Cofilin-1 is involved in regulation of actin reorganization during influenza A virus assembly and budding

Liu, Ge; Xiang, Yangfei; Guo, Chaowan; Pei, Ying; Wang, Yifei; Kitazato, Kaio

doi:10.1016/j.bbrc.2014.10.036

Cited by 19 publications

(17 citation statements)

References 40 publications

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“…The over-expression of cofilin can increase the velocity of cell migration in dictyostelium and in human glioblastoma cells [ 11 , 12 ]. Cofilin-1 is a key factor in cell cycle regulation and plays crucial roles in the pathogenesis and development of neoplasms [ 13 , 14 ]. The over-expression of Cofilin-1 has been detected in the invasive tumor cells in cervical cancer, liver cancer, colon cancer, gastric cancer, pancreatic cancer, and kidney cancer [ 15 – 18 ].…”

Section: Discussionmentioning

confidence: 99%

Expression of Cofilin-1 and Transgelin in Esophageal Squamous Cell Carcinoma

Zhang

Liao

et al. 2015

Med Sci Monit

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BackgroundEsophageal squamous cell carcinoma (ESCC) has attracted much research attention around the world, and the number of ESCC cases has increased gradually in recent years. Identifying the specific biomarkers of ESCC is an effective approach for the early diagnosis of tumors.Material/MethodsImmunohistochemical streptavidin-peroxidase method was used to determine the expressions of Cofilin-1 and transgelin in 68 patients with esophageal squamous cell carcinoma (ESCC) and 48 individuals with normal esophageal tissues. In addition to the relationships between the expression of Cofilin-1 and transgelin, the clinicopathologic features of ESCC were also discussed. The correlation between Cofilin-1 and transgelin protein expression in ESCC was analyzed.Results(1) The positive expression rates of Cofilin-1 and transgelin were 60.3% (41/68) and 54.4% (37/68) in esophageal carcinoma tissue, respectively. The positive expression rates of Cofilin-1 and transgelin in normal esophageal tissue were 27.1% (13/48) and 29.1% (14/48), respectively. The differences were statistically significant (P<0.05). (2) The positive expression rate of Cofilin-1 did not differ significantly (P>0.05) with sex, age, ethnicity, tumor size, or infiltration depth; but did have a statistically significant (P<0.05) difference with various degrees of tumor differentiation, lymph node metastasis, and clinical stages. (3) The positive expression rate of transgelin did not differ significantly (P>0.05) with sex, age, ethnicity, tumor size, infiltration depth, and clinical stage, but did significantly (P<0.05) differ with degree of tumor differentiation and lymph node metastasis.ConclusionsCofilin-1 and transgelin may play roles in the carcinogenesis and development of esophageal squamous cell carcinoma. Cofilin-1 may be useful as an important biomarker for indicating the degree of malignancy of esophageal squamous cell carcinoma, and the detection of transgelin is valuable in early diagnosis of esophageal squamous cell carcinoma.

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Section: Discussionmentioning

confidence: 99%

Expression of Cofilin-1 and Transgelin in Esophageal Squamous Cell Carcinoma

Zhang

Liao

et al. 2015

Med Sci Monit

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“…IAV proteins NP and M1 were found to bind to host cell cytoskeletal elements 39 , 40 ; and, using superresolution or FRET microscopy, the IAV HA protein was recently observed to be localized to actin-rich membrane regions in infected cells 41 , 42 . Increased actin polymerization at the plasma membrane of infected cells promotes proper assembly and budding of IAV 43 , 44 . The binding of Influenza viral proteins to microfilaments and the reorganization of the cytoskeleton in infected cells, which seems to serve the virus, might be particularly detrimental to skeletal muscle fibers given the critical role of stabilized cytoskeletal-ECM linkages for muscle structure and function.…”

Section: Discussionmentioning

confidence: 99%

Influenza A Virus Infection Damages Zebrafish Skeletal Muscle and Exacerbates Disease in Zebrafish Modeling Duchenne Muscular Dystrophy

