endothelial barrier  (MedChemExpress)

Journal: Acta Pharmaceutica Sinica. B

Article Title: Inhalable songorine-integrated lipid nanomedicine for targeted ARDS therapy via repairing endothelial barrier and inactivating NLRP3 inflammasome

doi: 10.1016/j.apsb.2025.10.048

Figure Lengend Snippet: Son-lipo ameliorated the phenotypes of LPS-induced ARDS in vivo . (A) Schedule of the construction and treatments of ARDS mouse model. (B‒E) The results of pulmonary function indexes (EF50, Penh, TV/body weight, and EEP) by non-invasive whole-body plethysmography ( n = 4‒5). (F) Immunohistochemistry staining of ZO-1 and CLAUDIN-5 protein (Scale bar = 100 μm), and immunofluorescent staining of VE-CADHERIN protein (red, VE-CADHERIN; blue, Hoechst33342; Scale bar = 20 μm). (G) Statistical analysis of ZO-1 and CLAUDIN-5 protein expression in F ( n = 3). (H) The mRNA expressions of tight junction factors, Tjp1 , Cldn5 , and, Cdh5 in lung tissues by RT-qPCR analysis ( n = 3). Internal control, α -Tubulin. (I) HE staining of lung tissues. Black arrows, the degree of inflammatory cell infiltration and destroyed alveoli structures. Red arrows, alveoli wall. Blue arrows, the degree of alveoli leakage. Scale bar = 1000 μm for the upper panels and 100 μm for the lower panels. (J) Pathological scores of HE staining results ( n = 5‒6). (K) Total cell number and (L) protein content in BALF ( n = 4‒5). (M) Lung index of mice ( n = 5). (N‒P) The change in folds of mRNA levels of inflammatory factors, Il1b , Tnfa , and Nos2 , in lung tissues ( n = 3). (Q, R) The ELISA analysis of IL-6 and TNF- α levels ( n = 4). (S) TUNEL staining and (T) statistics of positive cells in lung tissues ( n = 3). Blue, Hoechst33342. Scale bar = 50 μm. Data are represented as mean ± SD. ∗ P < 0.05 vs Control. # P < 0.05 vs Model. † P < 0.05.

Article Snippet: The primary antibody was the endothelial barrier marker VE-Cadherin (1:100, Santa Cruz, sc-9989, CA, USA).

Techniques: In Vivo, Immunohistochemistry, Staining, Expressing, Quantitative RT-PCR, Control, Enzyme-linked Immunosorbent Assay, TUNEL Assay

Journal: Molecular Therapy. Nucleic Acids

Article Title: Targeting long non-coding RNA MALAT1 preserves endothelial cell integrity and protects against kidney fibrosis

doi: 10.1016/j.omtn.2025.102689

Figure Lengend Snippet: Loss of vascular integrity during kidney fibrosis and differential lncRNA expression in endothelial cells (A) Schematic overview of study setup. (B) Representative images of tdTomato-positive cells (red) in healthy contralateral (CLK), IRI, and UUO kidneys. (C) Volcano plots visualizing differential lncRNA expression between indicated conditions. The blue and red dots correspond to lncRNAs with p < 0.05 and −11 that are down- or up-regulated, respectively. Gray dots indicate non-significantly changed lncRNAs ( n = 3 per condition). (D) Hierarchical clustering shows a distinguishable lncRNA expression pattern in VE-cadherin-derived cells in IRI and UUO compared to healthy CLK kidneys ( n = 3 per condition). (E) Venn diagram indicating number of differentially expressed lncRNAs in IRI and UUO. (F) Scatterplot and heatmap of lncRNAs that are significantly differentially expressed in both models. The blue and red dots correspond to lncRNAs with p < 0.05 and −11 that are down- or up-regulated, respectively. Gray dots indicate non-significantly changed lncRNAs.

Article Snippet: Using the electric cell-substrate impedance sensing system (ECIS Zθ, Applied Biophysics) and ECIS plates (96W20idf PET, Applied Biophysics), endothelial barrier function was assessed by measuring trans-endothelial electrical resistance, as previously described.

Techniques: Expressing, Derivative Assay

Journal: Molecular Therapy. Nucleic Acids

Article Title: Targeting long non-coding RNA MALAT1 preserves endothelial cell integrity and protects against kidney fibrosis

