Shu‐Hui Juan

ORCID: 0000-0002-8033-0522
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About
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Research Areas
  • Heme Oxygenase-1 and Carbon Monoxide
  • Cancer, Lipids, and Metabolism
  • Nitric Oxide and Endothelin Effects
  • Iron Metabolism and Disorders
  • Eicosanoids and Hypertension Pharmacology
  • Neonatal Health and Biochemistry
  • Adipose Tissue and Metabolism
  • Toxic Organic Pollutants Impact
  • Trace Elements in Health
  • Estrogen and related hormone effects
  • Alcohol Consumption and Health Effects
  • Peroxisome Proliferator-Activated Receptors
  • Thermal Regulation in Medicine
  • Per- and polyfluoroalkyl substances research
  • Metabolism, Diabetes, and Cancer
  • Cancer-related Molecular Pathways
  • Angiogenesis and VEGF in Cancer
  • Folate and B Vitamins Research
  • NF-κB Signaling Pathways
  • Retinoids in leukemia and cellular processes
  • Diabetes Treatment and Management
  • Acute Kidney Injury Research
  • High Altitude and Hypoxia
  • Lipid metabolism and biosynthesis
  • Aldose Reductase and Taurine

Taipei Medical University
2014-2023

Institute of Medical Sciences
2010-2017

Post Graduate Medical Institute
2017

Institute of Biomedical Sciences, Academia Sinica
2001-2014

China Medical University
2014

Tzu Chi University
2014

Taipei Medical University Hospital
2014

Zero to Three
2007

Wan Fang Hospital
2004

Utah State University
1997-1999

Background Increasing evidence supports the role of heme oxygenase-1 (HO-1) in cytoprotective response and iron homeostasis. The object this study was to investigate whether adenovirus-mediated gene transfer HO-1 arteries reduces overload inhibits lesion formation apolipoprotein E (apoE)–deficient mice. Methods Results Infection rat aortic smooth muscle cells with adenovirus carrying human (Adv-HO-1) resulted a high-level expression protein, which effectively reduced hemin-induced these...

10.1161/hc3801.095663 article EN Circulation 2001-09-25

Quercetin (QUE; 3,5,7,3′,4′-tetrahydroxyflavone) has been shown to possess several beneficial biological activities including antitumor, anti-inflammation and antioxidant properties; however, the effects of QUE in preventing invasion by breast carcinoma cells are still undefined. Increases protein, messenger RNA enzyme activity levels matrix metalloproteinase (MMP)-9 were observed 12- O -tetradecanoylphorbol-13-acetate (TPA)-treated MCF-7 cells, these blocked QUE, but not quercitrin or...

10.1093/carcin/bgn162 article EN Carcinogenesis 2008-06-09

Gentamicin, a widely used antibiotic for the treatment of bacterial infection, can cause nephrotoxicity. Tetramethylpyrazine (TMP) is compound purified from rhizome Ligusticum wallichi (Chuanxiong) and has been found to protect against ischaemia-reperfusion injury, nephritis alcohol-induced toxicity in rat kidneys.We renal tubular cells (RTCs), NRK-52E, this study. The cytotoxicity gentamicin was checked with transferase-mediated deoxyuridine triphosphate nick end-labeling (TUNEL) staining,...

10.1093/ndt/gfl699 article EN Nephrology Dialysis Transplantation 2006-11-29

Background. Gentamicin, a widely used antibiotic for the treatment of bacterial infection, can cause nephrotoxicity. Tetramethylpyrazine (TMP) is compound purified from rhizome Ligusticum wallichi (called chuanxiong in Chinese). Besides its protection against ischaemia–reperfusion injury and nephritis mice, we previously reported that TMP reverses gentamicin-induced apoptosis rat kidneys. Haem oxygenase-1 (HO-1) induction by has also been shown to attenuate myocardial ischaemia/reperfusion...

10.1093/ndt/gfn545 article EN Nephrology Dialysis Transplantation 2008-10-08

We have previously reported that perfluorooctanesulfonate (PFOS) causes cell apoptosis in renal tubular epithelial cells (RTCs). Here, we extend our findings and provide evidence of epithelial-mesenchymal transition (EMT)-associated fibrosis caused by PFOS the protection l-carnitine. Our results demonstrate increased expression EMT injury biomarkers (eg, N-cadherin, vimentin, Snail, Kim1, Lcn2). In addition, induction through Sirt1-mediated PPARγ deacetylation inactivation. l-carnitine...

10.1093/toxsci/kfx183 article EN Toxicological Sciences 2017-08-29

Perfluorinated chemicals (PFCs) are ubiquitously distributed in the environments including stainless pan-coating, raincoat, fire extinguisher, and semiconductor products. The PPAR family has been shown to contribute toxic effects of PFCs thymus, immune excretory systems. Herein, we demonstrated that perfluorooctanesulfonate (PFOS) caused cell apoptosis through increasing ratio Bcl-xS/xL, cytosolic cytochrome C, caspase 3 activation renal tubular cells (RTCs). In addition, PFOS increased...

10.1371/journal.pone.0155190 article EN cc-by PLoS ONE 2016-05-12

Abstract We previously reported that perfluorooctanesulfonate (PFOS) causes autophagy-induced apoptosis in renal tubular cells (RTCs) through a mechanism dependent on reactive oxygen species (ROS)/extracellular signal-regulated kinase. This study extended our findings and determined the therapeutic potency of l -Carnitine PFOS-treated RTCs. (10 mM) reversed effects PFOS (100 µM) autophagy induction impaired flux. Furthermore, it downregulated protein level p47Phox, which is partly related to...

