Editorial Material
Cell Biology
Liliana Felicia Iannucci, Giulietta Di Benedetto, Konstantinos Lefkimmiatis
Summary: Macroautophagy/autophagy is a cellular process responsible for eliminating and recycling aggregated proteins and damaged organelles. The compartmentalization of PRKA/PKA determines its effects on autophagy, with increased cAMP levels generating different PRKA activity signatures. The distribution of PRKA holoenzymes plays a role in affecting the autophagic flux in specific cell types.
Article
Pharmacology & Pharmacy
Linyi Li, Yunyun Yang, Huina Zhang, Yunhui Du, Xiaolu Jiao, Huahui Yu, Yu Wang, Qianwen Lv, Fan Li, Qiuju Sun, Yanwen Qin
Summary: Salidroside effectively ameliorated IH-aggravated endothelial barrier injury and atherosclerosis through the cAMP/PKA/RhoA signaling pathway.
FRONTIERS IN PHARMACOLOGY
(2021)
Article
Oncology
Jinghuan Wang, Wen Zhong, Qianwen Cheng, Chenxi Xiao, Jie Xu, Zhenghua Su, Haibi Su, Xinhua Liu
Summary: Smyd2 plays a vital role in disrupting blood-brain barrier integrity in ischaemic stroke through methylation-mediated Sphk/S1PR, and knocking down Smyd2 reduces blood-brain barrier permeability and improves functional recovery.
CLINICAL AND TRANSLATIONAL MEDICINE
(2022)
Review
Biochemistry & Molecular Biology
Qonita Afinanisa, Min Kyung Cho, Hyun-A Seong
Summary: AMP-activated protein kinase (AMPK) plays a central role in maintaining energy homeostasis by regulating signaling input and metabolic pathways. Its subcellular compartmentalization is crucial for accessing proper targets and generating appropriate responses to various stressors. Tissue-specific distribution and nucleo-cytoplasmic shuttling are influenced by factors such as starvation, exercise, and heat shock, highlighting the importance of AMPK localization in coordinating signaling and metabolism.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2021)
Article
Biochemistry & Molecular Biology
Simona Federica Spampinato, Giuseppe Costantino, Sara Merlo, Pier Luigi Canonico, Maria Angela Sortino
Summary: Modulating S1P receptors in microglia may contribute to the reinforcement of the endothelial barrier at the blood-brain barrier, suggesting an additional effect of the drug in the treatment of multiple sclerosis.
Article
Biochemistry & Molecular Biology
Qiuling Liu, Tujing Song, Bing Chen, Jingjing Zhang, Wen Li
Summary: Hypoxia is crucial for the development of various disorders, especially hypoxic cerebropathy. The damage to the blood-brain barrier (BBB) caused by hypoxia is well known. This study explored the correlation between endothelial ferroptosis and hypoxia-induced BBB damage using in vivo zebrafish and in vitro bEnd.3 cells. The results showed that hypoxic treatment could induce BBB disruption by down-regulating claudin-5 (CLDN5) expression in both zebrafish cerebrovascular endothelial cells and bEnd.3 cells.
Article
Chemistry, Multidisciplinary
Yujia Jiang, Yansong Liu, Xinyi Yang, Runze Pan, Lu Mou, Wankui Jiang, Wenming Zhang, Fengxue Xin, Min Jiang
Summary: This study successfully increased the efficiency of cellulose acid production from 7.36 g L-1 (native microbial consortium) to 57.57 g L-1 by re-assembling a simplified microbial consortium consisting of lignocellulose degrader Trichoderma asperellum and lactic acid (LA) producer Lactobacillus paracasei. The analysis of interactions between these two members provides insights for the construction of synthetic microbial consortia for the synthesis of other chemicals.
Article
Cell Biology
Huaping Zheng, Linna Gu, Fulei Zhao, Chen Zhang, Zhen Wang, Hong Zhou, Zhonglan Hu, Xiaoqiong Wei, Xiao Liu, Feng Luo, Fanlian Zeng, Qixiang Zhao, Yan Hao, Yawen Hu, Xiaoyan Wang, Jing Hu, Jiadong Yu, Wenling Wu, Yifan Zhou, Pei Zhou, Chengcheng Yue, Nongyu Huang, Kaijun Cui, Wei Li, Jiong Li
Summary: This study reveals the critical role of SerpinB7 in the regulation of keratinocyte differentiation and psoriatic microenvironment mediated via keratinocytes' intracellular calcium flux. SerpinB7 deficiency leads to excessive proliferation and impaired differentiation of keratinocytes, as well as increased expression of chemokines and antimicrobial peptides. The deficiency of SerpinB7 affects keratinocyte differentiation and proinflammatory cytokines possibly by affecting calcium ion channel-related proteins. These findings propose SerpinB7 as a potential therapeutic target for psoriasis.