doi: 10.1016/j.omtn.2025.102689

Figure Lengend Snippet: In vivo Malat1 knockdown inhibits kidney fibrosis and preserves vascular integrity (A) Quantification of in situ hybridization for Malat1 in the kidney upon Malat1 -targeting GapmeR treatment (gap Malat1 ), compared to control GapmeR (gapC)-treated mice, n = 3; one-way ANOVA. (B and C) Representative whole-mount images (B) and zoomed-in images (C) of in situ hybridization for Malat1 . (D and E) Representative images of Sirius Red staining (D) and corresponding quantification (E). (F and G) Representative images of α-SMA staining (F) and corresponding quantification (G). (H and I) Representative western blots for α-SMA (H) and corresponding quantification (I), normalized for glyceraldehyde 3-phosphate dehydrogenase (GAPDH). (J and K) Representative images of endothelial cell marker MECA32 (J) and corresponding quantification (K). (L and M) Representative images of endogenous Tomato label (L) and corresponding quantification (M). For (D)–(M), n = 5 (gapC) and n = 8 (gap Malat1 ); student’s t test. ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗ p < 0.001. CLK, healthy contralateral kidney; UUO, fibrotic kidney from unilateral ureteral obstruction model; gapC, control GapmeR; gap Malat1 , Malat1 GapmeR.

Article Snippet: Using the electric cell-substrate impedance sensing system (ECIS Zθ, Applied Biophysics) and ECIS plates (96W20idf PET, Applied Biophysics), endothelial barrier function was assessed by measuring trans-endothelial electrical resistance, as previously described.

Techniques: In Vivo, Knockdown, In Situ Hybridization, Control, Staining, Western Blot, Marker

Journal: Molecular Therapy. Nucleic Acids

Article Title: Targeting long non-coding RNA MALAT1 preserves endothelial cell integrity and protects against kidney fibrosis

doi: 10.1016/j.omtn.2025.102689

Figure Lengend Snippet: Virtual Hi-C analysis indicates possible coregulation with NEAT1 , while MALAT1 directly binds SUZ12 (A and B) Virtual Hi-C analysis in HUVECs (A) and mouse C2C12 (B) within the 300 kb region of MALAT1 or Malat1 , respectively. (C) Expression of Malat1 neighboring genes in sorted mouse kidney endothelial cells after gapMalat1 treatment or gapC, n = 3. (D) Gene set enrichment analysis for enriched molecular functions based on differentially expressed genes in sorted endothelial cells from mouse kidneys upon Malat1 knockdown, compared to control. (E) “Rummagene” analysis compared differentially expressed genes with other datasets. In parentheses the specific subset of data is indicated that overlaps. (F) RNA-binding domain prediction analysis of both human and mouse MALAT1 . (G) CatRAPID analysis of both human and mouse MALAT1 . (H) ChEA analysis on differentially expressed genes in sorted mouse kidney endothelial cells after gapMalat1 treatment or gapC. (I) SUZ12 RNA immunoprecipitation in HUVECs demonstrates direct binding of MALAT1 to SUZ12; n = 3; student’s t test. ∗ p < 0.05.

Article Snippet: Using the electric cell-substrate impedance sensing system (ECIS Zθ, Applied Biophysics) and ECIS plates (96W20idf PET, Applied Biophysics), endothelial barrier function was assessed by measuring trans-endothelial electrical resistance, as previously described.

Techniques: Hi-C, Expressing, Knockdown, Control, RNA Binding Assay, RNA Immunoprecipitation, Binding Assay

Journal: Molecular Therapy. Nucleic Acids

Article Title: Targeting long non-coding RNA MALAT1 preserves endothelial cell integrity and protects against kidney fibrosis

doi: 10.1016/j.omtn.2025.102689

Figure Lengend Snippet: Knockdown of MALAT1 in ECs increases barrier function and reduces angiogenesis (A–C) Representative images (A) of vascular endothelial growth factor (VEGF)-, basic fibroblast growth factor (bFGF)-, and sphingosine-1-phosphate (S1P)-induced angiogenesis upon knockdown of MALAT1 (gap MALAT1 ) or control (gapC) and corresponding quantification of average sprout length (B) and total area (C); n = 8; student’s t test. (D and E) Trans-endothelial electrical resistance of ECs after treatment with gap MALAT1 or gapC over time (D), attributable to cell-matrix contacts (alpha) and cell-cell contacts (Rb) (E); n = 4; student’s t test. (F) Schematic representation of the leakage assay, with HUVEC-based 3D capillary-like vessels in the upper perfusion channel, separated from a collagen gel in the lower channel with a phaseguide. Leak tight vessels have limited leakage of fluorescently labeled albumin, while increased permeability of the vessels results in increased fluorescent signal in the gel channel. (G and H) Analysis of leakage assay after knockdown of MALAT1 (gap MALAT1 ) or control (gapC) in HUVECs presented in (F), n = 5. Representative photographs (G) and quantification of the permeability of capillary-like vessels (H). ∗ p < 0.05 and ∗∗ p < 0.01.

Article Snippet: Using the electric cell-substrate impedance sensing system (ECIS Zθ, Applied Biophysics) and ECIS plates (96W20idf PET, Applied Biophysics), endothelial barrier function was assessed by measuring trans-endothelial electrical resistance, as previously described.

Techniques: Knockdown, Control, Labeling, Permeability