Biomedical subjects

Ying Luo

Publications and source records attributed to Ying Luo.

At least 19 recordsLinked to original sources

PubMed2026

Genetic Evidence That Stroke Causally Increases Circulating PDGFB Levels: a Two-Sample Mendelian Randomization Study.

Platelet-derived growth factor subunit B (PDGFB) is a key regulator of vascular remodeling, angiogenesis, and blood-brain barrier integrity. Although elevated PDGFB levels have been reported after ischemic injury, whether stroke liability itself causally influences circulating PDGFB levels remains unclear. We performed a two-sample Mendelian randomization (MR) analysis to assess the causal effects of genetically predicted all stroke, ischemic stroke, and cardioembolic stroke on plasma PDGFB concentrations. Genetic instruments were obtained from large-scale GIGASTROKE genome-wide association studies, and outcome data were derived from a proteomics GWAS. Instruments were then filtered by removing variants associated with established cardiovascular risk factors in a phenome-wide screen and outliers identified by RadialMR. The inverse variance-weighted (IVW) method was used as the primary analysis, complemented by weighted median, weighted mode, and MR-Egger approaches. Sensitivity analyses included Cochran's Q statistics, MR-Egger intercept tests, single-SNP analyses, leave-one-out analyses, and MR-PRESSO. IVW analysis demonstrated a significant positive causal association between genetic liability to all stroke and plasma PDGFB levels (β = 0.209, SE = 0.062, 95% CI 0.088 to 0.331, p = 7.3 × 10-4). A similar association was observed for ischemic stroke (β = 0.155, SE = 0.059, 95% CI 0.039 to 0.270, p = 0.009), with directionally consistent results across sensitivity analyses. MR-Egger regression for ischemic stroke initially suggested pleiotropy.After removal of a radial-MR outlier (rs2289252), the intercept was attenuated and no longer statistically significant (- 0.0190, p = 0.282). In contrast, no evidence of a causal association was found between cardioembolic stroke liability and plasma PDGFB levels across all MR methods (β = - 0.078, SE = 0.087, 95% CI - 0.248 to 0.092, p = 0.368). These findings provide genetic evidence that liability to stroke, particularly ischemic stroke, is causally associated with increased circulating PDGFB levels, whereas cardioembolic stroke does not show such an effect. This suggests that elevated PDGFB reflects vascular responses specific to ischemic stroke rather than a general consequence of all stroke subtypes.

Humans↗

PubMed2026

Nuclear class 3 PI3K co-activates fasting-specific chromatin remodelling.

Transcriptional remodelling during fasting ensures metabolic adaptation and provides health benefits across species. Although several regulators of fasting-induced transcription and chromatin are known, how nutrient levels directly influence RNA polymerase II (RNAPII) and epigenetic writers remains unclear. Here we show that lipid kinase class 3 phosphatidylinositol 3-kinase (PI3K-3), a master regulator of autophagy, also functions on chromatin as a co-activator of epigenetic writers to promote RNAPII transcription. PI3K-3 overlaps with transcriptionally engaged RNAPII phosphorylated at Ser5 and with Setd1a/COMPASS, the complex that deposits the activating H3K4me3 mark. Nuclear PI3K-3 interacts with RNAPII and Setd1a/COMPASS and promotes their chromatin binding. PI3K-3 loss reduces RNAPII-S5p and H3K4me3 at selected genes, whereas PI3K-3 overexpression co-activates p300/CBP and chromatin-targeted PI3K-3 increases H3K4me3. During starvation, PI3K-3 induces autophagy genes and drives fasted liver towards ketogenesis and lipid degradation. These findings link nutrient stress to chromatin-mediated transcriptional activation.

Chromatin Assembly and Disassembly↗

PubMed2026

Light regulates capsaicinoid biosynthesis via the CaHY5-CaBBX2-CaACS8 module in pepper.

