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Sultan, Md. Tipu,Li, Hong-Mei,Lee, Yong Zu,Lim, Soon Sung,Song, Dong-Keun The Korean Society of Pharmacology 2016 The Korean Journal of Physiology & Pharmacology Vol.20 No.2
We fortuitously observed a human neutrophil intracellular free-calcium concentration ($[Ca^{2+}]_i$) increasing activity in the commercially available phosphodiesterase I (PDE I), which is actually dried crude venom of Crotalus atrox. As this activity was not observed with another commercially available pure PDE I, we tried to find out the causative molecule(s) present in 'crude' PDE, and identified Lys49-phospholipase A2 (Lys49-PLA2 or K49-PLA2), a catalytically inactive protein which belongs to the phospholipase A2 family, by activity-driven three HPLC (reverse phase, size exclusion, reverse phase) steps followed by SDS-PAGE and LC-MS/MS. K49-PLA2 induced $Ca^{2+}$ influx in human neutrophils without any cytotoxic effect. Two calcium channel inhibitors, 2-aminoetoxydiphenyl borate (2-APB) ($30{\mu}M$) and SKF-96365 ($20{\mu}M$) significantly inhibited K49-PLA2-induced $[Ca^{2+}]_i$ increase. These results suggest that K49-PLA2 modulates $[Ca^{2+}]_i$ in human neutrophils via 2-APB- and SKF-96365-sensitive calcium channels without causing membrane disruption.
Md. Tipu Sultan,Hong-Mei Li,Yong Zu Lee,Soon Sung Lim,Dong-Keun Song 대한생리학회-대한약리학회 2016 The Korean Journal of Physiology & Pharmacology Vol.20 No.2
We fortuitously observed a human neutrophil intracellular free-calcium concentration ([Ca<sup>2+</sup>]<sub>i</sub>) increasing activity in the commercially available phosphodiesterase I (PDE I), which is actually dried crude venom of <i>Crotalus atrox</i>. As this activity was not observed with another commercially available pure PDE I, we tried to find out the causative molecule(s) present in ‘crude’ PDE, and identified Lys49- phospholipase A2 (Lys49-PLA2 or K49-PLA2), a catalytically inactive protein which belongs to the phospholipase A2 family, by activity-driven three HPLC (reverse phase, size exclusion, reverse phase) steps followed by SDS-PAGE and LC-MS/MS. K49-PLA2 induced Ca<sup>2+</sup> influx in human neutrophils without any cytotoxic effect. Two calcium channel inhibitors, 2-aminoetoxydiphenyl borate (2-APB) (30 μM) and SKF- 96365 (20 μM) significantly inhibited K49-PLA2-induced [Ca<sup>2+</sup>]<sub>i</sub> increase. These results suggest that K49-PLA2 modulates [Ca<sup>2+</sup>]<sub>i</sub> in human neutrophils via 2-APB- and SKF- 96365-sensitive calcium channels without causing membrane disruption.
Fixture layout optimization for multi point respot welding of sheet metals
Zeshan Ahmad,Tipu Sultan,Muhammad Asad,Matteo Zoppi,Rezia Molfino 대한기계학회 2018 JOURNAL OF MECHANICAL SCIENCE AND TECHNOLOGY Vol.32 No.4
The high quality of welding in the automotive industry is achieved by proper positioning of the fixture elements. A new method, N-3-2-1 (N ≥ 1), is proposed for fixture layout optimization of sheet metals. The flexible nature of the sheet metals requires N+3 fixture elements to constrain it normal to the surface (primary plane), but 2-1 fixture elements for other two directions (secondary and tertiary). The objective function is to achieve high stiffness of the workpiece and is calculated in terms of strain energy. Finite element analysis (FEA) was combined with genetic algorithm. A method was also proposed to find the optimum fixturing position of the workpiece in multipoint respot welding operation. Two different kinds of case studies were solved and the performance of the proposed method was also tested in the industrial scenario by fixturing the workpiece and completing the respot welding operation with satisfactory results.
NF-κB signaling is key in the wound healing processes of silk fibroin
Park, Ye Ri,Sultan, Md. Tipu,Park, Hyun Jung,Lee, Jung Min,Ju, Hyung Woo,Lee, Ok Joo,Lee, Dong Jin,Kaplan, David L.,Park, Chan Hum Elsevier Science B.V. Amsterdam 2018 ACTA BIOMATERIALIA Vol. No.
