Aldolase B (ALDOB), a glycolytic enzyme, is uniformly depleted in clear cell renal cell carcinoma (ccRCC) tissues. We previously showed that ALDOB inhibited proliferation through a mechanism independent of its enzymatic activity in ccRCC, but the mechanism was not unequivocally identified. We showed that the corepressor C-terminal-binding protein 2 (CtBP2) is a novel ALDOB-interacting protein in ccRCC. The CtBP2-to-ALDOB expression ratio in clinical samples was correlated with the expression of CtBP2 target genes and was associated with shorter survival. ALDOB inhibited CtBP2-mediated repression of multiple cell cycle inhibitor, proapoptotic, and epithelial marker genes. Furthermore, ALDOB overexpression decreased the proliferation and migration of ccRCC cells in an ALDOB-CtBP2 interaction-dependent manner. Mechanistically, our findings showed that ALDOB recruited acireductone dioxygenase 1, which catalyzes the synthesis of an endogenous inhibitor of CtBP2, 4-methylthio 2-oxobutyric acid. ALDOB functions as a scaffold to bring acireductone dioxygenase and CtBP2 in close proximity to potentiate acireductone dioxygenase-mediated inhibition of CtBP2, and this scaffolding effect was independent of ALDOB enzymatic activity. Moreover, increased ALDOB expression inhibited tumor growth in a xenograft model and decreased lung metastasis in vivo. Our findings reveal that ALDOB is a negative regulator of CtBP2 and inhibits tumor growth and metastasis in ccRCC.
Humans ; Carcinoma, Renal Cell/genetics* ; Fructose-Bisphosphate Aldolase/metabolism* ; Co-Repressor Proteins/metabolism* ; Transcription Factors/genetics* ; Kidney Neoplasms/genetics* ; Cell Line, Tumor ; Cell Proliferation/genetics* ; Gene Expression Regulation, Neoplastic

It is of great significance to use biosynthesis to transform the inorganic substance formaldehyde into organic sugars. Most important in this process was to find a suitable catalyst combination to achieve the dimerization of formaldehyde. In a recent report, an engineered glycolaldehyde synthase was reported to catalyze this reaction. It could be combined with engineered D-fructose-6-phosphate aldolase, a "one-pot enzyme" method, to synthesize L-xylose using formaldehyde and the conversion rate could reach up to 64%. This process also provides a reference for the synthesis of other sugars. With the increasing consumption of non-renewable resources, it was of great significance to convert formaldehyde into sugar by biosynthesis.
Biocatalysis ; Formaldehyde ; chemistry ; Fructose-Bisphosphate Aldolase ; metabolism ; Xylose ; chemical synthesis

BACKGROUND AND PURPOSE: Amyloid beta (Aβ) is the main component of amyloid plaques, which are deposited in the brains of patients with Alzheimer's disease (AD). Biochemical and animal studies support the central role of Aβ in AD pathogenesis. Despite several investigations focused on the pathogenic mechanisms of Aβ, it is still unclear how Aβ accumulates in the central nervous system and subsequently initiates the disease at the cellular level. In this study, we investigated the pathogenic mechanisms of Aβ using proteomics and antibody microarrays. METHODS: To evaluate the effect of Aβ on neural stem cells (NSCs), we treated primary cultured cortical NSCs with several doses of Aβ for 48 h. A 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide assay, trypan blue staining, and bromodeoxyuridine cell proliferation assay were performed. We detected several intracellular proteins that may be associated with Aβ by proteomics and Western blotting analysis. RESULTS: Various viability tests showed that Aβ decreased NSCs viability and cell proliferation in a concentration-dependent manner. Aβ treatment significantly decreased lactate dehydrogenase B, high-mobility group box 1, aldolase C, Ezrin, and survival signals including phosphorylated phosphoinositide 3-kinase, Akt, and glycogen synthase kinase-3β. CONCLUSIONS: These results suggest that several factors determined by proteomics and Western blot hold the clue to Aβ pathogenesis. Further studies are required to investigate the role of these factors.
Alzheimer Disease ; Amyloid* ; Animals ; Blotting, Western ; Brain ; Bromodeoxyuridine ; Cell Proliferation ; Central Nervous System ; Fructose-Bisphosphate Aldolase ; Glycogen Synthase ; Humans ; L-Lactate Dehydrogenase ; Neural Stem Cells* ; Plaque, Amyloid ; Proteomics ; Trypan Blue

OBJECTIVE: To investigate the association between angiopoietin-like 4 (ANGPTL4) and aldolase A (ALDOA) in human melanoma cell. 
 METHODS: Overexpression or knockdown of ANGPTL4 was performed in WM-115 or WM-266-4 cells, respectively. The expression of ANGPTL4 and ALDOA was measured by RT-PCR and Western blot, respectively. The promoter activity of ALDOA gene was determined by luciferase assay.
 RESULTS: The promoter activity of ALDOA gene and the expression of ALDOA (mRNA and protein) were increased or decreased in the melanoma cells with overexpression or knockdown of ANGPTL4, which was blocked by selective protein kinase C (PKC) inhibitor or restored by PKC agonist, respectively.
 CONCLUSION ANGPTL4 promotes ALDOA expression in human melanoma cell in a PKC dependent manner.
Angiopoietin-like 4 Protein ; Angiopoietins ; genetics ; metabolism ; Blotting, Western ; Cell Line, Tumor ; Fructose-Bisphosphate Aldolase ; metabolism ; Gene Knockdown Techniques ; Humans ; Melanoma ; genetics ; metabolism ; RNA, Messenger ; genetics ; metabolism