Capsaicinoids are a class of unique alkaloids that confer the pungent taste to pepper fruits. However, it remains largely unknown how light regulates the biosynthesis of capsaicinoids. We conducted a metabolic analysis on light- and dark-adapted pepper fruits. The results showed that dark-adapted pepper fruits had lower capsaicinoid contents and correspondingly downregulated transcription of capsaicinoid biosynthetic genes (CBGs), indicating that light plays a crucial role in capsaicinoid biosynthesis. Furthermore, silencing of CaHY5, a pivotal transcription factor gene in the light signaling pathway, decreased the content of capsaicinoid and suppressed the expression of CBGs, whereas transient overexpression of CaHY5 generated exactly opposite results. CaHY5 can bind to the G-box motif in the promoters of CaBBX2 and CaACS8, thereby enhancing their transcriptional levels. The activated CaBBX2 then binds to the T/G-box in the CaACS8 promoter to stimulate its expression. CaBBX2 or CaACS8 silencing led to decreased levels of capsaicinoids, while their transient overexpression produced increased capsaicinoid contents. Collectively, our results indicated that the light-activated CaHY5-CaBBX2-CaACS8 regulatory module plays a pivotal role in capsaicinoid biosynthesis. These findings provide new insights into the influence of light on capsaicinoid biosynthesis and potential targets for activation of this biosynthetic pathway in pepper.

Capsicum↗

PubMed2007

Identification of hepatitis B virus-specific lymphocytes in human liver grafts from HBV-immune donors.

Both animal and human studies have demonstrated the adoptive transfer of immunity against hepatitis B virus (HBV) through liver transplantation that may be attributed to the presence of HBV-specific immunocompetent cells of donor origin in liver grafts. In this study, we characterized the resident lymphocytes in 41 human liver grafts by immunohistochemical staining and flow cytometry and directly identified the intragraft HBV-specific lymphocytes in relation to the donor's and subsequent recipient's immunity using enzyme-linked immunospot assay. A significant number of HBV-specific T and B cells were detectable in 59.4% (19/32) and 28.1% (9/32), respectively, of liver grafts from HBV-immune donors. The presence of various HBV-specific lymphocytes was closely associated with each other and with a higher serum titer of antibody against hepatitis B surface antigen (anti-HBs) in donors (P < 0.05). After liver transplantation, 17 of 35 (48.6%) patients with chronic HBV infection showed a spontaneous anti-HBs production, which was significantly associated with a higher number of donor-derived T lymphocytes specific for hepatitis B surface antigen (P = 0.043). In conclusion, the presence of considerable numbers of donor-derived HBV-specific immunocompetent cells in grafts may account for the adoptive transfer of HBV immunity through liver transplantation.

Adult↗

PubMed2006

Mutations in the gene encoding the Sigma 2 subunit of the adaptor protein 1 complex, AP1S2, cause X-linked mental retardation.

In a systematic sequencing screen of the coding exons of the X chromosome in 250 families with X-linked mental retardation (XLMR), we identified two nonsense mutations and one consensus splice-site mutation in the AP1S2 gene on Xp22 in three families. Affected individuals in these families showed mild-to-profound mental retardation. Other features included hypotonia early in life and delay in walking. AP1S2 encodes an adaptin protein that constitutes part of the adaptor protein complex found at the cytoplasmic face of coated vesicles located at the Golgi complex. The complex mediates the recruitment of clathrin to the vesicle membrane. Aberrant endocytic processing through disruption of adaptor protein complexes is likely to result from the AP1S2 mutations identified in the three XLMR-affected families, and such defects may plausibly cause abnormal synaptic development and function. AP1S2 is the first reported XLMR gene that encodes a protein directly involved in the assembly of endocytic vesicles.

Adaptor Protein Complex sigma Subunits↗

PubMed2006

Adapter protein NRBP associates with Jab1 and negatively regulates AP-1 activity.

Jun activation domain-binding protein 1 (Jab1) is a coactivator of activating protein-1 (AP-1) and is the fifth component of the COP9 signalosome complex. It interacts with a variety of proteins and plays important roles in diverse signaling pathways and cellular function including oncogenesis. We show here that Jab1 interacts in vivo with nuclear receptor binding protein (NRBP), an evolutionarily conserved adapter protein with a kinase-like domain. We further show that NRBP inhibits Jab1-induced phosphorylation of c-Jun and AP-1 activation. Finally, overexpression of NRBP in mammalian cells specifically inhibits AP-1 activation by various stimuli. Taken together, our data suggest that NRBP may be an important negative regulator of Jab1-mediated functions such as gene transcription and tumor progression.

Binding Sites↗

PubMed2006

The X-linked lymphoproliferative disease gene product SAP associates with PAK-interacting exchange factor and participates in T cell activation.