CELL DEATH & DISEASE
(2022)
Article
Multidisciplinary Sciences
Ji Seul Han, Yong Geun Jeon, Minsik Oh, Gung Lee, Hahn Nahmgoong, Sang Mun Han, Jeehye Choi, Ye Young Kim, Kyung Cheul Shin, Jiwon Kim, Kyuri Jo, Sung Sik Choe, Eun Jung Park, Sun Kim, Jae Bum Kim
Summary: “The study demonstrates that HIF alpha plays a key role in regulating thermogenic function in response to cold and re-warming. Specifically, HIF2 alpha suppresses PKA activity by inducing miR-3085-3p expression, leading to downregulation of PKA C alpha. Ablation of adipocyte HIF2 alpha stimulates retention of beige adipocytes during re-warming after cold stimuli. Moreover, administration of miR-3085-3p promotes beige-to-white transition via downregulation of PKA C alpha and mitochondrial abundance in adipocyte HIF2 alpha deficient mice. These findings highlight the importance of HIF2 alpha-dependent PKA regulation in dynamic remodeling of beige adipocytes as thermostats.”
NATURE COMMUNICATIONS
(2022)
Article
Allergy
Suzanne Cole, Avneet Manghera, Lachrissa Burns, Janine Barrett, Nicole Yager, Hefin Rhys, Andrew Skelton, John Cole, Carl S. Goodyear, Meryn Griffiths, Dominique Baeten, Marta Bertolini, Stevan Shaw, Hussein Al-Mossawi, Asher Maroof
Summary: This study characterizes the regulation of IL-17A and IL-17F in psoriatic disease, showing that IL-17F is elevated preferentially over IL-17A and that each isoform is expressed in distinct cell populations. The study also reveals the plasticity of IL-17A and IL-17F expression, influenced by proinflammatory signaling and anti-inflammatory drugs. Higher IL-17F expression is linked to increased cell proliferation, suggesting the importance of neutralizing both IL-17A and IL-17F in inhibiting IL-17-driven pathology.
JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY
(2023)
Article
Biochemistry & Molecular Biology
Wangquan Ji, Qiang Hu, Mengdi Zhang, Chuwen Zhang, Chen Chen, Yujie Yan, Xue Zhang, Shuaiyin Chen, Ling Tao, Weiguo Zhang, Yuefei Jin, Guangcai Duan
Summary: The study in BALB/c mice model revealed that CVA2 infection induced lung damage by significantly increasing lung microvascular permeability, infecting lung endothelial cells, promoting apoptosis, and disrupting tight junctions. The infection also led to degradation of tight junction proteins, upregulation of genes related to endothelial dysfunction, activation of inflammatory cytokines, and p38-MAPK signaling pathways. Targeting p38-MAPK signaling may offer a therapeutic strategy for pulmonary edema in critical HFMD infections.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2021)
Article
Environmental Sciences
Yifan Huang, Jiahui Chen, Derui Zhang, Bo Fang, Tsering YangJin, Jianwen Zou, Yahua Chen, Nana Su, Jin Cui
Summary: The study found that exogenous glutathione reduces cadmium accumulation in roots by up-regulating BOT1/2 expression, promoting PC synthesis, and enhancing the expression of BcABCC1/2, all of which contribute to the compartmentalization of Cd in root vacuoles in pakchoi under Cd stress.
ECOTOXICOLOGY AND ENVIRONMENTAL SAFETY
(2021)
Article
Immunology
Qiancheng Deng, Puyu Zou, Pei Du, Yaqian Shi, Zixin Pi, Yangfan Xiao, Takuro Kanekura, Huiming Zhang, Yi Zhan, Xiangning Qiu, Yan Ding, Zhuotong Zeng, Rong Xiao
Summary: This study found increased CD8+ and perforin+ cells in the lesions of vitiligo patients. The expression levels of perforin were elevated in the CD8+ T cells from peripheral blood of vitiligo patients and their culture supernatants. The perforin promoter was hypomethylated in vitiligo CD8+ T cells. Treatment with the DNA methylation inhibitor 5-Azacytidine reduced the perforin methylation level and caused perforin overexpression.
