Biomedical subjects

Yu Huang

Publications and source records attributed to Yu Huang.

At least 37 records · Page 2Linked to original sources

PubMed2006

Synthesis and DNA cleavage activities of mononuclear macrocyclic polyamine zinc(II), copper(II), cobalt(II) complexes which linked with uracil.

Mononuclear macrocyclic polyamine zinc(II), copper(II), cobalt(II) complexes, which could attach to peptide nucleic acid (PNA), were synthesized as DNA cleavage agents. The structures of these new mononuclear complexes were identified by MS and (1)H NMR spectroscopy. The catalytic activities on DNA cleavage of these mononuclear complexes with different central metals were subsequently studied, which showed that copper complex was better catalyst in the DNA cleavage process than zinc and cobalt complexes. The effects of reaction time, concentration of complexes were also investigated. The results indicated that the copper(II) complexes could catalyze the cleavage of supercoiled DNA (pUC 19 plasmid DNA) (Form I) under physiological conditions to produce selectively nicked DNA (Form II, no Form III produced) with high yields. The mechanism of the cleavage process was also studied.

Cobalt↗

PubMed2006

Mechanism of non-capacitative Ca2+ influx in response to bradykinin in vascular endothelial cells.

Bradykinin is a potent vasoactive nonapeptide. It elicits a rise in cytosolic Ca(2+) (Ca(2+))(i) in endothelial cells, resulting in Ca(2+)-dependent synthesis and release of endothelial vasodilators. In the present study, we investigated the mechanism of bradykinin-induced Ca(2+) influx in primary cultured rat aortic endothelial cells and in a mouse heart microvessel endothelial cell line (H5V). Bradykinin-induced Ca(2+) influx was resolved into capacitative Ca(2+) entry (CCE) and non-CCE. The non-CCE component was inhibited by a B2 receptor antagonist (HOE140; 1 microM) and a phospholipase C (PLC) inhibitor (U73122; 10 microM). The action of bradykinin could be mimicked by 1-oleoyl-2-acetyl-glycerol, an analogue of diacylglycerol (DAG), and by RHC80267, a DAG-lipase inhibitor. Immunoblots showed that TRPC6 was one of the main TRPC channels expressed in endothelial cells. Transfection of H5V cells with two siRNA constructs against TRPC6 both markedly reduced the TRPC6 protein level and, at the same time, decreased the percentage of cells displaying bradykinin-induced non-CCE. siRNA transfection also reduced the magnitude of non-CCE among the cells responding to bradykinin. Taken together, our data suggest that bradykinin-induced non-CCE is mediated via the B2-PLC pathway, and that DAG may be involved in this process. Further, TRPC6 is one of the important channels participating in bradykinin-induced non-CCE in endothelial cells.

Animals↗

PubMed2006

Integrative Array Analyzer: a software package for analysis of cross-platform and cross-species microarray data.

The rapid accumulation of microarray data translates into an urgent need for tools to perform integrative microarray analysis. Integrative Array Analyzer is a comprehensive analysis and visualization software toolkit, which aims to facilitate the reuse of the large amount of cross-platform and cross-species microarray data. It is composed of the data preprocess module, the co-expression analysis module, the differential expression analysis module, the functional and transcriptional annotation module and the graph visualization module.

Algorithms↗

PubMed2006

Raloxifene prevents endothelial dysfunction in aging ovariectomized female rats.

