간행물

BMB Reports update

Biochemistry and Molecular Biology Reports

  • : 생화학분자생물학회
  • : 자연과학분야  >  화학
  • : KCI등재
  • : SCOPUS
  • : 연속간행물
  • : 월간
  • : 1976-6696
  • : 1976-670X
  • : Korean Biochemical Journal(~1994)→Journal of Biochemistry and Molecular Biology(1995~)→Biochemistry and Molecurar Biology Reports(2008~)

수록정보
수록범위 : 1권1호(1968)~55권5호(2022) |수록논문 수 : 4,593
BMB Reports
55권5호(2022년 05월) 수록논문
최근 권호 논문
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KCI등재 SCOPUS

1New therapeutic approach with extracellular vesicles from stem cells for interstitial cystitis/bladder pain syndrome

저자 : Ahmed Abdal Dayem , Kwonwoo Song , Soobin Lee , Aram Kim , Ssang-goo Cho

발행기관 : 생화학분자생물학회 간행물 : BMB Reports 55권 5호 발행 연도 : 2022 페이지 : pp. 205-212 (8 pages)

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Interstitial cystitis/bladder pain syndrome (IC/BPS) is a debilitating chronic disorder characterized by suprapubic pain and urinary symptoms such as urgency, nocturia, and frequency. The prevalence of IC/BPS is increasing as diagnostic criteria become more comprehensive. Conventional pharmacotherapy against IC/BPS has shown suboptimal effects, and consequently, patients with end-stage IC/BPS are subjected to surgery. The novel treatment strategies should have two main functions, anti-inflammatory action and the regeneration of glycosaminoglycan and urothelium layers. Stem cell therapy has been shown to have dual functions. Mesenchymal stem cells (MSCs) are a promising therapeutic option for IC/BPS, but they come with several shortcomings, such as immune activation and tumorigenicity. MSC-derived extracellular vesicles (MSC-EVs) hold numerous therapeutic cargos and are thus a viable cell-free therapeutic option. In this review, we provide a brief overview of IC/BPS pathophysiology and limitations of the MSC-based therapies. Then we provide a detailed explanation and discussion of therapeutic applications of EVs in IC/BPS as well as the possible mechanisms. We believe our review will give an insight into the strengths and drawbacks of EV-mediated IC/BPS therapy and will provide a basis for further development. [BMB Reports 2022; 55(5): 205-212]

KCI등재 SCOPUS

2Blood-brain barrier-on-a-chip for brain disease modeling and drug testing

저자 : Baofang Cui , Seung-woo Cho

발행기관 : 생화학분자생물학회 간행물 : BMB Reports 55권 5호 발행 연도 : 2022 페이지 : pp. 213-219 (7 pages)

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The blood-brain barrier (BBB) is an interface between cerebral blood and the brain parenchyma. As a gate keeper, BBB regulates passage of nutrients and exogeneous compounds. Owing to this highly selective barrier, many drugs targeting brain diseases are not likely to pass through the BBB. Thus, a large amount of time and cost have been paid for the development of BBB targeted therapeutics. However, many drugs validated in in vitro models and animal models have failed in clinical trials primarily due to the lack of an appropriate BBB model. Human BBB has a unique cellular architecture. Different physiologies between human and animal BBB hinder the prediction of drug responses. Therefore, a more physiologically relevant alternative BBB model needs to be developed. In this review, we summarize major features of human BBB and current BBB models and describe organ-on-chip models for BBB modeling and their applications in neurological complications. [BMB Reports 2022; 55(5): 213-219]

KCI등재 SCOPUS

3Hepatitis B virus X protein promotes epithelial-mesenchymal transition of hepatocellular carcinoma cells by regulating SOCS1

저자 : Inho Kang , Ji Ae Kim , Jinchul Kim , Ju Hyeon Lee , Mi-jee Kim , Jeong Keun Ahn

발행기관 : 생화학분자생물학회 간행물 : BMB Reports 55권 5호 발행 연도 : 2022 페이지 : pp. 220-225 (6 pages)