INTERNATIONAL IMMUNOPHARMACOLOGY
(2023)
Article
Cell Biology
Guolin Li, Linna Gu, Fulei Zhao, Yawen Hu, Xiaoyan Wang, Fanlian Zeng, Jiadong Yu, Chengcheng Yue, Pei Zhou, Ya Li, Yuting Feng, Jing Hu, Nongyu Huang, Wenling Wu, Kaijun Cui, Wei Li, Jiong Li
Summary: In this study, the researchers found that the WFDC12 gene plays a role in the pathogenesis of atopic dermatitis (AD). They discovered that WFDC12 is highly expressed in the skin tissue and lesions of AD patients. By overexpressing WFDC12 in the epidermis of transgenic mice, they observed increased migration of skin-presenting cells, enhanced Th cell infiltration, and upregulation of immune cells and cytokines. They also found that WFDC12 promotes arachidonic acid metabolism and platelet-activating factor (PAF) accumulation, exacerbating AD-like symptoms.
CELL DEATH & DISEASE
(2023)
Article
Biochemistry & Molecular Biology
Mariko Komuro, Masaki Nagane, Tomoki Fukuyama, Xiaolin Luo, Shinobu Hiraki, Masakatsu Miyanabe, Miyuki Ishikawa, Chiaki Niwa, Hironobu Murakami, Mariko Okamoto, Tadashi Yamashita
Summary: The study found that sphingomyelin plays a vital role in maintaining the cutaneous barrier through regulation of the STAT3 pathway. These results suggest that sphingomyelin could be a potential therapeutic target for treating dermatitis.
Article
Immunology
Franziska Vielmuth, Elias Walter, Michael Fuchs, Mariya Y. Radeva, Fanny Buechau, Thomas M. Magin, Volker Spindler, Jens Waschke
FRONTIERS IN IMMUNOLOGY
(2018)
Review
Immunology
Franziska Vielmuth, Volker Spindler, Jens Waschke
FRONTIERS IN IMMUNOLOGY
(2018)
Article
Immunology
Volker Spindler, Jens Waschke
FRONTIERS IN IMMUNOLOGY
(2018)
Letter
Dermatology
Daniela Kugelmann, Mariya Y. Radeva, Volker Spindler, Jens Waschke
JOURNAL OF INVESTIGATIVE DERMATOLOGY
(2019)
Article
Dermatology
D. T. Egu, A. M. Sigmund, E. Schmidt, V. Spindler, E. Walter, J. Waschke
BRITISH JOURNAL OF DERMATOLOGY
(2020)
Article
Biochemistry & Molecular Biology
Michael Fuchs, Marco Foresti, Mariya Y. Radeva, Daniela Kugelmann, Rene Keil, Mechthild Hatzfeld, Volker Spindler, Jens Waschke, Franziska Vielmuth
CELLULAR AND MOLECULAR LIFE SCIENCES
(2019)
Article
Immunology
Daniela Kugelmann, Vera Roetzer, Elias Walter, Desalegn Tadesse Egu, Michael Tobias Fuchs, Franziska Vielmuth, Hilda Vargas-Robles, Michael Schnoor, Michael Hertl, Ruediger Eming, Klemens Rottner, Ansgar Schmidt, Volker Spindler, Jens Waschke
FRONTIERS IN IMMUNOLOGY
(2019)
Article
Dermatology
Matthias Hiermaier, Felix Kliewe, Camilla Schinner, Chiara Studle, I. Piotr Maly, Marie-Therese Wanuske, Vera Roetzer, Nicole Endlich, Franziska Vielmuth, Jens Waschke, Volker Spindler
Summary: The loss of actin-binding protein alpha-adducin reduces desmosome numbers and impairs the ability of keratinocytes or epidermis to withstand mechanical stress. This is not mainly due to decreased levels or impaired adhesive properties, but rather altered turnover of desmosomal molecules.