Lack of an appropriate animal model has delayed the better understanding of mechanisms related to higher cardiovascular risk in women after menopause. The aging female rat may share some menopausal changes observed in women. However, most studies have attempted to mimic menopause by ovariectomizing young (6-12 weeks old) animals without taking into accounts the influence of aging and of declining ovarian function. Therefore, the present study examined changes in vascular reactivity in the aging (15 months old) female rat after ovariectomy and the effects of chronic raloxifene therapy on vascular reactivity and eNOS protein expression. Aortic rings were prepared from the three experimental groups of rats: sham-operated control, ovariectomized and ovariectomized aging rats receiving daily oral administration of raloxifene for 3 months. Aortic rings were suspended in organ baths for the measurement of isometric tension. Rings with endothelium contracted significantly more to phenylephrine after inhibition of nitric oxide/cyclic GMP-signaling pathway by L-NAME or ODQ (as an index of basal nitric oxide release) in control and raloxifene-treated ovariectomized rats than in ovariectomized rats. This effect was abolished upon mechanical removal of the endothelium. Phenylephrine induced greater contractions only in rings with endothelium from ovariectomized rats as compared with control rats and raloxifene treatment normalized this response. In the presence of L-NAME or ODQ, phenylephrine-induced contraction was similar in rings from the three groups. Rings relaxed more to thapsigargin and acetylcholine in raloxifene-treated ovariectomized rats than in ovariectomized rats. There was no significant difference in aortic eNOS protein contents among the different groups. These results suggest that chronic oral administration of raloxifene to aging ovariectomized female rats augmented the bioavailability of endothelial nitric oxide in isolated aortic rings without altering eNOS protein levels.

Acetylcholine↗

PubMed2006

Endothelial mediators of the acetylcholine-induced relaxation of the rat femoral artery.

This study examined endothelium-derived mediators of acetylcholine-induced relaxation in male rat femoral arteries. Arterial rings were suspended in a myograph for the measurement of isometric force. The generation of hydrogen peroxide (H2O2) in endothelial cells was detected using the fluorescent probe, 5-(and-6)-chloromethyl-2',7'-dichlorodihydrofluorescein diacetate acetyl ester. N(G)-nitro-L-arginine methyl ester (L-NAME, NOS inhibitor) and 1H-[1,2,4]oxadiazolo[4,2-alpha]quinoxalin-1-one (ODQ, guanylate cyclase inhibitor) alone or in combination with indomethacin (cycloxygenase inhibitor) diminished acetylcholine-induced endothelium-dependent relaxation to a similar extent. A small relaxation to acetylcholine in 60 mM KCl-constricted rings was abolished by L-NAME. Acetylcholine-induced relaxation was reduced by charybdotoxin plus apamin (intermediate- and small-conductance Ca2+-activated K+ channel blockers, respectively) or by 30 mM KCl. Both ouabain (Na+/K+ ATPase inhibitor) and BaCl2 (K(IR) channel blocker) also inhibited the relaxation albeit to a lesser degree. In the presence of L-NAME, ODQ plus indomethacin, charybdotoxin plus apamin or ouabain plus BaCl2 produced further inhibition. Catalase attenuated acetylcholine-induced relaxations and this attenuation was prevented by 3-amino-1,2,4-triazole (catalase inhibitor). Catalase did not affect acetylcholine-induced relaxations in rings treated with L-NAME or ODQ. Acetylcholine increased the dichlorofluorescein fluorescence intensity in native endothelial cells and this effect was abolished by catalase and by L-NAME. Exogenous H2O2 caused endothelium-independent relaxation that was slightly inhibited by iberiotoxin, ODQ or significantly reduced by elevated KCl, and abolished by catalase. The present results indicate that in addition to nitric oxide (NO) and endothelium-derived hyperpolarizing factor (EDHF, sensitive to charybdotoxin plus apamin, ouabain, and BaCl2), the endothelium of rat femoral artery can release H2O2 in response to acetylcholine, which was sensitive to L-NAME. Thus, the eNOS-dependent H2O2 is likely to be the third mediator of acetylcholine-mediated relaxations in rat femoral arteries.

Acetylcholine↗

PubMed2006

The human Pif1 helicase, a potential Escherichia coli RecD homologue, inhibits telomerase activity.

