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Biomedical subjects

D L Ma

Publications and source records attributed to D L Ma.

At least 19 recordsLinked to original sources
PubMed2006

Calcium binding protein containing neurons in the gliotic mouse hippocampus with special reference to their afferents from the medial septum and the entorhinal cortex.

In CA1 area and the hilus of the dentate gyrus of the mouse hippocampus, drastic reduction of NeuN, calbindin, calretinin, or parvalbumin immunopositive neurons was shown at 3, 7 and 60 days after pilocarpine-induced status epilepticus. In gliotic CA1 area at 60 days, few dendritic branches of calcium binding protein immunopositive neurons could be found suggesting reorganization of the afferents of surviving calcium binding protein immunopositive neurons. Calbindin, calretinin, or parvalbumin and 5-bromo-2'-deoxyuridine (BrdU) double labeling showed that calcium binding protein immunopositive neurons in gliotic CA1 area at 60 days were surviving instead of newly generated neurons. Iontophoretic injection of Phaseolus vulgaris leucoagglutinin into the medial septum and the nucleus of the diagonal band of Broca or the lateral entorhinal cortex showed contacts between Phaseolus vulgaris leucoagglutinin immunopositive en passant and terminal boutons and surviving calcium binding protein immunopositive neurons in the hippocampus. The presence in the gliotic hippocampus of enlarged and/or aggregated bouton-like structures 60 days after pilocarpine-induced status epilepticus is indicative for the reorganization of connections between the hippocampal afferents and surviving hippocampal neurons. This reconstruction could be a factor in the ongoing epileptic activity in this model of mesial temporal lobe epilepsy.

Afferent Pathways↗
PubMed2006

Short interfering RNA against the PDCD5 attenuates cell apoptosis and caspase-3 activity induced by Bax overexpression.

The programmed cell death 5 (PDCD5) protein plays an important apoptosis-accelerating role in cells undergoing apoptosis. Decreased expression of PDCD5 has been detected in various human carcinomas. Here we describe that one potent short interfering RNA (siRNA) against the PDCD5 (siPDCD5) specifically inhibits the expression of PDCD5 at both the mRNA and protein level. Cells with decreased PDCD5 expression displayed reduced sensitivity to an apoptotic stimulus induced by Bax overexpression in HeLa, HEK293 and 293T cell lines. Furthermore, we also show that siPDCD5 inhibited both caspase-3 activity and procaspase-3 cleavage. Suppressed expression of PDCD5 attenuates the release of cytochrome c from mitochondria to cytosol induced by Bax overexpression. This phenomenon is accompanied by the reduced translocation of Bax from the cytosol to mitochondria. MTT assay shows that targeted suppression of PDCD5 expression markedly promoted cell proliferation in Hela and HEK293 cell lines. Our data suggests that PDCD5 may exert its effects through pathway of mitochondria by modulating Bax translocation, cytochrome c release and caspase 3 activation directly or indirectly, and that decreased PDCD5 expression may be one of the mechanisms by which tumor cells achieve resistance to apoptotic stimulus induced by anticancer drugs.

Apoptosis↗
PubMed2006

Protein tyrosine phosphatase interacting protein 51 (PTPIP51) is a novel mitochondria protein with an N-terminal mitochondrial targeting sequence and induces apoptosis.

Apoptosis is a genetically determined cell suicide program. Mitochondria play a central role in this process and various molecules have been shown to regulate apoptosis in this organelle. In the present study, we firstly identified that protein tyrosine phosphatase interacting protein 51 (PTPIP51) is a novel mitochondrial protein, which may induce apoptosis in HEK293T and HeLa cell lines. PTPIP51 transfection resulted in the externalization of phosphatidylserine (PS), activation of caspase-3, cleavage of PARP, and condensation of nuclear DNA. Further investigation revealed that PTPIP51 over-expression caused a decrease in mitochondrial membrane potential and release of cytochrome c, suggesting that it may be involved in a mitochondria/cytochrome c mediated apoptosis pathway. We also found that a putative TM domain near the N terminus of PTPIP51 is required for its targeting to mitochondria, as evidenced by the finding that deletion of the PTPIP51 TM domain prevented the protein's mitochondiral localization. Furthermore, this deletion significantly influenced the ability of PTPIP51 to induce apoptosis. Taken together, the results of the present study suggest that PTPIP51 is a mitochondrial protein with apoptosis-inducing function and that the N-terminal TM domain is required for both the correct targeting of the protein to mitochondria and its apoptotic functions.

Amino Acid Sequence↗
PubMed2003

Association study of neuregulin 1 gene with schizophrenia.

