Publications by authors named "Xinan Meng"

8 Publications

  • Page 1 of 1

Redox-sensitive CDC-42 clustering promotes wound closure in C. elegans.

Cell Rep 2021 Nov;37(8):110040

Center for Stem Cell and Regenerative Medicine and Department of Cardiology of the Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310058, China; Zhejiang University-University of Edinburgh Institute, Key Laboratory of Tissue Engineering and Regenerative Medicine of Zhejiang Province, Zhejiang University School of Medicine, Hangzhou 310058, China. Electronic address:

Tissue damage induces immediate-early signals, activating Rho small GTPases to trigger actin polymerization essential for later wound repair. However, how tissue damage is sensed to activate Rho small GTPases locally remains elusive. Here, we found that wounding the C. elegans epidermis induces rapid relocalization of CDC-42 into plasma membrane-associated clusters, which subsequently recruits WASP/WSP-1 to trigger actin polymerization to close the wound. In addition, wounding induces a local transient increase and subsequent reduction of HO, which negatively regulates the clustering of CDC-42 and wound closure. CDC-42 CAAX motif-mediated prenylation and polybasic region-mediated cation-phospholipid interaction are both required for its clustering. Cysteine residues participate in intermolecular disulfide bonds to reduce membrane association and are required for negative regulation of CDC-42 clustering by HO. Collectively, our findings suggest that HO-regulated fine-tuning of CDC-42 localization can create a distinct biomolecular cluster that facilitates rapid epithelial wound repair after injury.
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http://dx.doi.org/10.1016/j.celrep.2021.110040DOI Listing
November 2021

Rapid and efficient wounding for in vivo studies of neuronal dendrite regeneration and degeneration.

J Genet Genomics 2021 02 7;48(2):163-166. Epub 2020 Nov 7.

Center for Stem Cell and Regenerative Medicine and Department of Cardiology of the Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310058 China. Electronic address:

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http://dx.doi.org/10.1016/j.jgg.2020.10.003DOI Listing
February 2021

Cryptosporidiosis outbreak caused by Cryptosporidium parvum subtype IIdA20G1 in neonatal calves.

Transbound Emerg Dis 2021 Jan 6. Epub 2021 Jan 6.

Center for Emerging and Zoonotic Diseases, College of Veterinary Medicine, South China Agricultural University, Guangzhou, China.

Cryptosporidium parvum is a major zoonotic pathogen responsible for outbreaks of severe diarrhoea in humans and calves. Almost all investigations of cryptosporidiosis outbreaks caused by C. parvum have focused on its IIa subtype family in industrialized nations. From December 2018 to April 2019, approximately 200 neonatal calves on a large cattle farm in Hebei Province, China, were diagnosed with watery diarrhoea and over 40 died. To investigate the cause of the outbreak, faecal samples were taken during and after the outbreak from neonatal calves of ≤4 weeks of age (n = 40 and n = 56) and older calves of 4-24 weeks of age (n = 79 and n = 38). A total of 18 faecal samples collected from ill calves at the peak of the outbreak were analysed for four common enteric pathogens using an enzymatic immunoassay (EIA). In addition, 75 samples from neonatal calves were tested for rotavirus by EIA. All samples were analysed for Cryptosporidium spp. using PCR and sequencing techniques. Of the initial 18 samples from sick calves, ten were positive for C. parvum, five for rotavirus, and one for coronavirus. The overall prevalence of rotavirus in neonatal calves was 20.0% (15/75), with no significant differences during and after the outbreak. In contrast, Cryptosporidium parvum infections were significantly higher during the outbreak (60.0%, 24/40) than after the outbreak (30.4%, 17/56; p = .004). Cryptosporidium parvum infection was associated with the presence of watery diarrhoea in neonatal calves (OR = 11.19), while no association was observed between C. bovis infection and diarrhoea. All C. parvum isolates were identified as subtype IIdA20G1. This is one of the few reports of outbreaks of severe diarrhoea caused by C. parvum IId subtypes in calves. More attention should be directed towards the dissemination of C. parvum in China.
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http://dx.doi.org/10.1111/tbed.13976DOI Listing
January 2021

Protocol to Induce Wounding and Measure Membrane Repair in Epidermis.

STAR Protoc 2020 Dec 21;1(3):100175. Epub 2020 Nov 21.

Center for Stem Cell and Regenerative Medicine and Department of Cardiology of The Second Affiliated Hospital, Zhejiang University School of Medicine, 310058 Hangzhou, China.

Efficient membrane repair after injury is essential for cell and animal survival. epidermal cell hpy7 has emerged as a powerful genetic system to investigate the molecular mechanism of membrane repair . This protocol describes detailed approaches for how to perform wounding on the epidermis and how to examine membrane repair by trypan blue staining, confocal imaging, and data analysis. For details on the use and execution of this protocol, please refer to Meng et al. (2020).
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http://dx.doi.org/10.1016/j.xpro.2020.100175DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7757402PMC
December 2020

Actin Polymerization and ESCRT Trigger Recruitment of the Fusogens Syntaxin-2 and EFF-1 to Promote Membrane Repair in C. elegans.