Telomeres, the protein-DNA complexes at the ends of eukaryotic chromosomes, are essential for chromosome stability, and their maintenance is achieved by the specialized reverse transcriptase activity of telomerase or the homologous recombination pathway in most eukaryotes. Here, we identified a human helicase, hPif1 that inhibits telomerase activity. The primary sequence and biochemical analysis suggest that hPif1 is a potential homologue of Escherichia coli RecD, an ATP-dependent 5' to 3' DNA helicase. Ectopic expression of wild-type, but not the ATPase/helicase-deficient hPif1, causes telomere shortening in HT1080 cells. hPif1 reduces telomerase processivity and unwinds DNA/RNA duplex in vitro. hPif1 preferentially binds telomeric DNA in vitro and in vivo. We propose that the mechanism of hPif1's inhibition on telomerase involves unwinding of the DNA/RNA duplex formed by telomerase RNA and telomeric DNA, and RecD homologues in eukaryotes may have evolved gaining additional functions.

Adenosine Triphosphatases↗

PubMed2006

Hen egg white lysozyme as an inhibitor of mushroom tyrosinase.

We report a kinetics study on hen egg white lysozyme's (HEWL) inhibitory effect on mushroom tyrosinase catalysis of 3-(3,4-dihydroxyphenyl)-L-alanine (L-DOPA) or L-tyrosine. For the first time, we demonstrate HEWL as a robust inhibitor against mushroom tyrosinase in catalysis of both substrates. The kinetics pattern matches a mixed (mostly non-competitive) partial inhibition. Ki and ID50 value of HEWL are more than 20-fold lower than that of kojic acid, a well-known chemical inhibitor of mushroom tyrosinase. Ki, alpha value and beta value, are almost identical in both experiments (L-DOPA and L-tyrosine as substrates, respectively), which suggests this common inhibition mechanism affects both steps. The inhibitory effect increases as both proteins were mixed and pre-incubated for less than 1 h. HEWL-depletion only removed about half of the inhibitory effect. Here we propose a novel function of HEWL, which combines the reversible inhibition and the irreversible inactivation toward mushroom tyrosinase. Discovery of HEWL as an inhibitor to mushroom tyrosinase catalysis may be commercially valuable in the food, medical and cosmetic industries.

Agaricales↗

PubMed2006

Role of NO and EDHF-mediated endothelial function in the porcine pulmonary circulation: comparison between pulmonary artery and vein.

OBJECTIVE: To compare electrophysiological measurement of nitric oxide (NO) release and endothelium-derived hyperpolarizing factor (EDHF)-mediated endothelial function in porcine pulmonary arteries and veins. METHODS: Isolated pulmonary interlobular arteries (PA) and veins (PV) were obtained from a local slaughterhouse. By using a NO-specific electrode and a conventional intracellular microelectrode, the amount of NO released from endothelial cells and hyperpolarization of smooth muscle cells were investigated. The bradykinin (BK)-induced relaxation in the precontraction by U(46619) was examined in the absence or presence of N(G)-nitro-l-arginine (l-NNA), indomethacin (INDO) plus oxyhemoglobin (HbO). RESULTS: The basal release of NO was 7.0+/-1.2 nmol/L in PA (n=8) and 5.5+/-1.6 nmol/L in PV (n=8, p<0.01). BK-induced release of NO was 160.4+/-10.3 nmol/L in PA (n=8) and 103.0+/-14.7 nmol/L in PV (n=8, p<0.001) with longer releasing duration in PA than in PV (14.3+/-1.3 vs. 12.1+/-0.8 min, p<0.01). BK evoked an endothelium-dependent hyperpolarization and relaxation that were reduced by l-NNA, INDO, and HbO (hyperpolarization: 12.8+/-1.3 vs. 8.0+/-1.4 mV in PA, n=6, p<0.001 and 8.3+/-1.4 vs. 3.0+/-0.8 mV in PV, n=6, p<0.001; relaxation: 92.8+/-3.1% vs. 19.6+/-11.1% in PA n=8, p<0.001 and 70.3+/-7.9% vs. 6.0+/-6.8% in PV, n=8, p<0.001). Both hyperpolarization (8.0+/-1.4 vs. 3.0+/-0.8 mV, p<0.001) and relaxation (19.6+/-11.1% vs. 6.0+/-6.8%, p<0.01) were greater in PA than in PV. CONCLUSIONS: Both NO and EDHF play an important role in regulation of porcine pulmonary arterial and venous tones. The more significant role of NO and EDHF is revealed in pulmonary arteries than in veins.