<P><B>Abstract</B></P> <P>Silk fibroin (SF) is a well-studied biomaterial for tissue engineering applications including wound healing. However, the signaling mechanisms underlying the impact of SF on this phenomenon have not been determined. In this study, through microarray analysis, regulatory genes of NF-ĸB signaling were activated in SF-treated NIH3T3 cells along with other genes. Immunoblot analysis confirmed the activation of the NF-ĸB signaling pathway as SF induced protein expression levels of IKKα, IKKβ, p65, and the degradation of IκBα. The treatment of NIH3T3 cells with SF also increased the expression of cyclin D1, vimentin, fibronectin, and vascular endothelial growth factor (VEGF). The expression of these factors by SF treatment was abrogated when NF-ĸB was inhibited by a pharmacological inhibitor Bay 11-7082. Knockdown of NF-ĸB using siRNA of IKKα and IKKβ also inhibited the SF-induced wound healing response of the NIH3T3 cells in a wound scratch assay. Collectively, these results indicated that SF-induced wound healing through the canonical NF-κB signaling pathway via regulation of the expression of cyclin D1, vimentin, fibronectin, and VEGF by NIH3T3 cells. Using an <I>in vivo</I> study with a partial-thickness excision wound in rats we demonstrated that SF-induced wound healing via NF-κB regulated proteins including cyclin D1, fibronectin, and VEGF. The <I>in vitro</I> and <I>in vivo</I> data suggested that SF induced wound healing via modulation of NF-ĸB signaling regulated proteins.</P> <P><B>Statement of Significance</B></P> <P>Silk fibroin has been effectively used as a dressing for wound treatment for more than a century. However, mechanistic insight into the basis for wound healing via silk fibroin has not been elucidated. Here we report a key mechanism involved in silk fibroin induced wound healing both <I>in vitro</I> and <I>in vivo.</I> Using genetic- and protein-level analyses, NF-κB signaling was found to regulate silk fibroin-induced wound healing by modulating target proteins. Thus, the NF-κB signaling pathway may be utilized as a therapeutic target during the formulation of silk fibroin-based biomaterials for wound healing and tissue engineering.</P> <P><B>Graphical abstract</B></P> <P>[DISPLAY OMISSION]</P>
Artificial Auricular Cartilage Using Silk Fibroin and Polyvinyl Alcohol Hydrogel
Lee, Jung Min,Sultan, Md. Tipu,Kim, Soon Hee,Kumar, Vijay,Yeon, Yeung Kyu,Lee, Ok Joo,Park, Chan Hum MDPI 2017 INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES Vol.18 No.8
<P>Several methods for auricular cartilage engineering use tissue engineering techniques. However, an ideal method for engineering auricular cartilage has not been reported. To address this issue, we developed a strategy to engineer auricular cartilage using silk fibroin (SF) and polyvinyl alcohol (PVA) hydrogel. We constructed different hydrogels with various ratios of SF and PVA by using salt leaching, silicone mold casting, and freeze-thawing methods. We characterized each of the hydrogels in terms of the swelling ratio, tensile strength, pore size, thermal properties, morphologies, and chemical properties. Based on the cell viability results, we found a blended hydrogel composed of 50% PVA and 50% SF (P50/S50) to be the best hydrogel among the fabricated hydrogels. An intact 3D ear-shaped auricular cartilage formed six weeks after the subcutaneous implantation of a chondrocyte-seeded 3D ear-shaped P50/S50 hydrogel in rats. We observed mature cartilage with a typical lacunar structure both in vitro and in vivo via histological analysis. This study may have potential applications in auricular tissue engineering with a human ear-shaped hydrogel.</P>
Scant Extracellular NAD Cleaving Activity of Human Neutrophils is Down-Regulated by fMLP via FPRL1
Hasan, Md. Ashraful,Sultan, Md. Tipu,Ahn, Won-Gyun,Kim, Yeon-Ja,Jang, Ji-Hye,Hong, Chang-Won,Song, Dong-Keun The Korean Society of Pharmacology 2014 The Korean Journal of Physiology & Pharmacology Vol.18 No.6
Extracellular nicotinamide adenine dinucleotide (NAD) cleaving activity of a particular cell type determines the rate of the degradation of extracellular NAD with formation of metabolites in the vicinity of the plasma membrane, which has important physiological consequences. It is yet to be elucidated whether intact human neutrophils have any extracellular NAD cleaving activity. In this study, with a simple fluorometric assay utilizing $1,N^6$-ethenoadenine dinucleotide (etheno-NAD) as the substrate, we have shown that intact peripheral human neutrophils have scant extracellular etheno-NAD cleaving activity, which is much less than that of mouse bone marrow neutrophils, mouse peripheral neutrophils, human monocytes and lymphocytes. With high performance liquid chromatography (HPLC), we have identified that ADP-ribose (ADPR) is the major extracellular metabolite of NAD degradation by intact human neutrophils. The scant extracellular etheno-NAD cleaving activity is decreased further by N-formyl-methionine-leucine-phenylalanine (fMLP), a chemoattractant for neutrophils. The fMLP-mediated decrease in the extracellular etheno-NAD cleaving activity is reversed by WRW4, a potent FPRL1 antagonist. These findings show that a much less extracellular etheno-NAD cleaving activity of intact human neutrophils compared to other immune cell types is down-regulated by fMLP via a low affinity fMLP receptor FPRL1.