A number of studies have indicated that 8p22-p12 is likely to harbor schizophrenia susceptibility loci. In this region, the candidate gene of interest, neuregulin 1 (NRG1), may play a role in the pathogenesis of schizophrenia. Then in the present study, we performed the linkage disequilibrium to determine the association between three genetic variants (SNPs: rs3924999, rs2954041, SNP8NRG221533) on NRG1 gene and schizophrenia in 246 Chinese Han schizophrenic family trios using PCR-based restriction fragment length polymorphism method and denaturing high-performance liquid chromatography. The transmission disequilibrium test analysis for each variant showed a significant difference between two transmitted alleles even after Bonferroni correction (rs3924999, P=0.007752; rs2954041, P=0.0009309; SNP8NRG221533, P=0.012606). The global chi(2) test for haplotype transmission also revealed a strong association (chi(2)=46.068, df=7, P&<0.000001). Our results suggest that the NRG1 gene may play a role in conferring susceptibility to the disease.

Adult↗
PubMed2001

[Stimulatory effect of chemokine-like factor 1 (CKLF1) on the growth of bone marrow cells].

OBJECTIVE: To investigate the activity of CKLF1 on the proliferation and differentiation of bone marrow cells. METHODS: Human low density bone marrow cells and mouse bone marrow cells were plated in 96-well microplate and supernatants from transfected COS-7 cell culture were added. The cell proliferation was assayed by MTT method after 5 days incubation. The enhancing effect of CKLF1 on the colony formation of human hematopoietic progenitor cells was identified in semi-solid culture. RESULTS: CKLF1 has obvious enhancing effect on both human and mouse bone marrow cells, it can stimulate the colony formation of human hematopoietic stem cells and has synergistic action with GM-CSF. CONCLUSION: CKLF1 can promote the proliferation and differentiation of bone marrow cells.

Animals↗
PubMed2001

[Expression in E. coli and chemotactic activity analyzing of recombinant CC-chemokine RANTES].

OBJECTIVE: To further understand the structure and function of RANTES and provide basis for research for application. METHODS: PCR product corresponding to region encoding mature RANTES protein was cloned into E. coli expression vector; purified recombinant protein was obtained by heparin affinity chromatography and its chemotactic activity was determined by Boyden chamber. RESULTS: The recombinant RANTES was expressed in E. coli with high efficiency. Purified protein showed chemotactic activity to peripheral blood lymphocytes, U937 cells, and CCR4 stable-transfected HEK293 cells. CONCLUSION: The purified recombinant protein exerted chemotactic activity on PBL and cultured cell lines, and we have established a experimental system for further study of structure and function of RANTES.

Animals↗
PubMed2001

[Eukaryotic expression and in vitro tumor cell apoptosis-induced effect of human TRAIL].

OBJECTIVE: To explore the tumor cell apoptosis induced by the effect in vitro of eukaryotic expression of full-length TRAIL cDNA and its extracellular region. METHODS: The eukaryotic expression vectors for both forms of the cDNA acquired from the fetal heart cDNA library were constructed. After gene transfecting, the stable expression cell lines were obtained by G418 screening. RESULTS: The supernatants from tansfectants could induce apoptosis of different tumor cell lines in vitro, and an enhanced effect was observed by adding TFAR19 (TF-1 cell apoptosis-related protein 19), a novel apoptosis gene product discovered in our laboratory. CONCLUSION: Eukaryotic expression products of TRAIL can induce apoptosis of the tumor cells, and TFAR19 could enhance the effect on apoptosis of tumor cells.

Animals↗
PubMed1999

Determination of interleukin-1 receptor antagonist, interleukin-10, and transforming growth factor-beta1 in synovial fluid aspirates of patients with temporomandibular disorders.

PURPOSE: This study was undertaken to examine the presence of interleukin-1 receptor antagonist (IL-1ra), IL-10, and transforming growth factor-beta1 (TGF-beta1) in the synovial fluid (SF) lavage specimens of patients with temporomandibular disorders (TMDs). PATIENTS AND METHODS: Synovial fluid lavage specimens were obtained from 14 temporomandibular joints (TMJs) of 12 patients with TMJ internal derangement (ID) and 17 TMJs of 15 patients with TMJ osteoarthritis (OA). Seven synovial fluid lavage samples of TMJs of four asymptomatic donors served as normal controls. The concentrations of IL-1ra, IL-10, and TGF-beta1 were detected with sensitive and specific sandwich enzyme-linked immunosorbent assay (sandwich-ELISA). RESULTS: IL-1ra, IL-10, and TGF-beta1 in all the normal controls were undetectable. IL-1ra concentrations were 175.78 +/- 52.43 pg/mL in the patients with TMJ ID and 187.85 +/- 59.51 pg/mL in those with TMJ OA. IL-10 was undetectable in all the TMJ ID and OA samples. The concentration of TGF-beta1 in TMJ ID patients (47.93 +/- 88.25 pg/mL) was significantly less than in patients with TMJ OA (143.61 +/- 108.00 pg/mL) (P < .01). CONCLUSION: The results suggest that deficiencies of IL-1ra, IL-10, and TGF-beta1 probably play an important role in the cause and pathogenesis of TMJ ID and OA.