Animals↗

PubMed2006

Chemokine CXCL16, a scavenger receptor, induces proliferation and invasion of first-trimester human trophoblast cells in an autocrine manner.

BACKGROUND: The aim of this study was to investigate whether CXCL16/CXCR6, a newly identified chemokine pair, is expressed in first-trimester human placenta and whether they affect the trophoblast cell biology, since we have found CXCR6 highly transcribed in first-trimester human trophoblast cells previously. METHODS: We analysed the transcription and translation of CXCR6 and CXCL16 in purified first-trimester human trophoblast cells by real-time RT-PCR and immunochemical staining. We then examined the kinetic secretion of CXCL16 in the supernatant of primary-cultured trophoblast by enzyme-linked immunosorbent assay. We further investigated effects of CXCL16 on the proliferation and invasion of trophoblast cells in vitro. RESULTS: We found the chemokine pair CXCL16/CXCR6 was transcribed and translated in first-trimester trophoblast cells and JAR line. In addition, the primary-cultured trophoblasts secreted CXCL16 spontaneously and continuously in 100-h culture. Treating trophoblasts with CXCL16 induced marked proliferation and invasion in vitro. CONCLUSION: The findings from this study have demonstrated for the first time that CXCR6 and CXCL16 are co-expressed by first-trimester human trophoblast cells and stimulate their proliferation and invasion in an autocrine/paracrine manner. It suggests that CXCL16 plays important roles in human extravillous cytotrophoblast invasion and placentation.

Autocrine Communication↗

PubMed2006

Cadmium-induced changes in pigments, total phenolics, and phenylalanine ammonia-lyase activity in fronds of Azolla imbricata.

This study was designed to examine the effects of cadmium on several color-related parameters (including chlorophyll, carotenoid, and anthocyanin), total phenolics, and phenylalanine ammonia-lyase (PAL) activity in an aquatic fern species Azolla imbricate (A. imbricata). Cd accumulation and effects in the fronds were closely related with Cd concentration in the growth medium. The fronds under 0.5 mg/L Cd treatment turned red on the 3rd day, and this color change also appeared under 0.05 and 0.1 mg/L Cd treatment on the 5th day. Correlated with the color change, the contents of chlorophyll and carotenoid in the fronds significantly decreased in the presence of high Cd concentrations, while the anthocyanin content increased during the experiment. Significant increase in total phenolics content and PAL activity were also detected during Cd treatment. The results suggested that the Cd-induced change in color of fronds might be due to the decrease in chlorophyll and carotenoid and the increase in anthocyanin. Anthocyanin, total phenolics and their biosynthesis-related PAL might play a role in detoxification of Cd in A. imbricata.

Anthocyanins↗

PubMed2006

Cilnidipine, a slow-acting Ca2+ channel blocker, induces relaxation in porcine coronary artery: role of endothelial nitric oxide and [Ca2+]i.