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Hepatocellular carcinoma (HCC), a primary type of liver cancer, is one of the leading causes of cancer related deaths worldwide. HCC patients have poor prognosis due to intrahepatic and extrahepatic metastasis. Hepatitis B virus (HBV) infection is one of the major causes of various liver diseases including HCC. Among HBV gene products, HBV X protein (HBx) plays an important role in the development and metastasis of HCC. However, the mechanism of HCC metastasis induced by HBx has not been elucidated yet. In this study, for the first time, we report that HBx interacts with the suppressor of cytokine signaling 1 (SOCS1) which negatively controls NF-κB by degrading p65, a subunit of NF-κB. NF-κB activates the transcription of factors associated with epithelial-mesenchymal transition (EMT), a crucial cellular process associated with invasiveness and migration of cancer cells. Here, we report that HBx physically binds to SOCS1, subsequently prevents the ubiquitination of p65, activates the transcription of EMT transcription factors and enhance cell migration and invasiveness, suggesting a new mechanism of HBV-associated HCC metastasis. [BMB Reports 2022; 55(5): 220-225]

KCI등재 SCOPUS

4Endoplasmin regulates differentiation of tonsil-derived mesenchymal stem cells into chondrocytes through ERK signaling

저자 : Hye Ryeong Kim , Hyeongrok Choi , Soon Yong Park , Young-chul Song , Jae-ho Kim , Sangin Shim , Woojin Jun , Kyung-jin Kim , Jin Han , Seung-wook Chi , Sun-hee Leem , Jin Woong Chung

발행기관 : 생화학분자생물학회 간행물 : BMB Reports 55권 5호 발행 연도 : 2022 페이지 : pp. 226-231 (6 pages)

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It is well-known that some species of lizard have an exceptional ability known as caudal autotomy (voluntary self-amputation of the tail) as an anti-predation mechanism. After amputation occurs, they can regenerate their new tails in a few days. The new tail section is generally shorter than the original one and is composed of cartilage rather than vertebrae bone. In addition, the skin of the regenerated tail distinctly differs from its original appearance. We performed a proteomics analysis for extracts derived from regenerating lizard tail tissues after amputation and found that endoplasmin (ENPL) was the main factor among proteins up-regulated in expression during regeneration. Thus, we performed further experiments to determine whether ENPL could induce chondrogenesis of tonsil-derived mesenchymal stem cells (T-MSCs). In this study, we found that chondrogenic differentiation was associated with an increase of ENPL expression by ER stress. We also found that ENPL was involved in chondrogenic differentiation of T-MSCs by suppressing extracellular signal-regulated kinase (ERK) phosphorylation. [BMB Reports 2022; 55(5): 226-231]

KCI등재 SCOPUS

5RNF152 negatively regulates Wnt/β-catenin signaling in Xenopus embryos

저자 : Gang-ho Yoon , Kyuhee Kim , Dong-seok Park , Sun-cheol Choi

발행기관 : 생화학분자생물학회 간행물 : BMB Reports 55권 5호 발행 연도 : 2022 페이지 : pp. 232-237 (6 pages)

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The Wnt/β-catenin signaling plays crucial roles in early development, tissue homeostasis, stem cells, and cancers. Here, we show that RNF152, an E3 ligase localized to lysosomes, acts as a negative regulator of the Wnt/β-catenin pathway during Xenopus early embryogenesis. Overexpression of wild-type (WT) RNF152 inhibited XWnt8-induced stabilization of β-catenin, ectopic expression of target genes, and activity of a Wnt-responsive promoter. Likewise, an E3 ligase-defective RNF152 had repressive effects on the Wnt-dependent gene responses but not its truncation mutant lacking the transmembrane domain. Conversely, knockdown of RNF152 further enhanced the transcriptional responses induced by XWnt8. RNF152 morphants exhibited defects in craniofacial structures and pigmentation. In line with this, the gain-of-RNF152 function interfered with the expression of neural crest (NC) markers, whereas its depletion up-regulated NC formation in the early embryo. Mechanistically, RNF152 inhibits the polymerization of Dishevelled, which is key to Wnt signaling, in an E3 ligase-independent manner. Together, these results suggest that RNF152 controls negatively Wnt/β-catenin signaling to fine-tune its activity for NC formation in Xenopus embryo. [BMB Reports 2022; 55(5): 232-237]

