was also blocked by monoclonal antibodies against ICAM‐1 and VCAM‐1. Taken together, these results show that resistin increases both the expression of ICAM‐1 and VCAM‐1 by endothelial cells and monocyte adhesion to HUVECs via p38MAPK‐dependent pathways. J. Cell. Physiol. 226: 2181–2188, 2011. © 2010 Wiley‐Liss, Inc.
Endothelin‐1 exacerbates lipid accumulation by increasing the protein degradation of the ATP‐binding cassette transporter G1 in macrophages
Authors: Lin Chun‐Yueh , Lee Tzong‐Shyuan , Chen Chin‐Chang , Chang Cheng‐An , Lin Yan‐Jie , Hsu Yung‐Pei , Ho Low‐Tone 
Published: December 2010

AbstractEndothelin‐1 (ET‐1), a potent proatherogenic vasoconstrictive peptide, is known to promote macrophage foam cell formation via mechanisms that are not fully understood. Excessive lipid accumulation in macrophages is a major hallmark during the early stages of atherosclerotic lesions. Cholesterol homeostasis is tightly regulated by scavenger receptors (SRs) and ATP‐binding cassette (ABC) transporters during the transformation of macrophage foam cells. The aim of this study was to investigate the possible mechanisms by which ET‐1 affects lipid accumulation in macrophages. Our results demonstrate that oxidized low‐density lipoprotein (oxLDL) treatment increases lipid accumulation in rat bone marrow‐derived macrophages. Combined treatment with ET‐1 and oxLDL significantly exacerbated lipid accumulation in macrophages as compared to treatment with oxLDL alone. The results of Western blotting show that ET‐1 markedly decreased the ABCG1 levels via ET type A and B receptors and activation of the phosphatidylinositol 3‐kinase pathway; however, ET‐1 had no effect on the protein expression of CD36, SR‐BI, SR‐A, or ABCA1. In addition, real‐time PCR analysis showed that ET‐1 treatment did not affect ABCG1 mRNA expression. We also found that ET‐1 decreases ABCG1 possibly due to the enhancement of the proteosome/calpain pathway‐dependent degradation of ABCG1. Moreover, ET‐1 significantly reduced the efficiency of the cholesterol efflux in macrophages. Taken together, these findings suggest that ET‐1 may impair cholesterol efflux and further exacerbate lipid accumulation during the transformation of macrophage foam cells. J. Cell. Physiol. 226: 2198–2205, 2011. © 2010 Wiley‐Liss, Inc.
The p53 tumor suppressor protein regulates hematopoietic stem cell fate
Authors: Asai Takashi , Liu Yan , Bae Narae , Nimer Stephen D. 
Published: December 2010

AbstractThe p53 tumor suppressor protein is a key transcription factor that regulates several signaling pathways involved in the cell's response to stress. Through stress‐induced activation, p53 accumulates and triggers the expression of target genes that protect the genetic integrity of all cells including hematopoietic stem cells (HSCs). These protective mechanisms include cell‐cycle arrest, DNA repair, induction of apoptosis, or initiation of senescence. In addition to its function under stress conditions, p53 has important functions during steady‐state hematopoiesis, regulating HSC quiescence and self‐renewal. In addition, it appears that p53 levels affect HSC competition for the hematopoietic niche, with the less p53 activated HSCs preferentially surviving. The specific genes and precise mechanisms underlying p53's effects on normal HSCs are slowly being clarified. p53 also plays an important role in leukemia stem cell (LSC) behavior, with p53 loss affecting drug resistance and disease progression. Pharmacologic activation of p53 function could overcome the adverse impact of p53 inactivation in LSCs. Thus, understanding the p53 regulatory mechanisms active in HSCs and LSCs may promote the development of new therapeutic strategies that could eliminate the population of largely quiescent LSCs. J. Cell. Physiol. 226: 2215–2221, 2011. © 2010 Wiley‐Liss, Inc.
Expression of members of the miRNA17–92 cluster during development and in carcinogenesis
Authors: Jevnaker Anne‐Marthe , Khuu Cuong , Kjøle Elisabeth , Bryne Magne , Osmundsen Harald 
Published: December 2010

