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Transforming growth factor-β1 regulates macrophage migration via RhoA
Kim, Jun-Sub,Kim, Jae-Gyu,Moon, Mi-Young,Jeon, Chan-Young,Won, Ha-Young,Kim, Hee-Jun,Jeon, Yee-Jin,Seo, Ji-Yeon,Kim, Jong-Il,Kim, Jaebong,Lee, Jae-Yong,Kim, Pyeung-Hyeun,Park, Jae-Bong American Society of Hematology 2006 Blood Vol.108 No.6
<B>Abstract</B><P>Brief treatment with transforming growth factor (TGF)-β1 stimulated the migration of macrophages, whereas long-term exposure decreased their migration. Cell migration stimulated by TGF-β1 was markedly inhibited by 10 μg/mL Tat-C3 exoenzyme. TGF-β1 increased mRNA and protein levels of macrophage inflammatory protein (MIP)-1α in the initial period, and these effects also were inhibited by 10 μg/mL Tat-C3 and a dominant-negative (DN)-RhoA (N19RhoA). Cycloheximide, actinomycin D, and antibodies against MIP-1α and monocyte chemoattractant protein-1 (MCP-1) abolished the stimulation of cell migration by TGF-β1. These findings suggest that migration of these cells is regulated directly and indirectly via the expression of chemokines such as MIP-1α and MCP-1 mediated by RhoA in response to TGF-β1. TGF-β1 activated RhoA in the initial period, and thereafter inactivated them, suggesting that the inactivation of RhoA may be the cause of the reduced cell migration in response to TGF-β1 at later times. We therefore attempted to elucidate the molecular mechanism of the inactivation of RhoA by TGF-β1. First, TGF-β1 phosphorylated RhoA via protein kinase A, leading to inactivation of RhoA. Second, wild-type p190 Rho GTPase activating protein (p190RhoGAP) reduced and DN-p190RhoGAP reversed the reduction of cell migration induced by TGF-β, suggesting that it inactivated RhoA via p190 Rho GAP.</P>
Oh, Soo-Jin,Heo, Jee-In,Kho, Yoon-Jung,Kim, Jeong-Hyeon,Kang, Hong-Joon,Park, Seong-Hoon,Kim, Hyun-Seok,Shin, Jong-Yeon,Kim, Min-Ju,Kim, Sung Chan,Park, Jae-Bong,Kim, Jaebong,Lee, Jae-Yong The Korean Society for Brain and Neural Science 2010 Experimental Neurobiology Vol.19 No.2
<P>Nitric oxide (NO) regulates proliferation, differentiation and survival of neurons. Although NO is reported to involve in NGF-induced differentiation of PC12 cells, the role of NO has not been characterized in primary neuron cells. Therefore, we investigated the role of NO in neuronal differentiation of primary cortical neuron cells. Primary cortical neuron cells were prepared from rat embryos of embryonic day 18 and treated with NMMA (NOS inhibitor) or PTIO (NO scavenger). Neurite outgrowth of neuron cells was counted and the mRNA levels of p21, p27, c-jun and c-myc were measured by RT-PCR. Neurite outgrowth of primary cortical neuron cells was inhibited a little by NOS inhibitor and completely by NO scavenger. The mRNA levels of p21 and p27, differentiation-induced growth arrest genes were increased during differentiation, but they were decreased by NOS inhibitor or NO scavenger. On the other hand, the level of c-jun mRNA was not changed and the level of c-myc mRNA was increased during differentiation differently from previously reported. The levels of these mRNA were reversed in NOS inhibitor- or NO scavenger-treated cells. The level of nNOS protein was not changed but NOS activity was inhibited largely by NOS inhibitor or NO scavenger. These results suggest that NO is an essential mediator for neuronal differentiation of primary cortical neuron cells.</P>
Kim, Kyong Hoon,Choi, Aryeong,Kim, Sang Hoon,Song, Heonju,Jin, Seohoon,Kim, Kyungim,Jang, Jaebong,Choi, Hanbyeul,Jung, Yong Woo Korean Society for Molecular and Cellular Biology 2021 Molecules and cells Vol.44 No.11
Memory T (T<sub>M</sub>) cells play an important role in the long-term defense against pathogen reinvasion. However, it is still unclear how these cells receive the crucial signals necessary for their longevity and homeostatic turnover. To understand how T<sub>M</sub> cells receive these signals, we infected mice with lymphocytic choriomeningitis virus (LCMV) and examined the expression sites of neural cadherin (N-cadherin) by immunofluorescence microscopy. We found that N-cadherin was expressed in the surroundings of the white pulps of the spleen and medulla of lymph nodes (LNs). Moreover, T<sub>M</sub> cells expressing high levels of killer cell lectin-like receptor G1 (KLRG1), a ligand of N-cadherin, were co-localized with N-cadherin<sup>+</sup> cells in the spleen but not in LNs. We then blocked N-cadherin in vivo to investigate whether it regulates the formation or function of T<sub>M</sub> cells. The numbers of CD127<sup>hi</sup>CD62L<sup>hi</sup> T<sub>M</sub> cells in the spleen of memory P14 chimeric mice declined when N-cadherin was blocked during the contraction phase, without functional impairment of these cells. In addition, when CD127<sup>lo</sup>KLRG1<sup>hi</sup> T<sub>M</sub> cells were adoptively transferred into anti-N-cadherin-treated mice compared with control mice, the number of these cells was reduced in the bone marrow and LNs, without functional loss. Taken together, our results suggest that N-cadherin participates in the development of CD127<sup>hi</sup>CD62L<sup>hi</sup> T<sub>M</sub> cells and homing of CD127<sup>lo</sup>KLRG1<sup>hi</sup> T<sub>M</sub> cells to lymphoid organs.
Kim, Hyun Su,Kim, Taewoo,Ahn, Jungmin,Yun, Hwayoung,Lim, Changjin,Jang, Jaebong,Sim, Jaehoon,An, Hongchan,Surh, Young-Joon,Lee, Jeeyeon,Suh, Young-Ger American Chemical Society 2018 Journal of organic chemistry Vol.83 No.4
<P>The asymmetric total synthesis of the marine natural product (+)-(3<I>E</I>)-pinnatifidenyne was accomplished. The key features of the synthesis involve the construction of an eight-membered cyclic ether by the abnormally regioselective Pd(0)-catalyzed cyclization, the installation of a double bond in the oxocene skeleton by sequential <I>in situ</I> deconjugative isomerization, and the efficient introduction of the crucial chloride mediated by the substrate-controlled diastereoselective reduction.</P> [FIG OMISSION]</BR>