SLAM (signaling lymphocyte activation molecule)-associated protein (SAP) is a Src homology 2 (SH2) domain-containing adaptor expressed in T cells and natural killer cells. Its essential role in immune responses is underscored by the recent finding that mutations in SAP result in a rare but fatal X-linked lymphoproliferative disease (XLP). Although SAP is known to associate with SLAM-family receptors, the exact molecular mechanism by which SAP regulates lymphocyte signaling remains elusive. We here report that in T cells, SAP associates with the PAK-interacting exchange factor (PIX), a guanine nucleotide exchange factor (GEF) specific for Rac/Cdc42 GTPases. Moreover, SAP, PIX, and an activated form of Cdc42 form a complex in mammalian cells. We demonstrate that the SAP-PIX interaction is specific and is mediated by the C-terminal region of the SAP SH2 domain and the PIX SH3 domain. We further show that SAP is required for the recruitment of PIX to the SLAM-family receptors. Interestingly, overexpression of SAP, but not its homolog EAT-2, leads to a synergistic activation of nuclear factor of activating T cells (NFAT) in combination with a calcium signal in T cells. This SAP-mediated activation appears to be receptor-dependent and can be blocked by a dominant negative form of PIX. Taken together, our data strongly suggest that, in addition to the known SAP-interacting kinase Fyn, PIX may be another key player in SAP-mediated T cell activation.

Antigens, CD↗

PubMed2006

A novel ARF-binding protein (LZAP) alters ARF regulation of HDM2.

The tumour suppressor ARF (alternative reading frame) is encoded by the INK4a (inhibitor of cyclin-dependent kinase 4)/ARF locus, which is frequently altered in human tumours. ARF binds MDM2 (murine double minute 2) and releases p53 from inhibition by MDM2, resulting in stabilization, accumulation and activation of p53. Recently, ARF has been found to associate with other proteins, but, to date, little is known about ARF-associated proteins that are implicated in post-translational regulation of ARF activity. Using a yeast two-hybrid screen, we have identified a novel protein, LZAP (LXXLL/leucine-zipper-containing ARF-binding protein), that interacts with endogenous ARF in mammalian cells. In the present study, we show that LZAP reversed the ability of ARF to inhibit HDM2's ubiquitin ligase activity towards p53, but simultaneously co-operated with ARF, maintaining p53 stability and increasing p53 transcriptional activity. Expression of LZAP, in addition to ARF, increased the percentage of cells in the G1 phase of the cell cycle. Expression of LZAP also caused activation of p53 and a p53-dependent G1 cell-cycle arrest in the absence of ARF. Taken together, our data suggest that LZAP can regulate ARF biochemical and biological activity. Additionally, LZAP has p53-dependent cell-cycle effects that are independent of ARF.

Alternative Splicing↗

PubMed2006

Interaction between Mnk2 and CBC(VHL) ubiquitin ligase E3 complex.

MAP kinase-interacting kinase-2 (Mnk2) is one of the downstream kinases activated by MAP kinases. It phosphorylates the eukaryotic initiation factor 4E (eIF4E), although the role of eIF4E phosphorylation and the role of Mnk2 in the process of protein translation are not well understood. Except for eIF4E, other physiological substrates of Mnk2 are still unidentified. To look for these unidentified substrates and to reveal the physiological function of Mnk2, we performed a yeast two-hybrid screening with Mnk2 as the bait. The results demonstrated Mnk2 could interact with VHL (von Hippel-Lindau tumor suppressor), Rbx1 (ring-box 1) and Cul2 (Cullin2) proteins in yeast cells. Furthermore, we validated the interaction between Mnk2 and VHL proteins in mammalian cells by co-immunoprecipitation analysis. Because the three proteins VHL, Rbx1 and Cul2 are all components of the CBC(VHL) ubiquitin ligase E3 complex, it has been shown that Mnk2 can interact with CBC(VHL) complex, and is probably one of the new substrates of the CBC(VHL) complex. Furthermore, during the interaction of Mnk2 with von Hippel-Lindau (VHL) tumor suppressor- binding protein 1 (VBP1), it appears that Mnk2 also joins to modulate cell shape as VBP1 plays an important role in the process of the maturation of the cytoskeleton and in the process of morphogenesis.

Carrier Proteins↗

PubMed2006

[Different expression and significance of VEGF and PCNA in aorta and pulmonary artery smooth muscle cells of rats with hypoxia pulmonary hypertension].

