Yes-associated protein 1 translocation through actin cytoskeleton organization in trophectoderm cells

Yamamura, Shota; Goda, Nanami; Akizawa, Hiroki; Kohri, Nanami; Balboula, Ahmed Z.; Kobayashi, Ken; Bai, Hanako; Takahashi, Masashi; Kawahara, Manabu

doi:10.1016/j.ydbio.2020.09.004

Cited by 8 publications

(11 citation statements)

References 51 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In line with our findings, other studies also report the involvement of actin cytoskeleton filament (25), or myosin II (26), or actomyosin-dependent (18) nucleocytoplasmic shuttling. Furthermore, studies also reported the role of ROCK in nuclear translocation of cytoplasmic molecules through regulation of the actin cytoskeleton (45).…”

Section: Discussionsupporting

confidence: 93%

“…Several previous studies have reported that NETosis induction requires functional cytoskeleton [18,21], and genetic disruption of actin polymerization by a deficiency of Wiskott-Aldrich syndrome protein blocks NET formation [19]. In line with our findings, other studies also report the involvement of actin cytoskeleton filament [34], or myosin II [35], or actomyosin-dependent [23] nucleocytoplasmic shuttling. Matoba et al reported the role of ROCK in nuclear translocation of cytoplasmic molecules through regulation of actin cytoskeleton organization [36].…”

Section: Discussionsupporting

confidence: 92%

“…These results demonstrated that not only actin cytoskeleton, but also the actomyosin cytoskeletal networks, are important for nuclear translocation of PKCα and nuclear envelope rupture (Fig 1E), which is required for nuclear chromatin extrusion and NET formation [9, 12]. In line, other studies also reported the involvement of actin cytoskeleton [34] or myosin II [35] in nuclear translocation of cytosolic molecules, and in actomyosin-dependent nucleocytoplasmic shuttling [23].…”

Section: Resultssupporting

confidence: 74%

“…In addition, actomyosin networks have been shown to be important in nucleocytoplasmic shuttling [25]. In the current study, we found that disruption of actin cytoskeleton filaments by inhibition of actin Along this line, other studies also reported the involvement of actin cytoskeleton [37] or myosin II [38] in nuclear translocation of cytosolic molecules, and in actomyosin-dependent nucleocytoplasmic shuttling [25].…”

Section: Disruption Of Actin Cytoskeleton or Actomyosin Cytoskeletal Network Attenuated Neutrophil Net Formationsupporting

confidence: 83%

“…In line, Hippenstiel demonstrated that inhibition of ROCK blocks nuclear translocation and activation of PKC in endothelial cells [17], and Matoba reported the role of ROCK in nuclear translocation of other cytosolic molecules through regulation of actin cytoskeleton organization [73]. Other studies also report the involvement of actin cytoskeleton filament [37], or myosin II [38], or actomyosindependent [25] in nucleocytoplasmic shuttling. Therefore, the current study provides a cellular mechanistic explanation for the role of actin cytoskeleton in early stage of NETosis induction [18,21], in which nuclear translocation of NETotic lamin kinase PKCα is mediated by actin cytoskeleton [16], and its upstream ROCK signaling pathway [17] during NETosis.…”

Section: Discussionmentioning

confidence: 87%

See 4 more Smart Citations

Rho Kinase regulates neutrophil NET formation that is involved in UVB-induced skin inflammation

Lyu

Liao

et al. 2021

Preprint

View full text Add to dashboard Cite

Objective. Ultraviolet B (UVB) is an important trigger of skin inflammation and lupus with recruitment of leukocytes to inflamed skin. Neutrophil NETosis has been implicated in pathogenesis of lupus erythematosus. We recently reported that nuclear envelope rupture and NET formation is driven by PKCα-mediated nuclear lamin B disassembly, with involvement of NETosis in UVB-induced skin inflammation. Studies have shown that cytoskeletal networks are involved in NETosis. However, it is still unknown how cytoskeletal networks and their upstream ROCK are involved in NET formation as well as UVB-induced skin inflammation. Methods. The involvements of actomyosin cytoskeletal networks and ROCK1 in NETosis were studied in vitro. Mice with hematopoietic specific ROCK1 deficiency were irradiated by UVB to investigate NET formation in vivo and its involvement in skin inflammation. Results. In time course studies, PKCα nuclear translocation was very well matched with actin polymerization and ROCK1 activation. Inhibition of actin polymerization or ROCK/MLCK/myosin pathway with chemical inhibitors decreased nuclear translocation of PKCα and NETosis in vitro. Furthermore, genetic deficiency of ROCK1 inhibited NET formation ex vivo. Hematopoietic specific ROCK1 deficiency ameliorated UVB-induced skin inflammation in mice with reduced skin thickness by attenuating NET formation and the extracellular display of NET-associated IL-17A, TNFα, IFNγ, and IFNα in the inflamed skin. Conclusion. ROCK1 regulated neutrophils for NET formation by modulation of PKCα nuclear translocation through actomyosin cytoskeletal networks. ROCK1 deficiency ameliorates UVB-induced skin inflammation by inhibition of NETosis and display of NET-associated cytokines. This study provides insights into novel therapeutics on NETosis-related diseases.

show abstract

Section: Discussionsupporting

confidence: 93%