Journal: Developmental cell

Article Title: Differential tissue deformability underlies fluid pressure-driven shape divergence of the avian embryonic brain and spinal cord.

doi: 10.1016/j.devcel.2025.04.010

Figure Lengend Snippet: Figure 3. Differential neural crest behavior underlies the acquisition of a thinned-out and expanded dorsal hindbrain roof (A) Confocal images of actin and phosphorylated myosin light chain kinase II in the hindbrain and spinal cord of HH12 stage embryos. (B and C) Quantification of apical actin signal intensity along the lumen circumference in the hindbrain and spinal cord of HH11-HH12 stage embryos (n = 3) (p = 0.012 and 0.53, paired t tests). (D) Confocal images showing Snail2+ cell migration in the hindbrain and spinal cord cross sections of embryos progressing toward brain-expansion stages (HH9 to HH12). (E) Confocal images showing laminin and actin organization in cross-section views of the hindbrain and spinal cord of HH12 stage embryos. (F) Confocal images showing laminin organization at the dorsal surface in a 3D rendering of the hindbrain and spinal cord of HH11 stage embryos. (G) Bright-field images of embryos treated with dimethyl sulfoxide (DMSO) or MMP inhibitor at HH11 and incubated for 20 h. Arrows indicate hindbrain at level of otic vesicle. (H) Dorsal views of DMSO- and MMP inhibitor-treated embryos. Yellow highlight fills the brain dorsal surface. (I) Confocal images showing the dorsal hindbrain of control and MMP inhibitor-treated embryos, ∼20 h post treatment. Bottom panels show laminin surface with arrows indicating breaks in laminin continuity. (J) Hindbrain roof length in control (n = 6) and inhibitor-treated (n = 8) embryos (p = 0.0000048, t test). White scale bars are 50 μm unless otherwise stated. See also Figure S3.

Article Snippet: The following antibodies and dyes where used: Laminin (DSHB, 3H11) 1:100, Snail2 (Cell Signaling Technology, 9585S) 1:200, pMLC2 (Cell Signaling Technology, 3671S) 1:100, Hoechst 1:1000, Phalloidin 647 (Thermo Scientific, A22287) 1:500, Donkey Anti-Mouse 488n IgG (Abcam, ab150105), Donkey Anti-Rabbit 594 (Abcam, ab150076).

Techniques: Migration, Incubation, Control

Journal: Developmental cell

Article Title: Differential tissue deformability underlies fluid pressure-driven shape divergence of the avian embryonic brain and spinal cord.

doi: 10.1016/j.devcel.2025.04.010

Figure Lengend Snippet: Figure 4. Hindbrain premigratory neural crest cells may be sufficient to generate neural tube expansion under lumen pres- sure (A) Bright-field images of pre-brain-expansion stage embryos with spinal cord-to-spinal cord graft and a hindbrain-to-spinal cord graft. (B and C) Confocal images showing dorsal surface of graft integration ∼20 h post-grafting and cross- sectional views at the levels corresponding to dashed lines in (B). White bracket highlights the thinned-out roof in the graft region. (D) Spinal cord tissue thickness in the region with spinal cord (n = 2) or hindbrain (n = 9) grafted cells. (E) Confocal images showing Snail2+ cells in graft regions. Arrows indicate Snail2+ cells within the GFP+ graft. (F) Model of brain expansion relative to the spinal cord. A greater extent of premigratory neural crest cell mesenchymal behavior and corresponding ECM remodeling underlies a more deformable dorsal roof in the early hindbrain compared with the spinal cord. This allows the hindbrain roof to deform more under internal lumen pressure, driving hindbrain expansion relative to the spinal cord during early embryo development. Black scale bars are 500 μm. White scale bars are 25 μm unless otherwise stated. See also Figure S4.

Article Snippet: The following antibodies and dyes where used: Laminin (DSHB, 3H11) 1:100, Snail2 (Cell Signaling Technology, 9585S) 1:200, pMLC2 (Cell Signaling Technology, 3671S) 1:100, Hoechst 1:1000, Phalloidin 647 (Thermo Scientific, A22287) 1:500, Donkey Anti-Mouse 488n IgG (Abcam, ab150105), Donkey Anti-Rabbit 594 (Abcam, ab150076).

Techniques:

Journal: Advanced Science

Article Title: Neoadjuvant Chemotherapy With Cisplatin Up‐Regulates GSDMD to Enhance Oral Squamous Cell Carcinoma Metastasis Through MMP14‐Mediated EMT Activation

doi: 10.1002/advs.202501149

Figure Lengend Snippet: Mass spectrometry analysis and validation of GSDMD‐interacting proteins. A) Coimmunoprecipitation (Co‐IP) identified proteins that bind to GSDMD. B) An intersection analysis of protein mass spectrometry data was performed to detect differentially expressed proteins that interact with GSDMD. C) Co‐IP confirmed the interaction between GSDMD and MMP14. D) Knockdown of GSDMD did not significantly alter the mRNA level of MMP14. E) Overexpression of GSDMD did not significantly alter the mRNA level of MMP14. F) Knockdown of GSDMD resulted in the synchronized downregulation of MMP14 protein expression in OSCC cells, along with the downstream downregulation of MMP9, MMP2, N‐cadherin, vimentin, and snail2 and upregulation of E‐cadherin, suggesting the inhibition of the EMT process. Overexpression of GSDMD resulted in the upregulation of MMP14 protein expression in OSCC cells, along with the downstream upregulation of MMP9, MMP2, N‐cadherin, vimentin, and snail2 and downregulation of E‐cadherin, suggesting the activation of the EMT process. G) Knockdown of GSDMD led to reduced secretion of MMP9 and MMP2 from OSCC cells. H) Overexpression of GSDMD led to increased secretion of MMP9 and MMP2 from OSCC cells.

Article Snippet: Antibodies specific for GSDMD (20770‐1‐AP), MMP14 (14552‐1‐AP), vimentin (60330‐1‐Ig), E‐cadherin (20874‐1‐AP), N‐cadherin (22018‐1‐AP), MMP2 (10373‐1‐AP), MMP‐9 (10375‐2‐AP), SNAIL2 (13099‐1‐AP), ubiquitin (10201‐2‐AP), Ki67 (27309‐1‐AP), and mCherry (26765‐1‐AP) were purchased from Proteintech.

Techniques: Mass Spectrometry, Biomarker Discovery, Co-Immunoprecipitation Assay, Knockdown, Over Expression, Expressing, Inhibition, Activation Assay