AIM: To study the expression of vascular endothelial growth factor (VEGF) and proliferating cell nuclear antigen(PCNA) in aorta and pulmonary artery smooth muscle cells of rats with hypoxia pulmonary hypertension(HPH). METHODS: The rat chronically HPH models were set up in the hypobaric hypoxia cabin. The experimental rats were divided into 3 groups: control group (rearing in a normoxia environment), two hypoxia groups (oxygen-deficient time being 2 weeks and 3 weeks, respectively). Expression of VEGF and PCNA were detected by immunohistochemical staining and image analysis. RESULTS: There was VEGF expression in vascular smooth muscle cells of aorta, pulmonary artery trunk and pulmonary arteriole in control group. In two hypoxia groups VEGF expression in vascular smooth muscle cells of pulmonary artery, trunk and pulmonary arteriole increased significantly, while no difference was found in smooth muscle cells of aorta. Expression of PCNA was very little in vascular smooth muscle cells of aorta, pulmonary artery trunk and pulmonary arteriole in control group. In two hypoxia groups, the PCNA expression increased only in vascular smooth muscle cells of pulmonary arteriole; there was no difference of PCNA expression in vascular smooth muscle cells of aorta and pulmonary artery trunk between hypoxia groups and control group. CONCLUSION: There is difference of VEGF expression in pulmonary artery trunk and aorta smooth muscle cells during the formation of chronic HPH, suggesting that VEGF expression may play very important role in the formation of chronic HPH.

Animals↗

PubMed2006

[Downregulation of Bcl-2 and survivin expression and release of Smac/DIABLO involved in bufalin-induced HL-60 cell apoptosis].

OBJECTIVE: To investigate the expression of mitochondria-mediated apoptosis pathway related genes bcl-2, Bax, survivin and Smac/DIABLO in bufalin induced HL-60 cell apoptosis. METHODS: Cell viability was determined by trypan blue exclusion, apoptosis by morphology and flow cytometry, expressions of Bcl-2, Bax, Survivin, Smac/DIABLO and caspase-3 protein by Western blot, and expression of survivin mRNA by RT-PCR. RESULTS: Proliferation of HL-60 cells was inhibited by bufalin and the IC(50) at 24, 48 and 72 h were 25.8, 8.0 and 2.1 nmol/L, respectively. Apoptosis was induced when the cells were treated with bufalin at concentrations of 50.0 nmol/L and higher. Compared with the control, HL-60 cells treated with bufalin at 50.0 nmol/L for 6, 12, 24 and 48 h showed decrease of Bcl-2 protein expression to 88.6%, 53.3%, 19.2% and 9.5%, Bcl-2/Bax ratio (control 2.0) to 1.7, 1.1, 0.4 and 0.2, Survivin protein expression to 75.2%, 54.8%, 37.5% and 20.3%, and survivin mRNA to 85.7%, 39.4%, 12.5%and 0%, respectively. The expression of Smac/DIABLO protein was downregulated to 77.5% (12 h), 21.2% (24 h) and 15.3% (48 h) in mitochondrial fraction and upregulated to 1.4-(12h), 2.0-(24 h) and 3.5- folds (48 h) in cytosolic fraction, respectively. The active subunits of caspase-3 were displayed after treatment for 8 h till 48 h. CONCLUSION: Apoptosis induced by bufalin is related to downregulation of expressions of bcl-2 and survivin, decrease of Bcl-2/Bax ratio, mitochondrial release of Smac/DIABLO, and activation of caspase-3. The mitochondria-mediated apoptotic pathway may be involved in the apoptosis induced by bufalin in HL-60 cells.

Apoptosis↗

PubMed2006

[Effect of Rho kinase on hypoxia stimulated proliferation of pulmonary arterial smooth muscle cells].

OBJECTIVE: To study whether Rho kinase is involved in the proliferation of pulmonary arterial smooth muscle cells (PASMCs) induced by hypoxia. METHODS: Rat's PASMCs were isolated and cultured. Methyl thiazolyl tetrazolium (MTT) was used to determine the growth of cells. The cell cycle was analyzed by flow cytometry. Western blot was used to assess the expression of Rho kinase. RESULTS: The results of MTT showed that the number of PASMCs was increased after exposure to low oxygen tension for 12 hours compared with PASMCs in normoxia. After exposure of PASMCs to hypoxia for 24 hours,the cellular proliferation peaked,and was higher than that of PASMCs exposed to normal oxygen tension, hypoxia and Y27632 (Rho kinase inhibitor) groups,then it declined when exposed for 48 hours. Analysis of cell cycle indicated that the ability of cell proliferation increased significantly in PASMCs exposed to hypoxia compared with normoxia. Rho kinase level was higher in PASMCs exposed to hypoxia compared with normoxia. CONCLUSION: Hypoxia stimulates proliferation of PASMCs and promotes PASMCs into the phase of mitosis. The expression of Rho kinase is increased in PASMCs that are exposed to hypoxia, and it shows that Rho kinase is activated by hypoxia in PASMCs. Rho kinase maybe involve in the proliferation of PASMCs induced by hypoxia.

