Cloning and characterization of five overlapping cDNAs specific for the human proα 1(I) collagen chain

Chu, Mon‐Li; Myers, Jeanne C.; Bernard, Michael P.; Ding, Jixiang; Ramirez, Francesco

doi:10.1093/nar/10.19.5925

Cited by 480 publications

(144 citation statements)

References 21 publications

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“…The blots were subsequently prehybridized in a solution containing 50% formamide, 0.9 M NaCl, 0.1 M NaPO4 (pH 7.4), 1% sodium dodecyl sulfate (SDS), 5´Denhart's solution and 10 mg/ml herring sperm DNA for 4 hr at 42°C and, hybridized overnight at 42°C in the same solution containing corresponding 32 P-labeled probes. cDNA probes were a1(I)Col (Chu et al, 1982), ON (Swaroop et al, 1988), TET (Wewer and Albrechtsen, 1992;Wewer et al, 1994), ALP and TGF-b1 from the American Type Culture Collection. The probes were labeled with 32 P using a multiprime DNA labeling system kit (Amersham).…”

Section: Northern Blot Analysismentioning

confidence: 99%

Phase-independent Inhibition by Retinoic Acid of Mineralization Correlated with Loss of Tetranectin Expression in a Human Osteoblastic Cell Line.

Iba¹,

Chiba

Yamashita³

et al. 2001

Cell Struct. Funct.

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ABSTRACT. We have recently reported that retinoic acid inhibits dexamethasone-induced alkaline phosphatase activity and mineralization in human osteoblastic cell line SV-HFO. In this study, we show that this inhibitory effect on alkaline phosphatase activity depends on the stage of cell differentiation; however, expression of tetranectin, which is a recently reported bone matrix protein, was completely inhibited by treatment with retinoic acid, irrespective of the stage of cell differentiation. Similarly, mineral deposit formation in SV-HFO cells was phase-independently inhibited by retinoic acid. To our knowledge, this is the first report that retinoic acid downregulates the tetranectin expression in human osteoblastic cells independent of the stage of cell differentiation, and is correlated with inhibition of mineralization. Key words: retinoic acid(RA)/tetranectin(TET)/mineralization/human/osteoblastRetinoids have a wide variety of effects on vertebrate embryogenesis and development, cellular differentiation, proliferation, and apoptosis, as well as homeostasis via two classes of ligand-dependent transactivators: the retinoic acid receptors (RARs) and the retinoid X receptors (RXRs), both of which are members of the nuclear receptor superfamily

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Section: Northern Blot Analysismentioning

confidence: 99%

Phase-independent Inhibition by Retinoic Acid of Mineralization Correlated with Loss of Tetranectin Expression in a Human Osteoblastic Cell Line.

Iba¹,

Chiba

Yamashita³

et al. 2001

Cell Struct. Funct.

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“…α1(I) collagen cDNA (Chu et al, 1982), α2(I) collagen cDNA (Myers et al, 1981) and pGEM β-actin probes were labelled with 32 P-dCTP by nick translation (Amersham). Approximately 1 × 10 6 cpm ml -1 of denatured probe was added to the prehybridization solution and the membranes were incubated overnight at 42°C.…”

Section: Northern Blot Analysismentioning

confidence: 99%

Breast tumour cell-induced down-regulation of type I collagen mRNA in fibroblasts

et al. 1999

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This study investigated the modulation of type I collagen gene expression in normal fibroblasts by breast tumour cells. Northern analysis of total RNA extracted from stages I, II and III breast tumour tissue revealed that collagen mRNA levels were elevated in stage I tumours compared to the adjacent normal breast tissues, whereas they were decreased in stages II and III breast tumours. This aberrant collagen gene expression was confirmed by non-radioactive RNA:RNA in situ hybridization analysis of 30 breast carcinomas which localized the production of type I collagen mRNA to the stromal fibroblasts within the vicinity of the tumour cells. In order to determine whether the tumour cells were directly responsible for this altered collagen production by the adjacent fibroblasts, breast tumour cell lines were co-cultured with normal fibroblasts for in vitro assessment of collagen and steady-state collagen RNA levels. Co-culture of tumour cells and normal fibroblasts in the same dish resulted in down-regulation of collagen mRNA and protein. Treatment of the fibroblasts with tumour-cell conditioned medium also resulted in decreased collagen protein levels but the mRNA levels, however, remained unaltered. These results suggested that the tumour cells either secrete a labile ‘factor’, or express a cell surface protein requiring direct contact with the fibroblasts, resulting in down-regulation of collagen gene expression. Modulation of the ECM is a common characteristic of invading tumour cells and usually involves increased production of collagenases by the tumour cells or stromal fibroblasts. This study showed that tumour cells were also able to modulate collagen mRNA production by stromal fibroblasts, which may facilitate tumour cell invasion and metastasis. © 1999 Cancer Research Campaign

