Organisation of the chicken annexin V gene and its correlation with the tertiary structure of the protein

Pfannmüller, Eva; Turnay, Javier; Bertling, Wolf; Mark, Klaus von der

doi:10.1016/0014-5793(93)80857-q

Cited by 15 publications

(14 citation statements)

References 26 publications

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“…Mouse and rat annexin A5 genes present two promoter regions; different transcripts and alternatively spliced mRNA species have been detected [Imai and Kohsaka, 1995;Rodrõ Âguez-Garcõ Âa et al, 1999]. However, we have only detected a unique transcript for chicken annexin A5; moreover, the analysis of its gene revealed only one promoter and the absence of TATA boxes and other cis-regulatory elements [Pfannmu È ller et al, 1993;Ferna Ândez et al, 1994], suggesting that the annexin A5 gene might be more related to that of a housekeeping gene. Here we show for the ®rst time that at least two regulatory mechanisms exist which control annexin A5 expression in a developmental and an environmentally regulated manner.…”

Section: Discussionmentioning

confidence: 73%

“…However, it reappears in the calci®cation zone of hypertrophic cartilage, both in hypertrophic chondrocytes and in osteoblasts as detected by in situ hybridization and by immunohistochemistry [Hofmann et al, 1992;Kirsch et al, 1997]. We have previously reported on the structure of the chicken annexin A5 gene and shown that the promoter region lacks the typical TATA-box but contains a GCrich region, with multiple Sp1 sites typical of housekeeping genes which may possibly promote transcription from several start sites [Pfannmu È ller et al, 1993]. Little is still known, however, on the regulatory mechanisms of annexin gene expression and on its regulation by growth stimuli, such as the c-fos protooncogene [Braselmann et al, 1992], cell differentiation degree [Hofmann et al, 1992;Kirsch et al, 1997], or even in cartilage diseases such as osteoarthritis [Mollenhauer et al, 1999;Kirsch et al, 2000b].…”

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confidence: 93%

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Changes in the expression of annexin A5 gene during in vitro chondrocyte differentiation: Influence of cell attachment

Turnay

Olmo

Lizarbe

et al. 2001

J of Cellular Biochemistry

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Several lines of evidence indicate that annexin A5, a membrane-associated protein with calcium-channel activity, plays a key role in cartilage calcification during endochondral ossification. As a major constituent of cartilage matrix vesicles, which are released from microvilli of hypertrophic chondrocytes, it is involved in calcium uptake necessary for the initial stages of cartilage calcification. Little is known, however, concerning transcriptional regulation of the annexin A5 gene during chondrocyte differentiation. Here, we report on changes in annexin A5 expression by measuring mRNA and protein levels during in vitro differentiation of chick sternal chondrocytes to the hypertrophic phenotype. Terminal differentiation of mature sternal chondrocytes was achieved in the presence of sodium ascorbate in high-density cultures growing either in monolayer or over agarose as cell aggregates. Differentiation of chondrocytes to hypertrophic cells was followed by morphological analysis and by the onset of type X collagen expression. High expression levels of annexin A5 mRNA were detected in chondrocytes freshly isolated from the sterna by enzymatic digestion and subsequently in cells growing in monolayer, but annexin A5 gene transcription was rapidly downregulated when cells were grown in suspension as aggregates over agarose. However, protein levels did not decrease probably due to its low turnover rate. In suspension culture, annexin A5 mRNA reappeared after 3 weeks concomitantly with segregation of the aggregates into single cells and onset of chondrocyte hypertrophy. The downregulation of annexin A5 expression in cells growing as matrix-rich aggregates was reverted when extracellular matrix components were removed and cells were reseeded onto tissue culture plastic, suggesting that cell spreading, formation of focal contacts and stress fibers stimulated annexin A5 expression in proliferating as well as in hypertrophic chondrocytes.