AbstractThe six microRNAs (miRNA) encoded by the miR‐17–92 cluster, also named oncomir‐1, have been associated with carcinogenesis and typically exhibit‐increased expression in tumors. Despite the well‐established role for the miR‐17–92 cluster in an oncogenic network, the physiological function of these miRNAs in normal tissues remains unresolved. In order to investigate whether there are similar patterns of miR‐17–92 expression during embryogenesis and carcinogenesis, we have preformed a systematic study of the expression in cultured carcinoma cells, cultured primary human keratinocytes (KC), and during development of some murine tissues. Both levels of expression of the primary transcript (pri‐miRNA) and levels of expression of the individual members of the cluster were monitored. Irrespectively of tissue examined we found that the level of expression decreased markedly during development. With cultured primary human KCs their levels of expression of some of these microRNAs decreased as the number of cell passages increased. Their levels of expression in cultured carcinoma cells, in contrasts, increased, or remained unchanged, with increasing number of cell passages. The results suggest these microRNAs are involved in the regulation of foetal development and that they may promote proliferation and inhibit differentiation during embryogenesis and carcinogenesis. Additionally, the six microRNAs exhibit variable tissue expression, suggesting selective processing of these microRNAs. J. Cell. Physiol. 226: 2257–2266, 2011. © 2010 Wiley‐Liss, Inc.
R‐Ras interacts with filamin a to maintain endothelial barrier function
Authors: Griffiths G.S. , Grundl M. , Allen J.S. , Matter M.L. 
Published: December 2010

AbstractThe molecular mechanisms regulating vascular barrier integrity remain incompletely elucidated. We have previously reported an association between the GTPase R‐Ras and repeat 3 of Filamin A (FLNa). Loss of FLNa has been linked to increased vascular permeability. We sought to determine whether FLNa's association with R‐Ras affects endothelial barrier function. We report that in endothelial cells endogenous R‐Ras interacts with endogenous FLNa as determined by co‐immunoprecipitations and pulldowns with the FLNa‐GST fusion protein repeats 1–10. Deletion of FLNa repeat 3 (FLNaΔ3) abrogated this interaction. In these cells FLNa and R‐Ras co‐localize at the plasma membrane. Knockdown of R‐Ras and/or FLNa by siRNA promotes vascular permeability, as determined by TransEndothelial Electrical Resistance and FITC‐dextran transwell assays. Re‐expression of FLNa restored endothelial barrier function in cells lacking FLNa whereas re‐expression of FLNaΔ3 did not. Immunostaining for VE‐Cadherin in cells with knocked down R‐Ras and FLNa demonstrated a disorganization of VE‐Cadherin at adherens junctions. Loss of R‐Ras and FLNa or blocking R‐Ras function via GGTI‐2133, a selective R‐Ras inhibitor, induced vascular permeability and increased phosphorylation of VE‐Cadherin (Y731) and Src (Y416). Expression of dominant negative R‐Ras promoted vascular permeability that was blocked by the Src inhibitor PP2. These findings demonstrate that maintaining endothelial barrier function is dependent upon active R‐Ras and association between R‐Ras and FLNa and that loss of this interaction promotes VE‐Cadherin phosphorylation and changes in downstream effectors that lead to endothelial leakiness. J. Cell. Physiol. 226: 2287–2296, 2011. © 2010 Wiley‐Liss, Inc.
Macrophage‐conditioned medium inhibits the activation of cyclin‐dependent kinase 2 by adipogenic inducers in 3T3‐L1 preadipocytes
Authors: Ide Jennifer , Gagnon AnneMarie , Molgat André S.D. , Landry Anne , Foster Charlie , Sorisky Alexander 
Published: December 2010

AbstractMacrophage infiltration into adipose tissue, associated with obesity, is thought to contribute to abnormal adipose tissue remodeling, low‐grade inflammation, and insulin resistance. Medium conditioned by macrophages (MacCM) inhibits 3T3‐L1 and human adipocyte differentiation, as well as early adipogenic cell cycle events including MCE and retinoblastoma protein (Rb) phosphorylation. Our objective was to determine if the inhibition of Rb phosphorylation was linked to changes in cell cycle‐related proteins. We treated 3T3‐L1 preadipocytes with adipogenic inducers for 24 h in control medium versus J774A.1‐MacCM. The differentiation‐induced mRNA and protein expression of cyclin A, an activator of cyclin‐dependent kinase (cdk) 2 which phosphorylates Rb, was inhibited by 82% and 73%, respectively, by J774A.1‐MacCM; adipogenic expression of Myc, a transcriptional regulator of cyclin A, was also suppressed significantly. Consistent with the reduction in cyclin A levels, the activation of cdk2 by adipogenic inducers was inhibited by 75% by J774A.1‐MacCM. J774A.1‐MacCM also lowered levels of cyclins D1 and D2. Inhibition studies demonstrated that platelet‐derived growth factor, an anti‐adipogenic factor found in J774A.1‐MacCM, was not responsible for the inhibitory effect on differentiation. The anti‐adipogenic effect of J774A.1‐MacCM was resistant to proteinase K and heat treatment, and was present in a <3 kDa fraction. Our data indicate that J774A.1‐MacCM interferes with the upregulation of cyclin A levels and cdk2 activity that are required for Rb phosphorylation and MCE in 3T3‐L1 adipogenesis. J. Cell. Physiol. 226: 2297–2306, 2011. © 2010 Wiley‐Liss, Inc.
Effects of insulin and high glucose on mobilization of slo1 BKCa channels in podocytes
Authors: Kim Eun Young , Dryer Stuart E. 
Published: December 2010

