Biomedical subjects

C Di

Publications and source records attributed to C Di.

7 recordsLinked to original sources

PubMed2001

Nuclear translocation of PDCD5 (TFAR19): an early signal for apoptosis?

The programmed cell death 5 (PDCD5) protein is a novel protein related to regulation of cell apoptosis. In this report, we demonstrate that the level of PDCD5 protein expressed in cells undergoing apoptosis is significantly increased compared with normal cells, then the protein translocates rapidly from the cytoplasm to the nucleus of cells. The appearance of PDCD5 in the nuclei of apoptotic cells precedes the externalization of phosphatidylserine and fragmentation of chromosome DNA. This phenomenon is parallel to the loss of mitochondrial membrane potential, independent of the feature of apoptosis-inducing stimuli and also independent of the cell types and the apoptosis modality. In conclusion, the nuclear translocation of PDCD5 is a universal earlier event of the apoptotic process, and may be a novel early marker for apoptosis.

Active Transport, Cell Nucleus↗

PubMed2001

Molecular cloning and characterization of chemokine-like factor 1 (CKLF1), a novel human cytokine with unique structure and potential chemotactic activity.

Cytokines are small proteins that have an essential role in the immune and inflammatory responses. The repertoire of cytokines is becoming diverse and expanding. Here we report the identification and characterization of a novel cytokine designated as chemokine-like factor 1 (CKLF1). The full-length cDNA of CKLF1 is 530 bp long and a single open reading frame encoding 99 amino acid residues. CKLF1 bears no significant similarity to any other known cytokine in its amino acid sequence. Expression of CKLF1 can be partly inhibited by interleukin 10 in PHA-stimulated U937 cells. Recombinant CKLF1 is a potent chemoattractant for neutrophils, monocytes and lymphocytes; moreover, it can stimulate the proliferation of murine skeletal muscle cells. These results suggest that CKLF1 might have important roles in inflammation and in the regeneration of skeletal muscle.

Amino Acid Sequence↗

PubMed2000

[Preparation and identification of monoclonal antibodies against human apoptosis-related protein TFAR19].

OBJECTIVE: To obtain mouse anti-human TFAR19 monoclonal antibodies for further study of the structure and function of the apoptosis-related protein TFAR19. METHODS: BALB/c mice were immunized with recombinant human TFAR19, hybridoma cells were screened by cell fusion and subcloning approach. The monoclonal antibodies were identified by ELISA and Western blotting. RESULTS: Three hybridoma cells (C1, C10, 2C12) stable in secreting anti-TFAR19 monoclonal antibodies were obtained. The monoclonal antibodies showed high specificity and high titer to TFAR19 with various affinity. All of them belong to IgG1 subclass. CONCLUSIONS: These monoclonal antibodies could bind specifically to TFAR19 protein.

Animals↗

PubMed2000

[Construction and expression of eukaryotic expression vector pBK-IL-1ra].

OBJECTIVE: Construction of eukaryotic vector with high expression of interleukin-1 receptor antagonist (IL-1ra) for IL-1ra gene delivery. METHODS: (1) Eukaryotic expression vector pBK-IL-1ra was constructed by recombinant DNA technique, and identified by restriction mapping enzymes, PCR, and DNA sequence analysis. (2) Expressions of the IL-1ra mRNA and IL-1ra in vitro and in vivo were detected by in situ hybridization, ELISA, and immunohistochemistry. RESULTS: (1) The correct construction of pBK-IL-1ra was identified by the method above. (2) The higher levels of IL-1ra in the supernate of COS-7 cells (24 h, (P < 0.001; 48 h, P < 0.01) and the over expression of IL-1ra mRNA (P < 0.01) and IL-1ra (P < 0.05) in the synoviocytes have been detected after 48 h of the transfection with pBK-IL-1ra. (3) The over expression of IL-1ra in muscle of the mice was detected by immunohistochemistry after 4 days of pBK-IL-1ra injection (P < 0.01) CONCLUSIONS: We have successfully constructed eukaryotic expression vector pBK-IL-1ra which could highly expressed IL-1ra in vitro and in vivo, and it offers a novel possibility in the research of IL-1ra gene therapy.

Animals↗

PubMed1999

TFAR19, a novel apoptosis-related gene cloned from human leukemia cell line TF-1, could enhance apoptosis of some tumor cells induced by growth factor withdrawal.

Using the cDNA-representative differences analysis (cDNA-RDA) approach, we identified a novel gene, TFAR19 (TF-1 cell apoptosis related gene-19), from TF-1 cells undergoing apoptosis. The human TFAR19 encodes a protein which shares significant homology to the corresponding proteins of species ranging from yeast to mice. TFAR19 exhibits a ubiquitous expression pattern and its expression is upregulated in the tumor cells undergoing apoptosis. Overexpression of TFAR19 in tumor cells enhances apoptosis triggered by growth factor or serum deprivation. We propose that TFAR19 may play a general role in the apoptotic process.

Amino Acid Sequence↗

PubMed1997

[Study on the effect of continuous administration of IL-1ra in BXSB mice].

OBJECTIVE: To explore the consequences of IL-1 blocking in BXSB mice which is an experimental model for human SLE. METHODS: rh IL-1ra was expressed in E. coli and injected in BXSB mice. 13 of 4.5 month-age male BXSB mice were divided into two groups, one group was injected rh IL-1ra 10 times (twice a week) at dose of 400 micrograms per mouse each time, another group was injected PBS at the same time as control. We monitored serum ANA and proteinuria weekly, and detected IgG, C3 deposition and IL-6 expression in kidneys at 40th day. RESULTS: The results showed that the increased level of serum ANA and proteinuria in treatment group were not higher than in control group, the IgG, C3 deposition and IL-6 expression in kidneys and IL-6 activity in serum of the treaed group were lower than the control group, whereas no difference of GPT level in the two groups. CONCLUSION: IL-1 might play a pathogenic role in BXSB mice. Blocking or reducing IL-1 secretion would be of beneficial to the treatment of SLE.

Animals↗

PubMed1996

Protective effect of interleukin-1 receptor antagonist on oleic acid-induced lung injury.

OBJECTIVE: To observe the changes of interleukin-1 (IL-1), nitric oxide (NO) and nitric oxide synthase (NOS) in mice with oleic acid-induced acute lung injury (ALI) and the protective effects of interleukin-1 receptor antagonist (IL-1ra). MATERIAL AND METHODS: Male Kunming mice were divided into control, oleic acid and IL-1ra groups. The control group mice were injected saline; the oleic acid group mice were injected oleic acid (0.2 ml/kg): and the IL-1ra group mice were injected the IL-1ra (20 mg/kg). Lung index, lung wet-to-dry weight ratio, and total protein, cell analysis, nitric oxide measurement, NOS activity in BALF, lung pathology examination were made after an hour of administration of drug. RESULTS: Preadministration of IL-1ra to the mouse with ALI decreased the lung index, lung wet-to-dry weight ratio and leakage of protein from pulmonary capillary, elevated PaO2, and attenuated lung histologic injury. It was found that in bronchoalveolar lavage fluid (BALF), NO amount and lung NOS activity increased in oleic acid group, BALF NO amount and lung NOS activity decreased obviously after given IL-1ra. CONCLUSIONS: This study demonstrated the protective effect of IL-1ra on oleic acid-induced lung injury, NO may participate in the pathological process of lung injury.

Animals↗