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“…22 cDNAs for procollagen a1(IV), 25 procollagen a1(I), 26 a-smooth muscle actin (a-SMA), 27 Smad1, Smad2 and Smad3 (provided by Dr Keiji Miyazawa, University of Yamanashi) were used to prepare radio-labeled probes. Levels of glyceraldehyde-3-phosphate dehydrogenase (GAPDH) and 28S ribosomal RNA were used as loading controls.…”

Section: Northern Blot Analysismentioning

confidence: 99%

Blockade of Smad signaling by 3′-deoxyadenosine: a mechanism for its anti-fibrotic potential

Johno

Nakajima

et al. 2013

Laboratory Investigation

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Cordyceps militaris has been used in Eastern countries for the treatment of various diseases including chronic kidney diseases. However, there are no reports that identified its active entities and molecular mechanisms underlying its therapeutic effectiveness. 3 0 -Deoxyadenosine is a major nucleoside derivative isolated from C. militaris. Some reports suggested that both C. militaris and 3 0 -deoxyadenosine have anti-inflammatory and anti-fibrotic effects. In the present report, we investigated whether and how 3 0 -deoxyadenosine interferes with fibrogenic processes in the kidney. For this purpose, we examined effects of 3 0 -deoxyadenosine on the expression of collagens triggered by transforming growth factor-b (TGF-b1) and bone morphogenetic protein-4 (BMP-4), especially focusing on the regulation of Smad signaling in vitro and in vivo. We found that 3 0 -deoxyadenosine suppressed expression of collagens induced by TGF-b1 and BMP-4 dose dependently. This suppression occurred at the transcriptional level and was correlated with blunted activation of the CAGA box and the BMP-responsive element. The suppressive effect on the TGF-b/BMP signaling was mediated mainly by adenosine transporter and partially by the A3 adenosine receptor, but not A1/A2 adenosine receptors. 3 0 -Deoxyadenosine reduced levels of both phosphorylated and total Smad proteins (Smad1, 2 and 3) dose dependently. It was mainly ascribed to transcriptional suppression, but not to enhanced protein degradation and eIF2a-mediated translational suppression. Consistent with the in vitro results, in vivo administration with 3 0 -deoxyadenosine reduced the levels of phosphorylated and total Smad proteins, as well as the levels of Smad mRNAs, in the kidney subjected to unilateral ureteral obstruction. It was associated with blunted induction of type I collagen and a-smooth muscle actin, a decrease in the number of interstitial myofibroblasts and reduced fibrotic area. These results suggest that 3 0 -deoxyadenosine interferes with the TGF-b and BMP signaling via downregulation of Smads, which may underlie the anti-fibrotic effect of this agent. 3 0 -Deoxyadenosine may be useful for therapeutic intervention in various TGF-b-related fibrotic disorders.

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Cloning and characterization of five overlapping cDNAs specific for the human proα 1(I) collagen chain

Cited by 480 publications

References 21 publications

Phase-independent Inhibition by Retinoic Acid of Mineralization Correlated with Loss of Tetranectin Expression in a Human Osteoblastic Cell Line.

Phase-independent Inhibition by Retinoic Acid of Mineralization Correlated with Loss of Tetranectin Expression in a Human Osteoblastic Cell Line.

Breast tumour cell-induced down-regulation of type I collagen mRNA in fibroblasts

Blockade of Smad signaling by 3′-deoxyadenosine: a mechanism for its anti-fibrotic potential

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