BACKGROUND: We intended to clarify the hypothesis that minimally invasive total hip arthroplasty (MI-THA) leads to less tissue damage and inflammatory response than does conventional total hip arthroplasty (C-THA). METHODS: We performed 30 cases of THA between September 2005 and May 2006 and evaluated these cases prospectively. We chose 15 MI-THA cases for the study group and another 15 C-THA cases for the control group. We checked skeletal muscle marker enzymes, such as serum creatinine kinase and aldolase, the pro-inflammatory cytokines, interleukin (IL)-6 and 8, and the anti-inflammatory cytokines, IL-10 and IL-1 receptor antagonist (ra) the day before surgery and at postoperative days 1, 7, and 14. RESULTS: On postoperative days 1 and 3, the study group showed significantly lower serum creatinine kinase, IL-6, IL-10, and IL-1ra values than those in the control group. Additionally, IL-8 was significantly lower on day 7 after surgery. CONCLUSIONS: These data show that MI-THA decreased the release of muscle marker enzymes due to tissue damage immediately after surgery and minimized the inflammatory response related to the surgery during the early postoperative period.
Adult ; Aged ; Aged, 80 and over ; Arthroplasty, Replacement, Hip/*adverse effects ; Biological Markers/blood ; Creatine Kinase/blood ; Female ; Fructose-Bisphosphate Aldolase/blood ; Humans ; Interleukin 1 Receptor Antagonist Protein/blood ; Interleukin-10/blood ; Interleukin-6/blood ; Interleukin-8/blood ; Male ; Middle Aged ; Minimally Invasive Surgical Procedures/adverse effects ; Soft Tissue Injuries/*blood/etiology

BACKGROUND AND PURPOSE: Hypoxia, or ischemia, is a common cause of neurological deficits in the elderly. This study elucidated the mechanisms underlying ischemia-induced brain injury that results in neurological sequelae. METHODS: Cerebral ischemia was induced in male Sprague-Dawley rats by transient ligation of the left carotid artery followed by 60 min of hypoxia. A two-dimensional differential proteome analysis was performed using matrix-assisted laser desorption ionization-time-of-flight mass spectrometry to compare changes in protein expression on the lesioned side of the cortex relative to that on the contralateral side at 0, 6, and 24 h after ischemia. RESULTS: The expressions of the following five proteins were up-regulated in the ipsilateral cortex at 24 h after ischemia-reperfusion injury compared to the contralateral (i.e., control) side: aconitase 2, neurotensin-related peptide, hypothetical protein XP-212759, 60-kDa heat-shock protein, and aldolase A. The expression of one protein, dynamin-1, was up-regulated only at the 6-h time point. The level of 78-kDa glucose-regulated protein precursor on the lesioned side of the cerebral cortex was found to be high initially, but then down-regulated by 24 h after the induction of ischemia-reperfusion injury. The expressions of several metabolic enzymes and translational factors were also perturbed soon after brain ischemia. CONCLUSIONS: These findings provide insights into the mechanisms underlying the neurodegenerative events that occur following cerebral ischemia.
Aconitate Hydratase ; Aged ; Anoxia ; Brain Injuries ; Brain Ischemia ; Carotid Arteries ; Cerebral Cortex* ; Dynamin I ; Fructose-Bisphosphate Aldolase ; Geriatrics ; Heat-Shock Proteins ; Humans ; Ischemia ; Ligation ; Male ; Mass Spectrometry ; Proteome ; Proteomics ; Rats, Sprague-Dawley ; Reperfusion Injury*

Proximal muscle weakness can be induced by many diseases, such as muscular dystrophies, inflammatory muscle diseases, and polymyalgia rheumatica. Differential diagnosis of these diseases is important. The patient had proximal muscle weakness with a normal creatine kinase (CK) level. Our initial diagnosis was polymyalgia rheumatica because the CK level was normal. The patient was treated with low-dose corticosteroid. However, the muscle weakness did not improve. The diagnosis of polymyositis was confirmed by a muscle biopsy. We suggest that if the patient has typical symptoms with normal CK, then evaluations for inflammatory muscle diseases are essential.
Biopsy ; Creatine Kinase* ; Creatine* ; Diagnosis ; Diagnosis, Differential ; Fructose-Bisphosphate Aldolase ; Humans ; Muscle Weakness ; Muscles ; Muscular Dystrophies ; Myositis ; Polymyalgia Rheumatica ; Polymyositis*