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Section: Discussionmentioning

confidence: 73%

mentioning

confidence: 93%

Changes in the expression of annexin A5 gene during in vitro chondrocyte differentiation: Influence of cell attachment

Turnay

Olmo

Lizarbe

et al. 2001

J of Cellular Biochemistry

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Section: Anchorin CII a Collagen-binding Protein Of The Annexin Familymentioning

confidence: 99%

“…Preliminary evidence was presented for tissue-specific differences of annexins from chondrocytes, bone cells, fibroblasts or other tissues [5]. The analysis of the annexin V gene, however, provided no evidence for more than one annexin V gene, splice variants or isoforms [6,7].The concept of anchorin CII as a collagen-receptor of chondrocyte membranes was consistent with its localization on the chondrocyte surface by immunofluorescence [2]. This was questioned, however, when the analysis of the protein structure [8] revealed homology to calpactin I and lipocortin II, and thus documented the absence of a hydrophobic signal peptide and transmembrane sequences.…”

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confidence: 99%

Annexin V interactions with collagen

Mark

Mollenhauer

1997

Cellular and Molecular Life Sciences (CMLS)

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Annexin V was originally identified as a collagen-binding protein called anchorin CII and was isolated from chondrocyte membranes by affinity chromatography on native type II collagen. The binding of annexin V to native collagen type II is stable at physiological ionic strength when annexin V is reconstituted in liposomes. The binding to native collagen types II and X, and to some extent to type I as well, was confirmed using recombinant annexin V. A physiological role for annexin V interactions with extracellular collagen is consistent with the localization of annexin V on the outer cell surface of chondrocytes, microvilli of hypertrophic chondrocytes, fibroblasts and osteoblasts. A breakthrough in our understanding of the function of annexin V was made with the discovery of its calcium channel activity. At least one of several putative functions of annexin V became obvious from studies on matrix vesicles derived from calcifying cartilage. It was found that calcium uptake by matrix vesicles depend on collagen type II and type X binding to annexin V in the vesicles and was lost when collagens were digested with collagenase: calcium influx was reconstituted after adding back native collagen II or V. These findings indicate that annexin V plays a major role in matrix vesicle-initiated cartilage calcification as a collagen-regulated calcium channel.

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“…(13) Briefly, a full-length chicken annexin II, chicken annexin V, and human annexin VI complementary DNA (cDNA) clones were subcloned into the pGEX expression vector. (29)(30)(31) Recombinant annexin II, V, and VI glutathione S-transferase (GST) fusion proteins were expressed in Escherichia coli DH5␣FЈ and purified. The fusion proteins were subjected to PreScission protease (Pharmacia, Piscataway, NJ, USA) cleavage to release the annexin molecules from the GST moiety.…”

Section: Recombinant Annexin II V and Vi Moleculesmentioning

confidence: 99%

Regulatory Roles of Zinc in Matrix Vesicle-Mediated Mineralization of Growth Plate Cartilage

Kirsch

Harrison

Worch

et al. 2000

Journal of Bone and Mineral Research

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Zinc (Zn 2؉ ) has long been known to play important roles in mineralization and ossification of skeletal tissues, but the mechanisms of Zn 2؉ action are not well understood. In this study we investigated the effects of Zn 2؉ on mineralization in a cell culture system in which terminal differentiation and mineralization of hypertrophic growth plate chondrocytes was induced by retinoic acid (RA) treatment. Addition of Zn 2؉ to RA-treated cultures decreased mineralization in a dose-dependent manner without affecting alkaline phosphatase (APase) activity. Characterization of matrix vesicles (MVs), particles that initiate the mineralization process, revealed that vesicles isolated from RA-treated and RA/Zn 2؉ -treated cultures showed similar APase activity, but vesicles from RA/Zn 2؉ -treated cultures contained significantly less Ca 2؉ and P i . MVs isolated from RA-treated cultures were able to take up Ca 2؉ and mineralize in vitro, whereas vesicles isolated from RA/Zn 2؉ -treated cultures were not able to do so. Detergent treatment, which ruptures the MV membrane and exposes preformed intravesicular Ca 2؉ -P i -phospholipid complexes, did not restore the Ca 2؉

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Organisation of the chicken annexin V gene and its correlation with the tertiary structure of the protein

Cited by 15 publications

References 26 publications

Changes in the expression of annexin A5 gene during in vitro chondrocyte differentiation: Influence of cell attachment

Changes in the expression of annexin A5 gene during in vitro chondrocyte differentiation: Influence of cell attachment

Annexin V interactions with collagen

Regulatory Roles of Zinc in Matrix Vesicle-Mediated Mineralization of Growth Plate Cartilage

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