imatinib mesilate (glivec  (Novartis)

Journal: bioRxiv

Article Title: Loss of endothelial ALK1 signaling induces the emergence of a KIT+ angiogenic endothelial cluster driving brain arteriovenous malformations

doi: 10.1101/2025.06.05.657957

Figure Lengend Snippet: A , Experimental timeline of tamoxifen and KIT inhibitor administration in Alk1iECKO and control mice. B, D, F , CD31 immunostaining of the PNVP of P8 Alk1iECKO mice injected with imatinib ( B ), masitinib ( D ), and KIT blocking antibody ( F ), along with their corresponding vehicle controls. C, E, G , Quantification of vessel diameter in the PNVP of P8 Alk1iECKO mice injected with the indicated inhibitor. Each dot represents one mouse. Error bars represent means ± s.e.m, *P<0.05, **P<0.01, ***P<0.001, Mann-Whitney test, Welch’s t test or Unpaired t test (B, D, F) were performed.

Article Snippet: Imatinib Mesylate (100 mg/kg, Selleckchem, S1026), Masitinib Mesylate (100mg/Kg, Cerdalane, E0814), KIT blocking antibody (500 µg, InVivo MAb anti-mouse c-Kit, BioxCell, BE0293-5MG-A) were administered intraperitoneally at P6, 3 hours following tamoxifen injection, and again at P7.

Techniques: Control, Immunostaining, Injection, Blocking Assay, MANN-WHITNEY

Journal: bioRxiv

Article Title: Loss of endothelial ALK1 signaling induces the emergence of a KIT+ angiogenic endothelial cluster driving brain arteriovenous malformations

doi: 10.1101/2025.06.05.657957

Figure Lengend Snippet: A , C , CD31 immunostaining of the PNVP of P8 Alk1l/l mice injected with imatinib (A), and masitinib (C), along with their corresponding vehicle controls. B, D , Quantification of vessel diameter in the PNVP of P8 Alk1l/l mice injected with the indicated inhibitor. Each dot represents one mouse. Error bars represent means ± s.e.m, Mann-Whitney test or Unpaired t test (B, D) were performed. D , Schematic model illustrating how 48 hours of Alk1 deletion induces the emergence of angiogenic 1 ECs in both PNVP and INVP. In the PNVP, angiogenic 1 ECs further differentiate into angiogenic 2 ECs, which drive AVM formation. Both angiogenic populations express KIT, with angiogenic 2 showing stronger expression. Pharmacological inhibition of KIT effectively prevents AVM development in this model. Each dot represents one mouse.

Article Snippet: Imatinib Mesylate (100 mg/kg, Selleckchem, S1026), Masitinib Mesylate (100mg/Kg, Cerdalane, E0814), KIT blocking antibody (500 µg, InVivo MAb anti-mouse c-Kit, BioxCell, BE0293-5MG-A) were administered intraperitoneally at P6, 3 hours following tamoxifen injection, and again at P7.

Techniques: Immunostaining, Injection, MANN-WHITNEY, Expressing, Inhibition

Journal: JCI Insight

Article Title: Endothelial HIF α /PDGF-B to smooth muscle Beclin1 signaling sustains pathological muscularization in pulmonary hypertension

doi: 10.1172/jci.insight.162449

Figure Lengend Snippet: ( A ) Experimental strategy for B – D . ( B ) Acta2-CreER T2 ROSA26R Zs/+ mice were exposed to hypoxia or normoxia for 31 days and STI571 was administered at 0, 50, or 100 mg/kg/d by daily intraperitoneal injections on hypoxia days 21–31. Lung Zs + SMCs were isolated by FACS, and expression levels of Atg5 , Atg7 , Becn1 , and Map1lc3b with hypoxia relative to normoxia, no STI571 were analyzed by qRT-PCR. n = 3 mice (2 males, 1 female) per experimental group. ( C ) Vibratome lung sections were stained for Beclin1, SMA, and nuclei (DAPI). Closeups of boxed regions are shown below. ( D ) Quantification of the percentage of distal arteriole SMCs that are Belclin1 + . n = 3 mice (1 male, 2 female) per experimental group, 3–4 arterioles analyzed per mouse. Significance assessed by multifactor ANOVA with Tukey’s multiple-comparison test ( B and D ). Scale bar: 20 μm.

Article Snippet: Starting on hypoxia day 21, mice received daily intraperitoneal injections of STI571 (imatinib mesylate, Selleckchem, S1026) at a dose of 50–100 mg/kg suspended in 0.9% sterile saline for 10 days, as previously described ( ).

Techniques: Isolation, Expressing, Quantitative RT-PCR, Staining, Comparison