Anti_Mouse, pab VEGF_A Source Rabbit
- Known as:
- Anti_Mouse, pab VEGF_A Source Rabbit
- Catalog number:
- 103-PA03S
- Product Quantity:
- 100 µg
- Category:
- -
- Supplier:
- Reliatech
- Gene target:
- Anti_Mouse pab VEGF_A Source Rabbit
Related genes to: Anti_Mouse, pab VEGF_A Source Rabbit
- Gene:
- VEGFA NIH gene
- Name:
- vascular endothelial growth factor A
- Previous symbol:
- VEGF
- Synonyms:
- VEGF-A, VPF
- Chromosome:
- 6p21.1
- Locus Type:
- gene with protein product
- Date approved:
- 1994-01-10
- Date modifiied:
- 2016-10-05
Related products to: Anti_Mouse, pab VEGF_A Source Rabbit
Related articles to: Anti_Mouse, pab VEGF_A Source Rabbit
- Management of highly refractory exudative neovascular age-related macular degeneration (nAMD) remains challenging when multiple antivascular endothelial growth factor (VEGF) therapies fail to control the disease. Faricimab, through dual inhibition of VEGF-A and angiopoietin-2, may represent a potential therapeutic alternative for this difficult-to-treat population. However, real-world evidence in highly refractory nAMD remains limited and is lacking in the Portuguese population. - Source: PubMed
Publication date: 2026/07/14
Mira FilipeDonato SofiaVaz FernandaMadeira FilipaPicoto MariaMendes AntónioBeato JoãoTorres-Costa SóniaPinto CarolinaOliveira NunoFeliciano SusanaLume MiguelCarreiro RitaCouto MarianaCarneiro Ângela - Exemestane (EMT) is a third-generation steroidal aromatase inhibitor extensively used in hormone receptor (HR)-positive breast cancer therapy and has been known to exert cardiovascular effects during prolonged treatment. The current study was planned to investigate the dose-dependent cardiotoxic effects of EMT. Thirty-two Sprague Dawley rats were randomly divided into four groups i.e., control group, EMT (5mg/kg), EMT (15mg/kg) and EMT (25mg/kg) groups. Gene expression analysis showed downregulated expression of ATP2A2 (SERCA2a), CACNA1C, NOS3 (eNOS) and KLF2 coupled with marked upregulation in the expression of RYR2, PLN, CAMK2D, VEGFA, EDN1 and ICAM1, suggesting impaired calcium handling and endothelial dysfunction. The antioxidant enzymes (CAT, SOD, GPx, GST, GSR, HO-1 and GSH) were decreased significantly by EMT while the concentrations of ROS and MDA were increased in dose-dependent manner. Cardiac function assessment by echocardiography showed that EMT caused dose-dependent cardiac dysfunction as evidenced by reduced heart rate, wall thickness and cardiac chamber volumes of the ventricles thereby suggesting progressive ventricular remodeling, myocardial hypertrophy, and chamber enlargement particularly at 25mg/kg EMT administration. Furthermore, EMT intoxication caused elevation in the levels of CK-MB, CPK, troponins, LDH, BNP, NT-proBNP and CRP. Significant upregulation observed in the levels of NF-κB, TNF-α, IL-1β, IL-6 and COX-2 after EMT administration. Moreover, EMT exposure promoted the levels of Bax, Caspase-3 and Caspase-9 while suppressing the levels of Bcl-2. Histopathological analysis demonstrated progressive myocardial degeneration, edema, inflammatory infiltration and peripheral necrosis. Overall, chronic EMT exposure leads to severe, dose-dependent cardiotoxicity, characterized by calcium dysregulation, oxidative stress, inflammatory responses, endothelial dysfunction and apoptosis, and thus warrants cardiac monitoring during prolonged EMT therapy. - Source: PubMed
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Alotaibi Reem NasserHayat Muhammad FaisalJamil SalimHassan Hesham MHalawani Ibrahim FAlzahrani Fuad MAlzahrani Khalid J - Extracorporeal shock wave therapy (ESWT) improves tendon-bone healing after rotator cuff injury (RCI), but its underlying cellular mechanisms remain unknown. This study aimed to explore the therapeutic effects of ESWT on RCI, with a particular focus on endothelial cells and tenocytes. The RCI model was established in rabbits by rotator cuff tear surgery, followed by ESWT intervention. Histological evaluation, blood perfusion analysis, biomechanical testing, and assessment of inflammation and extracellular matrix (ECM) degradation were performed in RCI-treated rabbits at week (W) 2, W4, and W8. For the in vitro experiments, human umbilical vein endothelial cells (HUVECs) and human tenocytes were treated with ESWT. ESWT reduced Bonar scores, increased the fibrocartilage area and collagen-positive area, and enhanced blood perfusion and biomechanical strength at most time points in RCI rabbits (all p < 0.05). Moreover, ESWT reduced inflammation and ECM degradation, as reflected by reduced tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and IL-6 and decreased matrix metalloproteinase (MMP)-1 and MMP-9 at most time points in RCI rabbits (all p < 0.05). In HUVECs, ESWT increased proliferation, invasion, branch points, MMP-2, MMP-9, vascular endothelial growth factor A (VEGFA), and fibroblast growth factor 2 (FGF2) (all p < 0.05). In tenocytes, ESWT increased proliferation, collagen I, thrombospondin-4 (TSP4), VEGFA, FGF2, tenomodulin (TNMD), and scleraxis (SCX) (all p < 0.05). ESWT improves tendon integrity, blood perfusion, and biomechanical strength while reducing inflammation and ECM degradation after RCI, possibly via enhanced angiogenic activity in endothelial cells and maintenance of the tenogenic phenotype in tenocytes. - Source: PubMed
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