Animals↗

PubMed2005

Polycystin-1 and polycystin-2 regulate the cell cycle through the helix-loop-helix inhibitor Id2.

Autosomal-dominant polycystic kidney disease (ADPKD) is the most common hereditary kidney disease and is characterized by progressive cyst formation and ultimate loss of renal function. Increased cell proliferation is a key feature of the disease. Here, we show that the ADPKD protein polycystin-2 (PC2) regulates the cell cycle through direct interaction with Id2, a member of the helix-loop-helix (HLH) protein family that is known to regulate cell proliferation and differentiation. Id2 expression suppresses the induction of a cyclin-dependent kinase inhibitor, p21, by either polycystin-1 (PC1) or PC2. The PC2-Id2 interaction is regulated by PC1-dependent phosphorylation of PC2. Enhanced Id2 nuclear localization is seen in human and mouse cystic kidneys. Inhibition of Id2 expression by RNA interference corrects the hyperproliferative phenotype of PC1 mutant cells. We propose that Id2 has a crucial role in cell-cycle regulation that is mediated by PC1 and PC2.

Active Transport, Cell Nucleus↗

PubMed2005

[An investigation of the sexual physiological and psychological development of 2,770 high school students in Yibin].

OBJECTIVE: To investigate the actual condition of the sexual physiological and psychological development of the high school students in Yibin in order to get a reliable basis for sexual education of the teenagers. METHODS: With a proportion of 1% to the whole, 2,770 students were randomly selected from eight high schools in the urban and rural areas of the city. We devised a questionnaire and asked each student to fill in his or her answers presently. RESULTS: So far as sexual physiological and psychological development was concerned, the high school students of Yibin were found rather precocious, with very little sexual knowledge and psychological endurance in sexual affairs and a relative lack of sexual education. CONCLUSION: It is imperative to extend the scope of puberty sexual education in high schools. Teenagers must be taught different kinds of sexual knowledge at different periods of growth as well as how to avoid sexually transmitted diseases and gestation. The sexual knowledge level of the teachers must also be raised. It is a must to establish service or specialist consultation hot lines about sexual knowledge for teenagers. Parents are expected to change their traditional views and assume an active role in the joint efforts of sexual education for their children.

Adolescent↗

PubMed2005

[Effect of Twin-block appliance in the treatment of Class II and division I malocclusion: a cephalometric study in 12 patients].

PURPOSE: To quantitatively evaluate the skeletal and dentoalveolar changes induced by Twin-block appliance for treatment of Class II,division I malocclusions in growing children. METHODS: Twelve patients with Class II, division I malocclusions aged 10 to 12 years were investigated. The records were evaluated and compared with an age-matched sample of untreated Class II control subjects. The follow-up period was 12 months. Group t test was used for comparison. RESULTS: In the treatment group, the upper incisors retroclination of the upper incisors and the mandibular forward movement contributed more to the overjet reduction. The skeletal and dental effects changes molar correction were almost similar. The mandibular growth in the treatment group was 2.29 mm, greater than that in the control group. The posterior facial height and the anterior lower facial height increased by 2.28 mm and 2.58 mm respectively. On the other hand, unfavorable vertical changes were not observed. CONCLUSIONS: The treatment of Class II division I malocclusion with Twin-block appliance was effective in reducing overjet, correcting molar relationship and improving soft tissue profile. It can also enhance mandibular growth.

Case-Control Studies↗

PubMed2005

[Study on the association between gestational diabetes mellitus and tumor necrosis factor-alpha gene polymorphism].