Adolescent↗
PubMed1998

Existence of IL-8 degrading protease and anti-IL-8 immunoglobulin G in gingival crevicular fluid.

OBJECTIVE: The aim of this study is to identify the nature of the IL-8 inhibitor(s) in gingival crevicular fluid (GCF). METHODS: Part 1: Fourteen GCF samples were collected from 13 adult periodontitis (AP) patients, and 9 samples were taken from 8 healthy subjects. Each GCF sample was divided into two aliquots. A serine protease-specific inhibitor, PMSF, was added to one aliquot, and PBS was added to the other aliquot as control. ELISA was used to measure IL-8 level in the samples. Part 2: Forty-one GCF samples were collected from 15 AP patients and indirect ELISA was performed to detect the anti-IL-8 IgG antibody. RESULTS: Part 1: IL-8 level in the PMSF samples was significantly greater than that in the control group (3.01 +/- 5.79 mg/L vs 0.05 +/- 0.15 mg/L, respectively P < .001). Part 2: The mean value of anti-IL-8 IgG in GCF was greater than that of negative control + 3 x SD. CONCLUSIONS: A serine protease that can "cleave" IL-8 exists in GCF. Gingival crevicular fluid from AP sites contains an autoantibody against IL-8.

Adult↗
PubMed1997

Effects of recombinant human endothelial-derived interleukin-8 on hemorrhagic shock in rats.

AIM: To study the effects of recombinant human endothelial-derived interleukin-8 (IL-8) on hemorrhagic shock. METHODS: A profound hemorrhagic shock in rats was produced by exsanguination from femoral artery with mean arterial blood pressure (MABP) maintained at 5.32 kPa for 90 min. After transfusion, IL-8 250 micrograms.kg-1 was i.v. injected. Plasma endothelin-1 (ET-1) and 6 ketoprostaglandin F1 alpha (6-KPGF1 alpha) contents were determined with radioimmunoassay. RESULTS: After i.v. IL-8, the MABP in IL-8 group was elevated obviously (P < 0.01), the rat survival 2 h after infusion was increased (P < 0.05). During profound shock the plasma ET-1 levels were higher (21 +/- 4 vs 8.2 +/- 1.8 ng.L-1, P < 0.01) and the plasma 6-KPGF1 alpha contents lower than those in normal rats (107 +/- 12 vs 157 +/- 11 ng.L-1, P < 0.01). IL-8 remarkably reduced the plasma ET-1 levels (10 +/- 4 ng.L-1, P < 0.01) and enhanced plasma 6-KPGF1 alpha contents (368 +/- 16 ng.L-1, P < 0.01). CONCLUSION: IL-8 has beneficial antishock effects.

6-Ketoprostaglandin F1 alpha↗
PubMed1995

[The protective effect of IL-1 beta on stress-induced gastric mucosal damage in rat].

The effect of recombinant IL-1 beta on stress-induced gastric mucosal lessions was studied in rats. Pretreatment with IL-1 beta prevented formation of gastric mucosal damage in a dose-dependent manner. IL-1 receptor antagonist peptide (IRAP) could totally reverse the protective effect of IL-1 beta. IL-1 fragment peptide (163-171) had no effect on gastric ulcer formation in the experimental model, whereas sulfhydryl blocker N-ehtylmaleimide partially blocked the protective effect of IL-1 beta. The concentration of protein and noneprotein sulfhydryls in the gastric mucosa was significantly decreased 3 h after stress, and this decrease was partially prevented by IL-1 beta. IL-1 beta also decreased the concentration of molondialdehyde (MDA) in the gastric mucosa after 3 h stress. The results suggest that IL-1 beta could effectively lessen the degree of stress-induced gastric mucosal damage, due possibly to the production of endogenous sulfhydryl compounds in the gastric mucosa.

Animals↗
PubMed1995

[Effects of emodin, sennosides and rheum polysaccharides on free calcium in isolated rat liver cells].

The effects of emodin (EMD), sennosides (SEN) and Rheum polysaccharides (RPP) on the free calcium level in the isolated rat liver cells were studied with Ca2+ level 131.60 +/- 37.79 nmol/L in the liver cells. After adding CaCl2 (2 mmol/L) and KCl (120 mmol/L) to liver cell suspension sequentially, the free Ca2+ levels were significantly elevated compared with that of the resting status (P < 0.01). When the liver cells were pretreated with EMD (0.037 mmol/L) for 10 min, in the resting status or using the above doses of CaCl2 and KCl, the free Ca2+ levels were significantly increased compared with that of the control groups (P < 0.01). On the contrary, after administration of SEN (0.046-0.092 mmol/L) and RPP (0.1-0.2 mg/ml), the free Ca2+ levels were obviously decreased compared with that of the control groups (P < 0.01). Furthermore, the inhibitory effect was dose dependent. The opposite effects of the different active ingredients of rhubarb (EMD,SEN,RPP) on the free Ca2+ levels suggested that rhubarb has many kinds of regulatory function in the liver cells.