AbstractPodocytes are dynamic polarized cells that lie on the surface of glomerular capillaries and comprise an essential component of the glomerular filitration barrier. Podocytes are affected in the earliest stages of diabetic nephropathy and insulin signaling to podocytes is essential for normal glomerular function. Large‐conductance Ca2+‐activated K+ channels (BKCa channels) encoded by the Slo1 gene are expressed in podocytes in a complex with multiple glomerular slit diaphragm proteins including nephrin, TRPC6 channels, and several different actin‐binding proteins. Here we show that insulin increases cell surface expression of podocyte BKCa channels, which is accompanied by a corresponding increase in the density of current flowing through these channels. Insulin stimulation of BKCa channels was detectable in 15 min and required activation of both Erk and Akt signaling cascades. Exposure to high glucose (36.1 mM) for 24 h caused a marked reduction in the steady‐state surface expression of BKCa channels as well as of the slit diaphragm signaling molecule nephrin. High glucose treatment also abolished the stimulatory effects of insulin on BKCa current density, although insulin continued to increase phosphorylation of Erk and Akt under those conditions. Therefore, in contrast to most other cell types, high glucose abrogates the effects of insulin in podocytes at relatively distal steps in its signaling pathway. Insulin stimulation of BKCa channels in podocytes may prepare podocytes to adapt to changes in pressure gradients that occur during postprandial hyperfiltration. J. Cell. Physiol. 226: 2307–2315, 2011. © 2010 Wiley‐Liss, Inc.
A case of an epignathus with intracranial extension appearing as a persistently open mouth at 16 weeks and subsequently diagnosed at 20 weeks of gestation
Authors: Calda Pavel , Novotná Michaela , Čutka David , Břešt'ák Miroslav , Hašlík Lubomír , Goldová Barbara , Vítková Ivana , Vaněčková Manuela , Seidl Zdeněk 
Published: December 2010

AbstractWe report a rare case of oral mass (epignathus) with intracranial extension originally suspected antenatally at 16 weeks' gestation because of a persistent open mouth. Postmortem MRI and pathologic examination of the fetus confirmed an oral teratoma with bilateral ventricular dilatation, corpus callosum agenesis, and a neuroepithelial intracranial cyst. The relevant literature regarding this anomaly is reviewed. © 2010 Wiley Periodicals, Inc. J Clin Ultrasound, 2011
Multi‐residue analysis of pesticides in tea by online SEC‐GC/MS
Authors: Xu Xiao‐Min , Yu Cun , Han Jian‐Long , Li Jia‐Ping , El‐Sepai Fawzi , Zhu Yan , Huang Bai‐Fen , Cai Zeng‐Xuan , Wu Hong‐Wei , Ren Yi‐Ping 
Published: December 2010

AbstractA multi‐residue method for the analysis of pesticides in tea was developed by online size exclusion chromatography (SEC)‐GC/MS with full scan mode. The sample was fortified with chlorpyrifos‐d10 isotope internal standard and extracted by acetonitrile. After purification by primary secondary amine sorbent and solvent exchange by SEC mobile phase, the sample was detected by online SEC‐GC/MS. The purification result of the online system was evaluated by comparing the correlation between Chinese cabbage and tea matrix. The factors for method optimization included sample preparation, matrix effects and the instrument parameters of each online component. Scatter plot was introduced in this study to directly illustrate the results of the condition optimization and matrix effects in the online system. For most of the pesticides, the average recoveries ranged from 70 to 130% and the RSD were below 15%. The feasibility of the application of full scan mode in multi‐residue determination of trace amounts of pesticides (LODs below 0.01 mg/kg) in a complex matrix was discussed.