10.1038/s41598-022-08771-3 article EN cc-by Scientific Reports 2022-03-18

Abstract We previously reported that 3‐methylcholanthrene (3MC), an aryl‐hydrocarbon receptor (AhR) agonist, inhibits the proliferation of human umbilical vascular endothelial cells (HUVECs; Juan et al., 2006, Eur J Pharmacol 530: 1–8). Herein, pretreatment HUVECs with p21 or p27 small interfering (si)RNA reduced 3MC‐induced elimination [ 3 H]thymidine incorporation, demonstrating their essential roles in antiproliferation HUVECs. The molecular mechanisms and involved antiproliferative...

10.1002/jcp.21299 article EN Journal of Cellular Physiology 2007-11-16

Abstract The aryl hydrocarbon receptor (AhR) is a ligand‐activated transcription factor activated by dioxin and polyaromatic hydrocarbons. Recent studies have revealed that AhR activity in central neurons depends on the NMDA receptor. In this study, we investigated how neuronal influence AhR‐mediated dioxin‐responsive gene expression neurotoxicity. Our results show activation of selective agonist 2,3,7,8‐tetrachlorodibenzo‐ p ‐dioxin induced calcium entry, which were attenuated small...

10.1111/j.1471-4159.2007.05098.x article EN Journal of Neurochemistry 2007-10-31

Activating transcription factor 3 (ATF3), a cAMP response element-binding protein/ATF family factors member, has been implicated in the cardiovascular and inflammatory system is rapidly induced by ischemic-reperfusion injuries. We performed transverse aortic banding (TAB) experiments using ATF3 gene-deleted mice (ATF3<sup>−/−</sup>) wild-type (WT) to determine what effect it might have on heart failure pressure overloading. Compared with WT mice, ATF3<sup>−/−</sup> were found...

10.1124/mol.113.090092 article EN Molecular Pharmacology 2014-02-18

Endothelin-1 (ET-1) has been implicated in fibroblast proliferation. However, the mechanism involving ET-1 is not clear. The present study was performed to examine role of endogenous ET-1-stimulated proliferation and investigate regulatory ET-1-induced gene expression cardiac fibroblasts. Both ET(A) receptor antagonist [(hexahydro-1H-azepinyl)carbonyl-Leu-D-Trp-D-OH (BQ485)] endothelin-converting enzyme inhibitor (phosphoramidon) inhibited increased DNA synthesis caused by ET-1. induced...

10.1124/mol.63.5.1002 article EN Molecular Pharmacology 2003-04-14

The renin-angiotensin system and epithelial-mesenchymal transition play crucial roles in the development of kidney fibrosis. connection between transforming growth factor-β remains largely unknown.

10.1177/1470320318803009 article EN cc-by-nc Journal of the Renin-Angiotensin-Aldosterone System 2018-07-01

Abstract Previously, we showed that magnolol induces cell‐cycle arrest in cultured colon and liver cancer cells through an upregulation of the p21 protein [ 1 ]. The aim this study was to delineate molecular mechanism underlying magnolol‐induced increase protein. Thus our RT‐PCR analysis demonstrated mRNA levels were increased at h after treatment sustained for least 24 h. promoter activity also by treatment. Western blot COLO‐205 with phosphorylation extracellular signal‐regulated kinase...

10.1002/mc.20274 article EN Molecular Carcinogenesis 2007-02-12

Previous genome-wide association studies have indicated an between CDH13 genotypes and adiponectin levels. In this study, we used mediation analysis to assess the statistical locus variants levels, metabolic syndrome, related phenotypes.A sample population of 530 Taiwanese participants was enrolled. Four gene in promoter intron 1 regions were genotyped. After adjustment for clinical covariates, genotypes/haplotypes exhibited with levels (lowest P = 1.95 × 10-11 rs4783244 lowest 3.78 10-13...

10.1371/journal.pone.0122664 article EN cc-by PLoS ONE 2015-04-13

Endothelial nitric oxide synthase (eNOS) modulates vascular blood pressure and is predominantly expressed in endothelial cells activated through the protein kinase B (Akt/PKB)‐dependent pathway. We previously reported that 3‐methylcholanthrene (3MC) activates aryl hydrocarbon receptor (AhR) reduces PI3K/Akt phosphorylation. This study investigated mechanism underlying downregulatory effects of 3‐MC on (NO) production occurring AhR/RhoA/Akt‐mediated mechanism. The eNOS activity was examined...

10.1002/jcp.25497 article EN Journal of Cellular Physiology 2016-07-21

It has been well documented previously that 17β-estradiol (E 2 ) exerts a protective effect on cardiovascular tissue. The possible role of E in the regulation endothelin (ET)-1 production reported, although complex mechanisms by which inhibits ET-1 expression are not completely understood. aims this study were to examine whether was able alter strain-induced gene and also identify putative underlying signaling pathways exist within endothelial cells. For cultured cells, (1–100 nM), but...

10.1152/ajpheart.00723.2003 article EN AJP Heart and Circulatory Physiology 2004-05-11

Abstract Prostacyclin (PGI 2 ) has been shown to inhibit proliferation in vascular smooth muscle cells. To clarify the underlying molecular mechanism, we investigated vasoprotection of beraprost (a PGI agonist) both vivo and vitro. Beraprost eliminated increases rat aortic cells (RASMCs) by 12‐O‐tetradecanoylphorbol 13‐acetate, enhanced peroxisome proliferator‐activated receptor‐delta (PPARδ) inducible nitric oxide synthetase (iNOS) expressions, which were associated with antiproliferative...

10.1002/jcp.21214 article EN Journal of Cellular Physiology 2007-07-09
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