Dev Cell 2020 09 14;54(5):624-638.e5. Epub 2020 Jul 14.

Center for Stem Cell and Regenerative Medicine and Department of Cardiology of the Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310058, China; The Zhejiang University, University of Edinburgh Institute, 718 East Haizhou Road, Haining, Zhejiang 314400, China. Electronic address:

Membrane repair is essential for cell and organism survival. Exocytosis and endocytosis facilitate membrane repair in small wounds within a single cell; however, it remains unclear how large wounds in the plasma membrane are repaired in metazoans. Here, we show that wounding triggers rapid transcriptional upregulation and dynamic recruitment of the fusogen EFF-1 to the wound site in C. elegans epidermal cells. EFF-1 recruitment at the wounded membrane depends on the actin cytoskeleton and is important for membrane repair. We identified syntaxin-2 (SYX-2) as an essential regulator of EFF-1 recruitment. SYX-2 interacts with the C terminus of EFF-1 to promote its recruitment, facilitating both endoplasmic and exoplasmic membrane repair. Furthermore, we show that SYX-2-EFF-1 repair machinery acts downstream of the ESCRT III signal. Together, our findings identify a key pathway underlying membrane repair and provide insights into tissue repair and regenerative medicine after injury.
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http://dx.doi.org/10.1016/j.devcel.2020.06.027DOI Listing
September 2020

Wounding triggers MIRO-1 dependent mitochondrial fragmentation that accelerates epidermal wound closure through oxidative signaling.

Nat Commun 2020 02 26;11(1):1050. Epub 2020 Feb 26.

Center for Stem Cell and Regenerative Medicine and Department of Cardiology of The Second Affiliated Hospital, Zhejiang University School of Medicine, 310058, Hangzhou, China.

Organisms respond to tissue damage through the upregulation of protective responses which restore tissue structure and metabolic function. Mitochondria are key sources of intracellular oxidative metabolic signals that maintain cellular homeostasis. Here we report that tissue and cellular wounding triggers rapid and reversible mitochondrial fragmentation. Elevated mitochondrial fragmentation either in fzo-1 fusion-defective mutants or after acute drug treatment accelerates actin-based wound closure. Wounding triggered mitochondrial fragmentation is independent of the GTPase DRP-1 but acts via the mitochondrial Rho GTPase MIRO-1 and cytosolic Ca. The fragmented mitochondria and accelerated wound closure of fzo-1 mutants are dependent on MIRO-1 function. Genetic and transcriptomic analyzes show that enhanced mitochondrial fragmentation accelerates wound closure via the upregulation of mtROS and Cytochrome P450. Our results reveal how mitochondrial dynamics respond to cellular and tissue injury and promote tissue repair.
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http://dx.doi.org/10.1038/s41467-020-14885-xDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7044169PMC
February 2020

Influences of acid-treated multiwalled carbon nanotubes on fibroblasts: proliferation, adhesion, migration, and wound healing.

Ann Biomed Eng 2011 Jan 8;39(1):414-26. Epub 2010 Sep 8.

MOE Key Laboratory of Macromolecular Synthesis and Functionalization, Department of Polymer Science and Engineering, Zhejiang University, Hangzhou, 310027, China.

With the increasing applications of carbon nanotubes (CNTs) in fields of biomedical engineering and medical chemistry, it is important to understand the response of mammalian cells to the CNTs exposure and treatment. In this study, the influences of multiwalled carbon nanotubes (MWCNTs) on cellular behavior of human dermal fibroblasts and NIH 3T3 murine fibroblasts were investigated. Results showed that the MWCNTs treatment induced dose-dependent cytotoxicity and arrested the cell cycle in the G1 phase, indicating inhibition of DNA synthesis. The presence of MWCNTs also down regulated the expression level of adhesion-related genes, and simultaneously caused cytoskeleton damage and disturbance of actin stress fibers, thereby inducing dramatically adverse effects on the cell physiological functions such as cell spreading, adhesion, migration, and wound healing ability.
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http://dx.doi.org/10.1007/s10439-010-0151-yDOI Listing
January 2011

Fabrication of cellular polycaprolactone films for cell culture.

Colloids Surf B Biointerfaces 2010 Mar 14;76(1):38-43. Epub 2009 Oct 14.

MOE of Key Laboratory of Macromolecular Synthesis and Functionalization, Department of Polymer Science and Engineering, Zhejiang University, Hangzhou, PR China.

Hierarchical cellular structures consisting of multilayers of ordered pores were created on a poly-epsilon-caprolactone (PCL) film by introducing a colloidal crystal mask/template in thermomechanical lithography. The surface characteristics were measured by scanning electron microscopy, atomic force microscopy, water contact angle and analyzed by Fourier Transform (FT). The resultant PCL films present a metastable superhydrophobicity. Their water contact angles were initially 150 degrees and then declined with time eventually to 115-120 degrees . In vitro culture of human fibroblasts found that the cells could spread on the cellular PCL surface as normal, but showed higher viability compared with the control cells on a flat substrate.
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http://dx.doi.org/10.1016/j.colsurfb.2009.10.006DOI Listing
March 2010
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