Publications by authors named "Hongying Fu"

4 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.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.celrep.2021.110040DOI Listing
November 2021

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.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1038/s41467-020-14885-xDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7044169PMC
February 2020

MiR-532 downregulation of the Wnt/β-catenin signaling via targeting Bcl-9 and induced human intervertebral disc nucleus pulposus cells apoptosis.

J Pharmacol Sci 2018 Dec 23;138(4):263-270. Epub 2018 Oct 23.

Department of Orthopedic, Guizhou Provincial People's Hospital, Guizhou, 550002, China. Electronic address:

Objective: Intervertebral disc degeneration was characterized with aberrant intervertebral disc nucleus pulposus cells apoptosis. MiR-532 was reported to be up-regulated in the patients with intervertebral disc degeneration. However, the role of miR-532 in intervertebral disc degeneration remains unclear. Thus, current study aim to investigate the effects of miR-532 on human intervertebral disc nucleus pulposus cells.

Methods: Quantitative PCR was firstly used to evaluate the level of miR-532 expression in intervertebral disc nucleus pulposus cells. Then, luciferase reporter assays was used to confirm the target genes of miR-532. The effects of miR-532 on cell proliferation were assayed using EdU transfection. Next, apoptosis level was examined by flow cytometry utilizing Annexin V-FITC/PI double staining, and the protein expression in cells was detected with Western blotting. Finally, The expression of β-catenin protein was demonstrated by fluorescence confocal microscopy and the interaction between β-catenin and Bcl-9 was detected by co-immunoprecipitation.

Results: MiR-532 was significantly upregulated in patient with intervertebral disc degeneration. In addition, intervertebral disc nucleus pulposus cells apoptosis was significantly increased in miR-532 mimics treated group. Moreover, Bcl-9 was confirmed to be a direct target of miR-532 via luciferase reporter assays and western blot assays.

Conclusion: MiR-532 downregulation of the Wnt/β-catenin signaling via targeting Bcl-9 and induced human intervertebral disc nucleus pulposus cells apoptosis.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.jphs.2018.10.007DOI Listing
December 2018

[The effect of aerobic exercise on serum IL-4 and TNF-alpha of patients with allergic rhinitis].

Authors:
Hongying Fu Ping Yu

Lin Chung Er Bi Yan Hou Tou Jing Wai Ke Za Zhi 2013 Dec;27(23):1321-3

Objective: To investigate the effect of aerobic exercise on immune factor IL-4, TNF-alpha in patients with allergic rhinitis, which provide a theoretical basis for the treatment of allergic rhinitis.

Method: Thirty-two allergic rhinitis patients were selected and divided into a control group (14 people) and the experimental group (18 people). During the treatment, both groups receive conventional symptomatic treatment. Meanwhile, aerobic exercise therapy is applied to the experimental group for 40 - 60 minutes a day, 3 - 4 days a week. Serum IL-4, TNF-alpha and allergic rhinitis symptoms graded scoring were tested before and after 6 month therapy.

Result: After six months of exercise intervention, the 11-4, and TNF-alpha levels of experimental group were significantly lower than the level of control group. The symptoms score is also significantly decreased in experimental group.

Conclusion: Aerobic exercise had good therapeutic effect in patients with allergic rhinitis. The mechanism may be that aerobic exercise can reduce the level of IL-4 and TNF-alpha, which can relieve infiltration and activation of inflammatory cells.
View Article and Find Full Text PDF

Download full-text PDF

Source
December 2013
-->