Goody¹,

Jurczyszak²,

Kim³

et al. 2017

PLoS Curr

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INTRODUCTION: Both genetic and infectious diseases can result in skeletal muscle degeneration, inflammation, pain, and/or weakness. Duchenne muscular dystrophy (DMD) is the most common congenital muscle disease. DMD causes progressive muscle wasting due to mutations in Dystrophin. Influenza A and B viruses are frequently associated with muscle complications, especially in children. Infections activate an immune response and immunosuppressant drugs reduce DMD symptoms. These data suggest that the immune system may contribute to muscle pathology. However, roles of the immune response in DMD and Influenza muscle complications are not well understood. Zebrafish with dmd mutations are a well-characterized model in which to study the molecular and cellular mechanisms of DMD pathology. We recently showed that zebrafish can be infected by human Influenza A virus (IAV). Thus, the zebrafish is a powerful system with which to ask questions about the etiology and mechanisms of muscle damage due to genetic and/or infectious diseases.METHODS: We infected zebrafish with IAV and assayed muscle tissue structure, sarcolemma integrity, cell-extracellular matrix (ECM) attachment, and molecular and cellular markers of inflammation in response to IAV infection alone or in the context of DMD.RESULTS: We find that IAV-infected zebrafish display mild muscle degeneration with sarcolemma damage and compromised ECM adhesion. An innate immune response is elicited in muscle in IAV-infected zebrafish: NFkB signaling is activated, proinflammatory cytokine expression is upregulated, and neutrophils localize to sites of muscle damage. IAV-infected dmd mutants display more severe muscle damage than would be expected from an additive effect of dmd mutation and IAV infection, suggesting that muscle damage caused by Dystrophin-deficiency and IAV infection is synergistic.DISCUSSION: These data demonstrate the importance of preventing IAV infections in individuals with genetic muscle diseases. Elucidating the mechanisms of immune-mediated muscle damage will not only apply to DMD and IAV, but also to other conditions where the immune system, inflammation, and muscle tissue are known to be affected, such as autoimmune diseases, cancer, and aging. INTRODUCTIONSkeletal muscle is critical for homeostasis because skeletal muscle is required for breathing, posture, locomotion, metabolism, thermoregulation, and the immune response. Muscle tissue is remarkably plastic and can increase or decrease in mass in response to genetic and environmental factors. Muscle degeneration is a serious health issue that can reduce lifespan and quality of life. Muscle wasting can be caused by aging, injury, disuse, medications, genetic mutations, and infectious or inflammatory diseases. Understanding how muscle growth, regeneration, and degeneration are regulated in response to genetic and environmental insults alone and in combination is an important undertaking in order to be able to promote muscle health in cases of sickness and disease.Skeletal muscle damage occurs ...

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“…Therefore, downregulation of cortactin can be a potential strategy usurped by IAV for viral release. In addition, HDAC6 may regulate actin remodelling under the plasma membrane to restrict viral assembly and budding [93,94], when considering that actin cytoskeleton has been shown to associate with IAV infection [95][96][97].…”

Section: Assembly and Egressmentioning

confidence: 99%

Cellular defence or viral assist: the dilemma of HDAC6

Zheng

Jiang

et al. 2017

Journal of General Virology

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Histone deacetylase 6 (HDAC6) is a unique cytoplasmic deacetylase that regulates various important biological processes by preventing protein aggregation and deacetylating different non-histone substrates including tubulin, heat shock protein 90, cortactin, retinoic acid inducible gene I and b-catenin. Growing evidence has indicated a dual role for HDAC6 in viral infection and pathogenesis: HDAC6 may represent a host defence mechanism against viral infection by modulating microtubule acetylation, triggering antiviral immune response and stimulating protective autophagy, or it may be hijacked by the virus to enhance proinflammatory response. In this review, we will highlight current data illustrating the complexity and importance of HDAC6 in viral pathogenesis. We will summarize the structure and functional specificity of HDAC6, and its deacetylaseand ubiquitin-dependent activity in key cellular events in response to virus infection. We will also discuss how HDAC6 exerts its direct or indirect histone modification ability in viral lytic-latency switch.

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Cofilin-1 is involved in regulation of actin reorganization during influenza A virus assembly and budding

Cited by 19 publications

References 40 publications

Expression of Cofilin-1 and Transgelin in Esophageal Squamous Cell Carcinoma

Expression of Cofilin-1 and Transgelin in Esophageal Squamous Cell Carcinoma

Influenza A Virus Infection Damages Zebrafish Skeletal Muscle and Exacerbates Disease in Zebrafish Modeling Duchenne Muscular Dystrophy

Cellular defence or viral assist: the dilemma of HDAC6

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