This study aimed to evaluate the efficacy of fructose-1,6-bis phosphate aldolase (SMALDO) DNA vaccination against Schistosoma mansoni infection using different routes of injection. The SMALDO has been cloned into the eukaryotic expression vector pcDNA3.1/V5-His TOPO-TA and was used in injecting Swiss albino mice intramuscularly (IM), subcutaneously (SC), or intraperitoneally (IP) (50 microg/mouse). Mice vaccinated with non-recombinant pcDNA3.1 served as controls. Each group was immunized 4 times at weeks 0, 2, 4, and 6. Two weeks after the last booster dose, all mice groups were infected with 80 S. mansoni cercariae via tail immersion. At week 8 post-infection, animals were sacrificed for assessment of parasitological and histopathological parameters. High anti-SMALDO IgG antibody titers were detected in sera of all vaccinated groups (P<0.01) compared to the control group. Both the IP and SC vaccination routes resulted in a significant reduction in worm burden (46.2% and 28.9%, respectively, P<0.01). This was accompanied by a significant reduction in hepatic and intestinal egg counts (41.7% and 40.2%, respectively, P<0.01) in the IP group only. The number of dead eggs was significantly increased in both IP and IM groups (P<0.01). IP vaccination recorded the highest significant reduction in granuloma number and diameter (54.7% and 29.2%, respectively, P<0.01) and significant increase in dead miracidia (P<0.01). In conclusion, changing the injection route of SMALDO DNA vaccination significantly influenced the efficacy of vaccination. SMALDO DNA vaccination via IP route could be a promising protective and anti-pathology vaccine candidate against S. mansoni infection.
Animals ; Antibodies, Helminth/blood ; Disease Models, Animal ; Female ; Fructose-Bisphosphate Aldolase/genetics/*immunology ; Histocytochemistry ; Immunoglobulin G/blood ; Injections, Intramuscular ; Injections, Intraperitoneal ; Injections, Subcutaneous ; Mice ; Parasite Load ; Schistosoma mansoni/enzymology/genetics/*immunology ; Schistosomiasis mansoni/immunology/parasitology/pathology/*prevention & control ; Vaccination/methods ; Vaccines, DNA/administration & dosage/genetics/*immunology ; Vaccines, Synthetic/administration & dosage/genetics/immunology

OBJECTIVE: The idiopathic inflammatory myopathies (IIMs) are chronic systemic connective tissue diseases. The muscle biopsy is a definitive diagnostic tool but blind biopsy sometimes produces to negative results. Magnetic resonance imaging (MRI) as a tool for early diagnosis, guidance for biopsy, assessing extent of lesions and monitoring therapy in IIMs has been reported. The aim of this study is to assess the association of thigh inflammation through MRI and biopsy specimens with clinical findings. METHODS: Sixty patients diagnosed with dermatomyositis (DM) or polymyositis (PM) from 2004 to 2011 in one center of rheumatology were enrolled. We reviewed clinical, laboratory, histopathologic and MRI of thigh data at initial diagnosis. The inflammation grades by MRI and histopathology of muscles were evaluated through 4-point scoring systems. RESULTS: The laboratory findings for aldolase and CK differed significantly between DM patients (68.3%) and PM patients (31.7%). Fasciitis was detected by MRI in 43.3% of patients, of whom 88.5% had DM (p<0.05). The fasciitis was also associated with myalgia (p<0.05). Almost all MRI findings were symmetric except for two patients. The mean of total signal intensity was higher in patients with decreased muscle power. The signal intensity of affected muscle was slightly associated with muscle enzymes and histopathologic grading. CONCLUSION: Fasciitis was observed more in DM patients. MRI findings were associated with muscle enzymes and histopathologic grading. Signal intensity on MRI may be useful for measurement of disease activity in acute IIMs. The noninvasive nature and high sensitivity of muscle inflammation suggest that MRI images should be considered prior to muscle biopsy and treatment of IIMs.
Biopsy ; Connective Tissue Diseases ; Dermatomyositis ; Early Diagnosis ; Fasciitis ; Fructose-Bisphosphate Aldolase ; Humans ; Inflammation ; Magnetic Resonance Imaging* ; Magnetics* ; Magnets* ; Muscles ; Myositis* ; Polymyositis ; Rheumatology ; Thigh

A 48-year-old male visited the emergency room of the authors' hospital due to nausea, vomiting, and myalgia for four days. Acute hepatitis A was identified from the serologic marker of the hepatitis A virus. Mild elevation of the serum creatinine and creatinine phosphokinase (CPK) suggested rhabomyolysis, which was confirmed with the serum aldolase, myoglobin, and urine myoglobin. With supportive care, both the liver and renal functions were recovered gradually and fully. This case shows that rhabdomyolysis can be one of the mechanisms of renal complication in cases of acute symptomatic hepatitis A.
Acute Kidney Injury ; Creatinine ; Emergencies ; Fructose-Bisphosphate Aldolase ; Hepatitis ; Hepatitis A ; Hepatitis A virus ; Humans ; Kidney ; Liver ; Male ; Middle Aged ; Myoglobin ; Nausea ; Rhabdomyolysis ; Vomiting