Cilnidipine is a dual blocker of L-type voltage-gated Ca(2+) channels in vascular smooth muscle and N-type Ca(2+) channels in sympathetic nerve terminals that supply blood vessels. However, the clinical benefits of cilnidipine and underlying mechanisms are incompletely understood. This study was designed to compare the time course of relaxant responses to cilnidipine and nifedipine, and to examine the role of endothelial NO and [Ca(2+)](i) in the vasorelaxation. Porcine left circumflex coronary arteries were isolated and isometric tension was measured with Grass force transducers. Endothelial [Ca(2+)](i) in intact arteries was determined by a calcium fluorescence imaging technique. The free radical scavenging capacity was also assayed. Cilnidipine and nifedipine induced concentration-dependent relaxations in high KCl-precontracted artery rings, while the former-induced relaxation was slower as compared to the latter. Treatment with L-NAME or ODQ reduced relaxations to cilnidipine or nifedipine to the same extent as in rings without endothelium. Indomethacin or omega-conotoxin had no effects. L-Arginine antagonized the effect of L-NAME on cilnidipine-induced relaxations. Cilnidipine did not affect sodium nitroprusside-induced relaxation in rings with and without endothelium. Cilnidipine and nifedipine caused extracellular Ca(2+)-dependent increases in endothelial [Ca(2+)](i) in intact arteries and cilnidipine's action had a slower onset, similar to that of cilnidipine-induced relaxation. Neither cilnidipine nor nifedipine exhibited a free radical scavenging property. The present results demonstrate that cilnidipine can produce endothelium-dependent relaxation in porcine coronary arteries in vitro in addition to blocking Ca(2+) channels. Like short-acting nifedipine, cilnidipine-dependent relaxation, albeit to a slower onset, is partly mediated by endothelial NO but not by prostacyclin. The increased release or bioavailability of NO may causally result from elevated endothelial [Ca(2+)](i) in arteries. The Ca(2+) channel-independent effect suggests the usefulness of cilnidipine in the treatment of cardiovascular diseases associated with diminished NO release, such as atherosclerosis.

Animals↗

PubMed2006

Depletion of intracellular Ca2+ stores enhances flow-induced vascular dilatation in rat small mesenteric artery.

The effect of depleting intracellular Ca2+ stores on flow-induced vascular dilatation and the mechanism responsible for the vasodilatation were examined in rat isolated small mesenteric arteries. The arteries were pressurized to 50 mmHg and preconstricted with phenylephrine. Intraluminal flow reversed the effect of phenylephrine, resulting in vasodilatation. Flow dilatation consisted of an initial transient peak followed by a sustained plateau phase. The magnitude of dilatation was markedly reduced by removing Ca2+ from the intraluminal flow medium. Depletion of intracellular Ca2+ stores with either cyclopiazonic acid (CPA, 2 microM) or 1,4-dihydroxy-2,5-di-tert-butylbenzene (BHQ, 10 microM) significantly augmented the magnitude of flow dilatation. Flow-induced endothelial cell Ca2+ influx was also markedly enhanced in arteries pretreated with CPA or BHQ.Flow-induced dilatation was insensitive to Nw-nitro-L-arginine methyl ester (100 microM) plus indomethacin (3 microM) or to oxyhemoglobin (3 microM), but was markedly reduced by 30 mM extracellular K+ or 2 mM tetrabutylammonium (TBA), suggesting an involvement of EDHF. Catalase at 1200 U ml-1 abolished the flow-induced dilatation, while the application of exogenous H2O2 (90-220 microM) induced relaxation in phenylephrine-preconstricted arteries. Relaxation to exogenous H2O2 was blocked in the presence of 30 mM extracellular K+, and H2O2 (90 microM) hyperpolarized the smooth muscle cells, indicating that H2O2 can act as an EDHF. In conclusion, flow-induced dilatation in rat mesenteric arteries can be markedly enhanced by prior depletion of intracellular Ca2+ stores. Furthermore, these data are consistent with a role for H2O2 as the vasodilator involved.

Adenosine Triphosphate↗

PubMed2006

Mutation frequency for Charcot-Marie-Tooth disease type 1 in the Chinese population is similar to that in the global ethnic patients.