KCI등재 SCOPUS

6Autistic-like social deficits in hippocampal MeCP2 knockdown rat models are rescued by ketamine

저자 : Miyeon Choi , Seung Yeon Ko , Jee Young Seo , Do Gyeong Kim , Huiju Lee , Heekyoung Chung , Hyeon Son

발행기관 : 생화학분자생물학회 간행물 : BMB Reports 55권 5호 발행 연도 : 2022 페이지 : pp. 238-243 (6 pages)

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Autism or autism spectrum disorder (ASD) is a behavioral syndrome characterized by persistent deficits in social interaction, and repetitive patterns of behavior, interests, or activities. The gene encoding Methyl-CpG binding protein 2 (MeCP2) is one of a few exceptional genes of established causal effect in ASD. Although genetically engineered mice studies may shed light on how MeCP2 loss affects synaptic activity patterns across the whole brain, such studies are not considered practical in ASD patients due to the overall level of impairment, and are technically challenging in mice. For the first time, we show that hippocampal MeCP2 knockdown produces behavioral abnormalities associated with autism-like traits in rats, providing a new strategy to investigate the efficacy of therapeutics in ASD. Ketamine, an N-Methyl-D-aspartate (NMDA) blocker, has been proposed as a possible treatment for autism. Using the MeCP2 knockdown rats in conjunction with a rat model of valproic acid (VPA)-induced ASD, we examined gene expression and ASD behaviors upon ketamine treatment. We report that the core symptoms of autism in MeCP2 knockdown rats with social impairment recovered dramatically following a single treatment with ketamine. [BMB Reports 2022; 55(5): 238-243]

KCI등재 SCOPUS

7Inhibition of VRK1 suppresses proliferation and migration of vascular smooth muscle cells and intima hyperplasia after injury via mTORC1/β-catenin axis

저자 : Xiongshan Sun , Weiwei Zhao , Qiang Wang , Jiaqi Zhao , Dachun Yang , Yongjian Yang

발행기관 : 생화학분자생물학회 간행물 : BMB Reports 55권 5호 발행 연도 : 2022 페이지 : pp. 244-249 (6 pages)

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Characterized by abnormal proliferation and migration of vascular smooth muscle cells (VSMCs), neointima hyperplasia is a hallmark of vascular restenosis after percutaneous vascular interventions. Vaccinia-related kinase 1 (VRK1) is a stress adaption-associated ser/thr protein kinase that can induce the proliferation of various types of cells. However, the role of VRK1 in the proliferation and migration of VSMCs and neointima hyperplasia after vascular injury remains unknown. We observed increased expression of VRK1 in VSMCs subjected to platelet-derived growth factor (PDGF)-BB by western blotting. Silencing VRK1 by shVrk1 reduced the number of Ki-67-positive VSMCs and attenuated the migration of VSMCs. Mechanistically, we found that relative expression levels of β-catenin and effectors of mTOR complex 1 (mTORC1) such as phospho (p)-mammalian target of rapamycin (mTOR), p-S6, and p-4EBP1 were decreased after silencing VRK1. Restoration of β-catenin expression by SKL2001 and re-activation of mTORC1 by Tuberous sclerosis 1 siRNA (siTsc1) both abolished shVrk1-mediated inhibitory effect on VSMC proliferation and migration. siTsc1 also rescued the reduced expression of β-catenin caused by VRK1 inhibition. Furthermore, mTORC1 re-activation failed to recover the attenuated proliferation and migration of VSMC resulting from shVrk1 after silencing β-catenin. We also found that the vascular expression of VRK1 was increased after injury. VRK1 inactivation in vivo inhibited vascular injury-induced neointima hyperplasia in a β-catenin-dependent manner. These results demonstrate that inhibition of VRK1 can suppress the proliferation and migration of VSMC and neointima hyperplasia after vascular injury via mTORC1/β-catenin pathway. [BMB Reports 2022; 55(5): 244-249]

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