OBJECTIVE: To study allelic frequency of tumor necrosis factor-alpha (TNF-alpha) in gestational diabetes mellitus (GDM) of Han ethnicity in north China and to determine whether there is a specific allele of TNF-alpha associated with GDM susceptibility. METHODS: By using PCR-RFLP, we detected the distribution of TNF-alpha promoter alleles frequency in GDM women and control normal pregnant women. Plasma TNF-alpha levels and insulin levels were measured by radioimmunoassay. RESULTS: (1) There was a significant increase of A alleles frequency of TNF-alpha promoter -308 gene in GDM women compared with control group (61.4% vs 30.0%, P < 0.05) and an increase of the AA + GA genotype was observed in GDM group (71.4% vs 37.1%, P < 0.05). (2) In GDM group, the patients carrying the AA + GA genotype had higher plasma TNF-alpha levels (52 +/- 13 vs 14 +/- 4, P < 0.05) and a lower insulin sensitivity (13.6 +/- 6.5 vs 1.9 +/- 0.2, P < 0.05) compared with those carrying the other genotype (GG). CONCLUSIONS: The 308 G-->A polymorphism of TNF-alpha promoter gene is involved in the pathophysiology of insulin resistance and gestational diabetes mellitus.

Adult↗

PubMed2004

Identification and functional characterization of a novel human misshapen/Nck interacting kinase-related kinase, hMINK beta.

Misshapen/NIKs-related kinase (MINK) is a member of the germinal center family of kinases that are homologous to the yeast sterile 20 (Ste20) kinases and regulate a wide variety of cellular processes, including cell morphology, cytoskeletal rearrangement, and survival. Here, we present the cloning and functional characterization of a novel human Misshapen/NIKs-related kinase beta (hMINK beta) that encodes a polypeptide of 1312 amino acids. hMINK beta is ubiquitously expressed in most tissues with at least five alternatively spliced isoforms. Similar to Nck interacting kinase (NIK) and Traf2 and Nck-interacting kinase (TNIK), hMINK beta moderately activates c-Jun N-terminal kinase (JNK) and associates with Nck via the intermediate domain in the yeast two-hybrid system and in a glutathione S-transferase (GST) pull-down assay. Interestingly, overexpression of the kinase domain deleted and kinase-inactive mutants of hMINK beta in human fibrosarcoma HT1080 cells enhanced cell spreading, actin stress fiber formation, and adhesion to extracellular matrix, as well as decreased cell motility and cell invasion. Furthermore, these mutants also promoted cell-cell adhesion in human breast carcinoma MCF7 cells, evidenced with cell growth in clusters and increased membrane localization of beta-catenin, a multifunctional protein involved in E-cadherin-mediated cell adhesion. Finally, hMINK beta protein was found to colocalize with the Golgi apparatus, implicating that hMINK beta might exert its functions, at least in part, through the modulation of intracellular protein transport. Taken together, these results suggest that hMINK beta plays an important role in cytoskeleton reorganization, cell adhesion, and cell motility.

Adaptor Proteins, Signal Transducing↗

PubMed2004

Up-regulation of vascular endothelial growth factor (VEGF) in small-for-size liver grafts enhances macrophage activities through VEGF receptor 2-dependent pathway.

This study aims to investigate the potential role of vascular endothelial growth factor (VEGF) and VEGF-R2 (fetal liver kinase (Flk)-1) in mediating macrophage activities in small-for-size liver transplantation. A rat orthotopic liver transplantation model was performed using either whole, 50, or 30% liver grafts (both 50 and 30% were regarded as small-for-size) in syngeneic or allogeneic combinations, respectively. Firstly, the mRNA and protein levels of VEGF and Flk-1 in liver grafts were detected by RT-PCR and Western blot, and the number of Flk-1(+) macrophages (labeled by ED1) was determined by flow cytometry. It was found that the small-for-size isografts and allografts presented higher levels of VEGF and Flk-1 expression than the whole isograft and allograft. In addition, a higher number of Flk-1(+)ED1(+) cells were detected in the small-for-size isografts and allografts than the whole isograft and allograft. Secondly, our study revealed that macrophage cell lines did not initially express detectable Flk-1, but could be induced by VEGF, and the inducible expression of Flk-1 in macrophages was related to their migration and proliferation activities. Finally, our study demonstrated that the induction of Flk-1 expression on macrophages by VEGF was associated with the expression of NF-kappaB and heat shock protein 90. In conclusion, the present study showed that the up-regulated expression of VEGF and its interaction with Flk-1 in small-for-size liver grafts might facilitate the activities of macrophages.

Animals↗