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SuYeon LIM,Dahwun KIM,SiYan LYU,OuiBo HWANG,ByungDeok KIM,ChaeEun PARK,Ji hoon JEONG 한국생물공학회 2021 한국생물공학회 학술대회 Vol.2021 No.10
Microneedle (MN) has been desired as a therapeutic device which allow cutaneous administration of various drugs with easily and painlessly. Herein, nano-micelle generating dissolvable MN was designed by a biocompatible amphiphilic tri-block copolymer. When fabricating with doxorubicin (DOX) in the MN, the hydrophobic anticancer drug can be dissolved in an aqueous medium by entrapped in nano-micelles generated by dissolution of the MN. The intratumoral administration of the DOX-encapsulated MN can significantly inhibit the growth of melanoma in a mouse skin cancer model. Furthermore, owing to its small size (< 50 ㎚), the nano-micelle can efficiently migrate to the sentinel lymph nodes, killing the metastatic skin cancer cells. Therefore, the use of locally application of MN can be considered as a promising therapeutic device for the inhibition of metastatic melanoma.
( Suyeon Jin ),( Chan Joo Lee ),( Gibbeum Lim ),( Sungha Park ),( Sang-hak Lee ),( Ji Hyung Chung ),( Jaewon Oh ),( Seok-min Kang ) 생화학분자생물학회 2023 BMB Reports Vol.56 No.12
C-reactive protein (CRP) is an inflammatory marker and risk factor for atherosclerosis and cardiovascular diseases. However, the mechanism through which CRP induces myocardial damage remains unclear. This study aimed to determine how CRP damages cardiomyocytes via the change of mitochondrial dynamics and whether survivin, an anti-apoptotic protein, exerts a cardioprotective effect in this process. We treated H9c2 cardiomyocytes with CRP and found increased intracellular ROS production and shortened mitochondrial length. CRP treatment phosphorylated ERK1/2 and promoted increased expression, phosphorylation, and translocation of DRP1, a mitochondrial fission-related protein, from the cytoplasm to the mitochondria. The expression of mitophagy proteins PINK1 and PARK2 was also increased by CRP. YAP, a transcriptional regulator of PINK1 and PARK2, was also increased by CRP. Knockdown of YAP prevented CRP-induced increases in DRP1, PINK1, and PARK2. Furthermore, CRP-induced changes in the expression of DRP1 and increases in YAP, PINK1, and PARK2 were inhibited by ERK1/2 inhibition, suggesting that ERK1/2 signaling is involved in CRP-induced mitochondrial fission. We treated H9c2 cardiomyocytes with a recombinant TAT-survivin protein before CRP treatment, which reduced CRP-induced ROS accumulation and reduced mitochondrial fission. CRP-induced activation of ERK1/2 and increases in the expression and activity of YAP and its downstream mitochondrial proteins were inhibited by TAT-survivin. This study shows that mitochondrial fission occurs during CRPinduced cardiomyocyte damage and that the ERK1/2-YAP axis is involved in this process, and identifies that survivin alters these mechanisms to prevent CRP-induced mitochondrial damage. [BMB Reports 2023; 56(12): 663-668]