JOURNAL OF INVESTIGATIVE DERMATOLOGY
(2021)
Article
Physiology
Marie-Theres Wanuske, Dominique Brantschen, Camilla Schinner, Chiara Stuedle, Elias Walter, Matthias Hiermaier, Franziska Vielmuth, Jens Waschke, Volker Spindler
Summary: Dp is crucial for desmosome formation, while not influencing individual cadherin binding properties. Instead, macro-clustering of desmosomal adhesion molecules through Dp is crucial.
Article
Cell Biology
Jakob Mitgau, Julius Franke, Camilla Schinner, Gabriele Stephan, Sandra Berndt, Dimitris G. Placantonakis, Hermann Kalwa, Volker Spindler, Caroline Wilde, Ines Liebscher
Summary: This study provides information on the structural requirements and forces needed for ECM-mediated activation of the GPR126 receptor. The N terminus of GPR126 acts as an allosteric module that can fine-tune receptor activation in a context-specific manner.
FRONTIERS IN CELL AND DEVELOPMENTAL BIOLOGY
(2022)
Article
Cardiac & Cardiovascular Systems
Camilla Schinner, Lifen Xu, Henriette Franz, Aude Zimmermann, Marie-Theres Wanuske, Maitreyi Rathod, Pauline Hanns, Florian Geier, Pawel Pelczar, Yan Liang, Vera Lorenz, Chiara Studle, Piotr Maly, Silke Kauferstein, Britt M. Beckmann, Farah Sheikh, Gabriela M. Kuster, Volker Spindler
Summary: This study successfully induced a cardiac phenotype in mice that met the diagnostic criteria for ACM by causing defects in intercellular adhesion of cardiac cells through mutation. It confirmed integrin-alpha V beta 6 and transforming growth factor-beta signaling as key pathways leading to fibrosis. Blocking this pathway reduced fibrotic markers expression and fibrosis formation, offering a promising target for treating ACM.
Article
Dermatology
Christoph Hudemann, Yvonne Exner, Robert Pollmann, Karina Schneider, Anna Zakrzewicz, Simon Feldhoff, Thomas Schmidt, Volker Spindler, David Rafei-Shamsabadi, Frauke Voellner, Jens Waschke, Ritva Tikkanen, Michael Hertl, Ruediger Eming
Summary: The study demonstrates that an antibody called 2G4 can induce weakened intercellular keratinocyte adhesion and activate the p38MAPK signal transduction pathway, leading to a severe autoimmune skin disease called pemphigus vulgaris. This study provides further insights into the underlying mechanisms of desmosomal keratinocyte adhesion and blister formation in pemphigus vulgaris.
JOURNAL OF INVESTIGATIVE DERMATOLOGY
(2023)
Article
Biochemistry & Molecular Biology
Michael Fuchs, Mariya Y. Radeva, Volker Spindler, Franziska Vielmuth, Daniela Kugelmann, Jens Waschke
Summary: Desmoglein 3 (Dsg3) is a cadherin protein that mediates cell adhesion and is the antigen of pemphigus vulgaris. Using super resolution microscopy, researchers studied the cytoskeletal anchorage of Dsg3 on living keratinocytes and discovered the existence of two pools of Dsg3 with different anchorage mechanisms. These findings provide valuable insights into cell adhesion and keratinocyte formation.
CELLULAR AND MOLECULAR LIFE SCIENCES
(2023)
Article
Cell Biology
Volker Spindler, Brenda Gerull, Kathleen J. Green, Andrew P. Kowalczyk, Rudolf Leube, Ali J. Marian, Hendrik Milting, Eliane J. Mueller, Carien Niessen, Aimee S. Payne, Nicolas Schlegel, Enno Schmidt, Pavel Strnad, Ritva Tikkanen, Franziska Vielmuth, Jens Waschke
Summary: Desmosome diseases are caused by dysfunction of desmosomes, which anchor intermediate filaments (IFs) at sites of cell-cell adhesion. The understanding of the role of desmosomes has shifted from the focus on actin filament-associated adherens junctions to the interference with desmosome function and its molecular constituents. The Alpine desmosome disease meeting provided a platform for researchers and clinical experts to discuss the function and dysfunction of desmosomes in different cell types and their involvement in various diseases.
JOURNAL OF CELL SCIENCE
(2023)
Meeting Abstract
Biochemistry & Molecular Biology
Camilla Schinner, Henriette Franz, Chiara Studle, Lifen Xu, Vera Lorenz, Gabriela Kuster, Volker Spindler
