Annexin I and dexamethasone effects on phospholipase and cyclooxygenase activity in human synoviocytes

Sampey, Annaleise V.; Hutchinson, Paul; Morand, Eric Francis

doi:10.1080/09629350020018357

Cited by 18 publications

(13 citation statements)

References 45 publications

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“…In rheumatic diseases, the increases expression of ANXA1 in rheumatoid synovium and its inhibitory actions in animal models of arthritis suggests its involvement in human arthritis [32,33]. Regarding its role in OA, it has been reported that TNF-a and IL-1b increased ANXA1-binding sites on OA FLS [34].…”

Section: Discussionmentioning

confidence: 99%

Proteomic analysis of human osteoarthritic chondrocytes reveals protein changes in stress and glycolysis

et al. 2008

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Osteoarthritis (OA) is characterized by cartilage degradation. The chondrocyte is the only cell type present in mature cartilage, and it is important in the control of cartilage integrity. The aim of this study was to analyze, by a proteomic approach, the changes that are characteristic of OA chondrocytes, and to identify new OA-related proteins. Chondrocytes were isolated from the cartilage of ten OA patients undergoing joint replacement and ten donors with no history of joint disease. Whole-cell proteins were resolved by 2-DE and stained with SYPRO Ruby. Protein expression patterns of 2-DE gels from OA and normal chondrocyte proteins were analyzed with PDQuest 7.3.1 software. OA-related proteins were identified by MALDI-TOF or MALDI-TOF/TOF MS. The results were validated for ANXA1, GSTO1, GRP78, and HSP90beta in cells by Western blotting and in tissue cartilage by immunohistochemistry. Results showed an average of 700 protein spots that were present in the 2-DE gels. Compared to normal chondrocytes, 19 protein spots were found to be significantly increased in OA cells (ratio OA:N> or =2.0, p<0.05), whereas nine were decreased in OA chondrocytes (ratio OA:N< or =0.5, p<0.05). Three stress response proteins were increased (HSP90beta, GRP78, and GRP94) and three proteins involved in glycolysis were decreased (enolase, glyceraldehyde 3-phosphate dehydrogenase, and fructose biphosphate aldolase). Functionally, almost all proteins could be classified as proteins involved in cellular metabolism (33%), structure (21%), or protein targeting (21%).

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Section: Discussionmentioning

confidence: 99%

Proteomic analysis of human osteoarthritic chondrocytes reveals protein changes in stress and glycolysis

et al. 2008

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“…The protein was also secreted by the activated microglia [22]. Interestingly, the inhibition of COX-2 expression appears to be a unique feature of ANXA1 in microglia inasmuch as it has not been observed in macrophages [18], in A549 cells [23], or in synoviocytes [24].…”

Section: Effects Of Annexin 1 On Inducible Cyclooxygenase and Nitric mentioning

confidence: 92%

Annexin 1: more than an anti-phospholipase protein

Parente

Solito

2004

Inflammation Research

263

206

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Annexin 1 (ANXA1) is the first characterized member of the annexin family of proteins able to bind (i.e. to annex) to cellular membranes in a calcium-dependent manner. ANXA1 may be induced by glucocorticoids in inflammatory cells and shares with these drugs many anti-inflammatory effects. Originally described as a phospholipase A2 (PLA2)-inhibitory protein, ANXA1 can affect many components of the inflammatory reaction besides the metabolism of arachidonic acid. Recent data have shown that ANXA1 may specifically target cytosolic PLA2 by both direct enzyme inhibition and suppression of cytokine-induced activation of the enzyme. ANXA1 inhibits the expression and/or activity of other inflammatory enzymes like inducible nitric oxide synthase (iNOS) in macrophages and inducible cyclooxygenase (COX-2) in activated microglia. The inhibition of iNOS expression may be caused by the stimulation of IL-10 release induced by ANXA1 in macrophages. Like glucocorticoids, ANXA1 exerts profound inhibitory effects on both neutrophil and monocyte migration in inflammation. Several mechanisms may contribute to the protein effect on cell migration, namely the activation of receptors like the formyl peptide receptor (FPR) and the lipoxin A4 receptor (ALXR), the shedding of L-selectin, the binding to alpha4beta1 integrin and carboxylated N-glycans. Furthermore, again mimicking the action of glucocorticoids, ANXA1 promotes inflammatory cell apoptosis associated with transient rise in intracellular calcium and caspase-3 activation. Finally, ANXA1 has been recently identified as one of the 'eat-me' signals on apoptotic cells to be recognised and ingested by phagocytes. Thus, ANXA1 may contribute to the anti-inflammatory signalling that allows safe post-apoptotic clearance of dead cells.

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“…The activation of PPARG can also suppress expression of the PTGS2 gene [124]. Further, the expression of the PTGS2 gene can be up-regulated by IL1B [125,126]. In turn, IL1B can significantly suppress CTGF gene expression [127], of which expression can be induced by p53 protein [128].…”

Section: Apoptosis In Asthma/hypertension Gene Networkmentioning

confidence: 98%

Novel candidate genes important for asthma and hypertension comorbidity revealed from associative gene networks

et al. 2018

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Background: Hypertension and bronchial asthma are a major issue for people's health. As of 2014, approximately one billion adults, or~22% of the world population, have had hypertension. As of 2011, 235-330 million people globally have been affected by asthma and approximately 250,000-345,000 people have died each year from the disease. The development of the effective treatment therapies against these diseases is complicated by their comorbidity features. This is often a major problem in diagnosis and their treatment. Hence, in this study the bioinformatical methodology for the analysis of the comorbidity of these two diseases have been developed. As such, the search for candidate genes related to the comorbid conditions of asthma and hypertension can help in elucidating the molecular mechanisms underlying the comorbid condition of these two diseases, and can also be useful for genotyping and identifying new drug targets. Results: Using ANDSystem, the reconstruction and analysis of gene networks associated with asthma and hypertension was carried out. The gene network of asthma included 755 genes/proteins and 62,603 interactions, while the gene network of hypertension -713 genes/proteins and 45,479 interactions. Two hundred and five genes/proteins and 9638 interactions were shared between asthma and hypertension. An approach for ranking genes implicated in the comorbid condition of two diseases was proposed. The approach is based on nine criteria for ranking genes by their importance, including standard methods of gene prioritization (Endeavor, ToppGene) as well as original criteria that take into account the characteristics of an associative gene network and the presence of known polymorphisms in the analysed genes. According to the proposed approach, the genes IL10, TLR4, and CAT had the highest priority in the development of comorbidity of these two diseases. Additionally, it was revealed that the list of top genes is enriched with apoptotic genes and genes involved in biological processes related to the functioning of central nervous system.

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Annexin I and dexamethasone effects on phospholipase and cyclooxygenase activity in human synoviocytes

Cited by 18 publications

References 45 publications

Proteomic analysis of human osteoarthritic chondrocytes reveals protein changes in stress and glycolysis

Proteomic analysis of human osteoarthritic chondrocytes reveals protein changes in stress and glycolysis

Annexin 1: more than an anti-phospholipase protein

Novel candidate genes important for asthma and hypertension comorbidity revealed from associative gene networks

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