PURPOSE: To investigate the genetic loci/mutations among the Chinese Charcot-Marie-Tooth disease type 1 (CMT1), which accounts for approximately 70% of Charcot-Marie-Tooth; and to study the genetic heterogeneity and mutation frequency. METHODS: CMT1A duplication and mutations at loci of MPZ, Cx32/GJB1, EGR2, and LITAF/SIMPLE were analyzed among 32 clinically diagnosed CMT1 patients of Chinese ancestry. RESULTS: The CMT1A duplication was detected in 62.5% (20/32) CMT1 patients. This duplication accounts for the major mutation for Chinese CMT1. Among 12 cases that have no CMT1A duplication detected, three point mutations including one (3.1%) in MPZ and two (6.3%) in Cx32 were identified. No mutation was detected in genes PMP22, EGR2 and LITAF among the remaining nine (28.1%) CMT1 patients. CONCLUSION: The mutation frequency for the Chinese CMT1 is similar to that seen in the global ethnic population. Molecular testing of the CMT1A duplication, along with the loci of MPZ and Cx32, may detect the majority of Chinese CMT1 patients.

Amino Acid Substitution↗

PubMed2006

TRPC3 is involved in flow- and bradykinin-induced vasodilation in rat small mesenteric arteries.

AIM: To test the possible involvement of TRPC3 in agonist-induced relaxation and flow-induced vasodilation in rat small mesenteric arteries. METHODS: Male Sprague-Dawley rats were used in the present study. After 72 h-treatment of antisense oligo via tail vein injection, isometric tension and isobaric diameter measurement were carried out with isolated mesenteric artery segments by using either a Pressure Myograph or a Multi Myograph system. Endothelial [Ca(2+)]i changes were measured with a MetaFluor imaging system in response to flow or to 30 nmol/L bradykinin. RESULTS: Immunohistochemical study showed that the 72 h-treatment of antisense oligo via tail vein injection markedly decreased the TRPC3 expression in mesenteric arteries, indicating the effectiveness of the antisense oligo. Isometric tension and isobaric diameter measurement showed that, although the antisense oligo treatment did not affect histamine-, ATP-, and CPA-induced relaxation, it did reduce the magnitude of flow-induced vasodilation by approximately 13% and decreased bradykinin-induced vascular relaxation with its EC50 value raised by nearly 3-fold. Endothelial [Ca(2+)]i measurement revealed that treatment of the arteries with antisense oligos significantly attenuated the magnitude of endothelial [Ca(2+)]i rise in response to flow and to 30 nmol/L bradykinin. CONCLUSION: The results suggest that TRPC3 is involved in flow- and bradykinin-induced vasodilation in rat small mesenteric arteries probably by mediating the Ca(2+) influx into endothelial cells.

Animals↗

PubMed2006

Characterization of ATPase activity of recombinant human Pif1.

Saccharomyces cerevisiae Pif1p helicase is the founding member of the Pif1 subfamily that is conserved from yeast to human. The potential human homolog of the yeast PIF1 gene has been cloned from the cDNA library of the Hek293 cell line. Here, we described a purification procedure of glutathione S-transferase (GST)-fused N terminal truncated human Pif1 protein (hPif1deltaN) from yeast and characterized the enzymatic kinetics of its ATP hydrolysis activity. The ATPase activity of human Pif1 is dependent on divalent cation, such as Mg2+, Ca2+ and single-stranded DNA. Km for ATP for the ATPase activity is approximately 200 microM. As the ATPase activity is essential for hPif1's helicase activity, these results will facilitate the further investigation on hPif1.

Adenosine Triphosphatases↗

PubMed2006

Reactive oxygen species in vascular wall.

