Anti-ALDOA monoclonal antibody, clone FQS0835(C)

Increased production of methylglyoxal (MG) in vascular tissues is one of the causative factors for vascular remodelling in different subtypes of metabolic syndrome, including hypertension and insulin resistance. Fructose-induced up-regulation of aldolase B (AldoB) contributes to increased vascular MG production but the underlying mechanisms are unclear. Serum levels of MG and fructose were determined in diabetic patients with hypertension. MG level had significant positive correlations with blood pressure and fructose level respectively. C57BL/6 mice were fed with control or fructose-enriched diet for 3 months and ultrasonographic and histologic analyses were performed to evaluate arterial structural changes. Fructose-fed mice exhibited hypertension and high levels of serum MG with normal glucose level. Fructose intake increased blood vessel wall thickness and vascular smooth muscle cell (VSMC)proliferation. Western blotting and real-time PCR analysis revealed that AldoB level was significantly increased in both the aorta of fructose-fed mice and the fructose-treated VSMCs, whereas aldolase A (AldoA) expression was not changed. The knockdown of AldoB expression prevented fructose-induced MG overproduction and VSMC proliferation. Moreover, fructose significantly increased carbohydrate-responsive element-binding protein (ChREBP), phosphorylated FoxO1/3 alpha and Akt1 levels. Fructose induced translocation of ChREBP from the cytosol to nucleus and activated AldoB gene expression, which was inhibited by the knockdown of ChREBP. Meanwhile, fructose caused FoxO1/3 alpha shuttling from the nucleus to cytosol and inhibited its binding to AldoB promoter region. Fructose-induced AldoB up-regulation was suppressed by Akt1 inhibitor but enhanced by FoxO1/3 alpha siRNA. Collectively, fructose activates ChREBP and inactivates FoxO1/3 alpha pathways to up-regulate AldoB expression and MG production, leading to vascular remodelling.

BACKGROUND: Osteosarcoma, which is also termed osteogenic sarcoma or osteoma sarcomatosum, is the most common form of bone cancer. Typical osteosarcoma can occur at any age, including in infants, children, and the elderly, but more than half of cases occur in individuals who are 10-20 years old. OBJECTIVE: Here, the objective was to search for protein markers to indicate resistance to cisplatin in osteosarcoma and provide a theoretical basis for the early and accurate use of cisplatin to treat osteosarcoma. METHODS: Thirty patients with osteosarcoma were selected for the study. Experimental studies on the chemosensitivity of osteosarcoma using an in vitro kit method were performed, and cisplatin-resistant and cisplatin-sensitive osteosarcoma tissues were obtained. A representative sample was chosen to analyze and identify differentially expressed proteins in cisplatin-resistant tissues. RESULTS: The osteosarcoma-sensitive tissue was analyzed using 2-D electrophoresis and time-of-flight mass spectrometry. Differently expressed proteins were analyzed by western blotting to identify markers. Cisplatin-resistant and cisplatin-sensitive osteosarcoma tissues were obtained. Five significantly differentially expressed proteins were identified, including ALDOA and PGK1. CONCLUSIONS: The results indicate that ALDOA and PGK1 might be appropriate markers that can be used when treating osteosarcoma with cisplatin.