Does the chiral magnetic effect change the dynamic universality class in QCD?

In QCD matter under an external magnetic field, the chiral magnetic effect (CME) leads to the collective gapless mode called the chiral magnetic wave (CMW). Since dynamic universality class generally depends on low-energy gapless modes, it is nontrivial whether the CME and the resulting CMW change that of the second-order chiral phase transition in QCD. To address this question, we study the critical dynamics near the chiral phase transition in massless two-flavor QCD under an external magnetic field. By performing the dynamic renormalization-group analysis within the epsilon expansion, we find that the presence of the CME changes the dynamic universality class to that of model A. We also show that the transport coefficient of the CME is not renormalized by the critical fluctuations of the order parameter.Comment: 32 pages, 8 figures; v2: title and abstract modified, main results changed, discussions substantially extended, published in JHE

Novel transition dynamics of topological solitons

Continuous phase transitions can be classified into ones characterized by local order parameters and others that need additional topological constraints. The critical dynamics near the former transitions have been extensively studied, but the latter is less understood. We fill this gap in knowledge by studying the transition dynamics to a parity-breaking topological ground state called the chiral soliton lattice in quantum chromodynamics at finite temperature, baryon chemical potential, and external magnetic field. We find a slowing down of the soliton's translational motion as the critical magnetic field approaches while the local dissipation rate remains finite. Therefore, the characteristic time it takes to converge to the stationary state associated with a finite topological number strongly depends on the initial configuration: whether it forms a solitonic structure or not.Comment: 6 pages, 3 figures; affiliation update

Role of Dlg5/lp-dlg, a Membrane-Associated Guanylate Kinase Family Protein, in Epithelial-Mesenchymal Transition in LLc-PK1 Renal Epithelial Cells

Discs large homolog 5 (Dlg5) is a member of the membrane-associated guanylate kinase adaptor family of proteins, some of which are involved in the regulation of epithelial-to-mesenchymal transition (EMT). Dlg5 has been described as a susceptibility gene for Crohn's disease; however, the physiological function of Dlg5 is unknown. We show here that transforming growth factor-β (TGF-β)-induced EMT suppresses Dlg5 expression in LLc-PK1 cells. Depletion of Dlg5 expression by knockdown promoted the expression of the mesenchymal marker proteins, fibronectin and α-smooth muscle actin, and suppressed the expression of E-cadherin. In addition, activation of JNK and p38, which are stimulated by TGF-β, was enhanced by Dlg5 depletion. Furthermore, inhibition of the TGF-β receptor suppressed the effects of Dlg5 depletion. These observations suggest that Dlg5 is involved in the regulation of TGF-βreceptor-dependent signals and EMT

Dominant-negative mutants of JNK and p38 suppress the expression of mesenchymal marker proteins in Dlg5-depleted cells.

<p><b>A:</b> Six hours after transfection of a dominant-negative JNK mutant or a control plasmid into LLc-PK1 cells, the cells were further transfected with control or Dlg5 siRNA. After incubation for two days, expression of the indicated proteins was investigated by immunoblotting. <b>B:</b> Dominant-negative p38 mutant or a control plasmid was transfected into LLc-PK1 cells and treated and analyzed as in A. Expression of β-tubulin was detected as a loading control. The results are representative of at least three independent experiments. The expression levels of dominant-negative mutants were affected by Dlg5 knockdown by an unknown mechanism. Dominant-negative mutants of JNK and p38 suppressed the expression of fibronectin and SMA.</p

Dlg5 depletion disrupts epithelial cell morphology and induces the expression of mesenchymal marker proteins.

<p><b>A:</b> LLc-PK1 cells were transfected with Dlg5 siRNA (siDlg5#1: KD) or control siRNA and then incubated with 4 ng/ml of TGF-β for three days. The cells were lysed and immunoblotted using the indicated antibodies. Expression of β-tubulin was examined as a loading control. The upper band observed in immunoblotting with anti-Dlg5 is the larger variant of Dlg5. <b>B:</b> Cells were treated as in A and incubated for 60 hours. The cells were then photographed using phase contrast microscopy to examine cell morphology. <b>C:</b> Cells were transfected with Dlg5 siRNA or control siRNA and then immunostained using anti-Dlg5 or anti-E-cadherin antibodies. The asterisks indicate the cells that were transfected with Dlg5 siRNA. The scale bar indicates 10 µm. <b>D:</b> LLc-PK1 cells were transfected with Dlg5 siRNA or control siRNA and incubated for 24 hours. A GFP expression plasmid was then transfected into the cells with FLAG-Dlg5 or control plasmids. After incubation for two days, the cells were immunostained using an anti-SMA antibody. Fifty GFP-expressing cells were randomly selected, and the fluorescent intensity of SMA staining was examined. The graph shows the ratio of cells with higher SMA expression than background. <b>E:</b> LLc-PK1 cells were transfected with FLAG-Dlg5 or control plasmid and incubated for six hours. The cells were further transfected with Dlg5 siRNA or control siRNA. After two days of incubation, the cells were lysed and immunoblotted using the indicated antibodies. Arrows indicate endogenously expressed Dlg5, and an arrow head indicates FLAG-Dlg5. Dlg5 depletion induced the expression of mesenchymal marker proteins, and the re-expression of Dlg5 suppressed it.</p

TGF-β-mediated EMT decreases Dlg5 expression.

<p><b>A:</b> LLc-PK1 cells were incubated with 4 ng/ml of TGF-β for three days. Images were taken using phase contrast microscopy. TGF-β treatment induced morphological changes of LLc-PK1 cells. <b>B:</b> Three days after incubation with TGF-β, cells were lysed and immunoblotted using the indicated antibodies, which include an antibody for the epithelial marker E-cadherin, antibodies for the mesenchymal markers SMA and fibronectin, and antibodies for Dlg5 and β-catenin. As a loading control, vinculin expression was detected. <b>C:</b> LLc-PK1 cells were incubated with 4 ng/ml of TGF-β for three days. The cells were immunostained with anti-Dlg5 or anti-E-cadherin antibody. The scale bar indicates 10 µm. TGF-β treatment induced EMT and decreased Dlg5 expression. The results are representative of at least three independent experiments.</p

Dlg5 depletion promotes JNK and p38 activation.

<p><b>A:</b> LLc-PK1 cells were stimulated with 4 ng/ml TGF-β and incubated for the indicated periods. Cells were then lysed and immunoblotted using the indicated antibodies. <b>B, C, D, E:</b> LLc-PK1 cells were transfected with Dlg5 siRNA (KD) or control siRNA and incubated for two days. Cell lysates were then immunoblotted using the indicated antibodies, and the results were quantitated. The values represent the mean ± S.E. from at least three independent experiments. Dlg5 depletion promoted JNK and p38 activation but not Smad2/3 activation.</p