Reactive oxygen species (ROS) contribute to the pathogenesis of cardiovascular diseases including hypertension, atherosclerosis, cardiac hypertrophy, heart failure and diabetes mellitus. Oxidative stress is resulted from excessive generation of ROS that outstrips the antioxidant system. Various agonists, pathological conditions and therapeutic interventions lead to modulated expression and function of oxidant and antioxidant enzymes, including NAD(P)H oxidase, endothelial nitric oxide synthase, xanthine oxidase, myeloperoxidase, superoxide dismutases, catalase and glutathione peroxidase. ROS formed in vascular wall target a wide range of signaling molecules and cellular pathways in both endothelium and vascular smooth muscle, such as transcription factors, protein tyrosine phosphatase, protein tyrosine kinase, mitogen-activated protein kinase, Ca(2+)-transporting system and protein modification. ROS also have distinct physiological and pathophysiological impacts on vascular cells. ROS contribute to vascular dysfunction and remodeling through oxidative damage by (1) reducing the bioavailability of NO, (2) impairing endothelium-dependent vasodilatation and endothelial cell growth, (3) causing apoptosis or anoikis, (4) stimulating endothelial cell migration, and (5) activating adhesion molecules and inflammatory reaction, leading to endothelial dysfunction, an initial episode progressing toward hypertension and atherosclerosis. Cellular events underlying these processes involve changes in vascular smooth muscle cell growth, apoptosis/anoikis, cell migration, inflammation, and vasoconstriction. The present communication focuses on the biology of ROS signaling in vascular cells, discusses how oxidative stress contributes to vascular damage, and the therapeutic strategies/biotic factors that can prevent or treat ROS-associated cardiovascular disorders.

Animals↗

PubMed2006

[Expressions of CXCL16/CXCR6 and CXCL12/CXCR4 in first-trimester human trophoblast cells].

OBJECTIVE: To investigate the transcription and protein expressions of chemokines CXCL16, CXCL12 and their receptors CXCR6, CXCR4 in first-trimester human cytotrophoblast cells and human choriocarcinoma cell line JAR. METHODS: Transcriptions of CXCR6, CXCL16, CXCR4, CXCL12 in purified first-trimester human trophoblast cells and JAR line were assessed by semi-quantitative RT-PCR, and protein expressions of CXCR6, CXCL16, CXCR4, CXCL12 were analyzed in primary cultured villous cytotrophoblasts (VCT), extravillous cytotrophoblasts (EVCT), JAR line and placentas by immunostaining. RESULTS: CXCR6 and CXCR4 were highly transcribed in primary cultured trophoblast cells with mRNA relative level of 1.12 +/- 0.25 and 1.08 +/- 0.11 respectively, and their ligands CXCL16 and CXCL12 were transcribed moderately with mRNA relative level of 0.89 +/- 0.11 and 0.78 +/- 0.10 respectively. It was demonstrated that CXCL16, CXCL12, CXCR6 and CXCR4 were expressed in primary cultured VCT, EVCT, JAR line and placentas by immunostaining. CONCLUSION: The co-expression of CXCL16/CXCR6 and CXCL12/CXCR4 in trophoblast cells may play a role in the proliferation and differentiation of first-trimester trophoblast cells in a manner of autocrine.

Adult↗

PubMed2006

[Chemokine CXCL16 induces proliferation and invasion of human first-trimester cytotrophoblasts in autocrine manner].

To investigate the secretion and autocrine roles of chemokine CXCL16 in first-trimester human cytotrophoblast cells, enzyme-linked immunosorbent assay (ELISA) was used to detect the CXCL16 secretion of primary-cultured cytotrophoblast cells in various lengths of culture time and various plated densities in vitro. Then, the [3H] thymidine incorporation assay and matrigel invasion assay were applied respectively to investigate proliferation and invasion roles of CXCL16 on the cytotrophoblast cells treated with rhCXCL16. Our results showed that the primary cultured cytotrophoblasts were found to secrete in vitro CXCL16 spontaneously and continuously. CXCL16 stimulated the proliferation and invasion of cytotrophoblast cells in vitro. These results indicated that CXCL16 is secreted in first-trimester cytotrophoblast cells and induces the proliferation and invasion of cytotrophoblast cells in autocrine manner. CXCL16 plays important roles in human placentation and extravillous trophoblast invasiveness.

Cell Proliferation↗