Animals↗
PubMed1994

Triptolide suppresses T-lymphocyte proliferation by inhibiting interleukin-2 receptor expression, but spares interleukin-2 production and mRNA expression.

The purpose of this study was to elucidate the mechanism of action of triptolide on the T-lymphocyte-mediated immune response. Lymphocytes were incubated with a suboptimal dose of Con A or PHA in the presence or absence of varying doses of triptolide to assess the effect of triptolide on lymphocyte proliferation, interleukin-2 (IL-2) production and IL-2 receptor expression. Then, Con A or PHA induced T-blast cells were cultured with a sufficient dose of recombinant human IL-2 in the presence or absence of triptolide to evaluate the effect of triptolide on the interaction of IL-2 and IL-2 receptors. The effect of triptolide on the immune response in vivo was also investigated. The results of these studies clearly demonstrated that triptolide selectively inhibited the T-lymphocyte proliferative response to Con A and PHA, but had less effect on LPS-induced B-lymphocyte proliferation. Triptolide also suppressed the expression of IL-2 receptors on PHA induced T-blast cells, but did not alter the production of IL-2 by mouse splenic cells and human tonsil lymphocytes. Furthermore, the results also showed that triptolide at higher concentration had a slight inhibitory effect on the interaction of IL-2 and IL-2 receptors, and addition of exogenous IL-2 did not reverse the inhibiting action of triptolide on T-cell proliferation. Taken together, these results suggest that triptolide inhibits T-lymphocyte proliferation mainly by affecting IL-2 receptor expression rather than IL-2 production.

Animals↗
PubMed1994

Enhancement of interleukin-2 production and its mRNA expression by dihydroartemisinin.

Immunoregulatory properties of a novel antimalarial drug dihydroartemisinin (DHA) were investigated in vitro. DHA 0.5-5 mumol.L-1 enhanced the lymphocyte proliferation induced by Con A. Interleukin 2 (IL-2) production and its mRNA expression by both Con A-stimulated mouse splenocytes and a T cell line LBRM-33-1A5 were also augmented by DHA. In contrast, DHA 0.5-5 mumol.L-1 did not show any effect on the lipopolysaccharides (LPS)-induced lymphocyte proliferation and the spontaneous and mitogen-induced proliferation of transformed T cells. These results indicated that DHA might regulate lymphocyte responses through the induction of IL-2 production and that the enhanced T cell proliferation and IL-2 production might be mediated through different pathways.

Animals↗
PubMed1994

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

Thirty-six mice were divided into a control group, lung injury group by oleic acid and protected group with interleukin-1 receptor antagonist (IL-1ra). There were 12 mice in each group. Oleic acid was injected into the tail vein of the mouse with a dose of 0.2 ml/kg to produce a model of acute lung injury (ALI). The result indicates that preadministration of IL-1ra to the mouse with ALI can decrease the lung index, lung wet-to-dry weight ratio and leakage of protein from pulmonary capillary, elevate PaO2, and significantly attenuate lung histologic injury (alveoli edema, alveoli hemorrhage, lung necrosis, inflammatory cell invasion). It is suggested that IL-1ra has protective effect on oleic acid-induced lung injury and may be a potential tool for treatment of ARDS.

Animals↗
PubMed1994

[Study on effect of emodin on the isolated intestinal smooth muscle of guinea-pigs].

Emodin is an active principle of Rheum palmatum. It is reported that emodin possesses antibiotic and antineoplastic functions. The effect of emodin action on the isolated intestinal smooth muscle of guinea-pigs were dose dependent. When the dose of emodin was less than 29.6 mumol/L, the contraction effect enhanced obviously with increasing dosage; but whenever the dose increased to more than 29.6 mumol/L, on the contrary, the effect decreased gradually and ceased finally. Emodin with appropriate concentration (14.8 mumol/L) strengthened the effect of acetylcholine (Ach) on the isolated ileum and large intestine of guinea-pigs (P < 0.05 and P < 0.01). But high concentration of emodin could reduce even completely antagonize the effect of Ach. Under such condition, CaCl2 could restore the effect of Ach on the smooth muscle. It is suggested that emodin has biphasic regulatory effect on the intestinal smooth muscle, and its effect is related to calcium ion.

Animals↗