Xiaoliang Liu
China Medical University (PRC)
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Featured researches published by Xiaoliang Liu.
Kidney International | 2009
Xiaoliang Liu; Yanyan Zhao; Luzeng Wang; Xianghong Yang; Zhihong Zheng; Yuanyuan Zhang; Fangjie Chen; Hong Liu
Cytochrome P450 4F2 (CYP4F2) activity is thought to be a factor in the pathogenesis of hypertension through its bioactive metabolite 20-hydroxyeicosatetraenoic acid (20-HETE). We previously found that a gain-in-function CYP4F2 variant in a Chinese cohort was associated with elevated urinary 20-HETE and hypertension. To further explore this association we generated a transgenic mouse model expressing CYP4F2 driven by a modified mouse kidney androgen-regulated protein promoter. This heterologous promoter regulated the expression of luciferase and his-tagged CYP4F2 in transfected HEK 293 cells. In the kidney of transgenic mice, CYP4F2 was localized to renal proximal tubule epithelia and was expressed at a higher level than in control mice, leading to increased urinary 20-HETE excretion. Assessment of CYP4F2 activity by an arachidonic acid hydroxylation assay showed that 20-HETE production was significantly higher in kidney microsomes of transgenic mice compared to control mice, as was their systolic blood pressure. There was a positive correlation of blood pressure with urinary 20-HETE levels. Our results show that increased expression of CYP4F2 in mice enhanced 20-HETE production and elevated blood pressure.
Gene | 2012
Xiaoliang Liu; Jingjing Wu; Hong Liu; Guangrui Lai; Yanyan Zhao
We have previously established a cytochrome P450 4F2 (CYP4F2) transgenic mouse model. The present study elucidated the molecular foundation of hypertension by androgen-induction in this model. The renal expression of CYP4F2 in transgenic mice was highly expressed and strongly induced with 5α-dihydrotestosterone (DHT) treatment determined by Western blot. DHT also increased the renal arachidonic acid ω-hydroxylation and urinary 20-hydroxyeicosatetraenoic acid (20-HETE) excretion (P<0.01), and furthermore elevated the systolic blood pressure by 10 and 22 mm Hg (P<0.05) in female and castrated male transgenic mice, respectively. HET0016 completely eliminated the androgen-induced effects (P<0.01). Endogenous Cyp4a ω-hydroxylases, evaluated by real-time quantitative PCR, were significantly suppressed in transgenic mice (P<0.05). Importantly, transgenic mice with increased 20-HETE showed decreased epoxyeicosatrienoic acids (EETs) and increased dihydroxyeicosatetraenoic acids determined by liquid chromatography-tandem mass spectrometry, contributing to significantly raised ratio of 20-HETE/EETs in the urine and kidney homogenate (P<0.01). These data demonstrate that the androgen aggravated hypertension possibly through an altered ratio of 20-HETE/EETs in CYP4F2 transgenic mice.
BioMed Research International | 2014
Qiang Du; Zheng Li; Yongfeng Pan; Xiaoliang Liu; Pan Bc; Bin Wu
Purpose. To evaluate the significance of molecular detection of cystic fibrosis transmembrane conductance regulator (CFTR) M470V, intron 8 poly-T, and intron 8 TG-repeats in congenital bilateral absence of the vas deferens (CBAVD). Methods. Eighty-nine male patients with CBAVD and 103 healthy males were included in this study. Polymerase chain reaction was performed to amplify the polymorphic regions using primers from conserved regions. M470V was genotyped using real-time PCR by cycling probe. The exon 9 DNA sequence was determined using an automated sequencer. TG-repeats and poly-T were identified by direct sequencing analysis. Results. The 5T allele distribution was 0.32, 0.66 for 7T, and 0.02 for 9T in CBAVD males, respectively. In contrast, the 5T allele distribution was 0.03, 0.96 for 7T, and 0.01 for 9T in healthy control. Study of the polymorphisms of the upstream of exon 9 revealed a higher frequency of 5T allele in the CBAVD males. All cases with TG13T5 haplotype and TG12T5 homozygous led to CBAVD. The CFTR TG12T5-V470 variant haplotype was associated with CBAVD. Conclusion. The 5T allele of intron 8 of CFTR has clinically significant association with CBAVD. TG13T5 and TG12T5 homozygously led to CBAVD, and TG12T5-V470 may also lead to CBAVD.
Gene | 2014
Dan Huang; Shujuan Jiang; Yuanyuan Zhang; Xiaoliang Liu; Jiubin Zhang; Rong He
Brachydactyly type B, an autosomal dominant disorder that is characterized by hypoplasia of the distal phalanges and nails, can be divided into brachydactyly type B1 (BDB1) and brachydactyly type B2 (BDB2). BDB1 is caused by mutations in the receptor tyrosine kinase gene ROR2, which maps to chromosome 9q22, whereas BDB2 is caused by point mutations in the bone morphogenetic protein antagonist NOGGIN. Here, we report a three-generation Chinese family with dominant inheritance of the BDB1 limb phenotype. Sequence analysis identified a novel heterozygous base deletion (c.1396-1398delAA) in the gene ROR2 in all affected family members. This new deletion is expected to produce a truncated Ror2 protein with a new polypeptide of 57 amino acids at the C-terminal.
International Journal of Molecular Medicine | 2011
Guangrui Lai; Xiaoliang Liu; Jingjing Wu; Hong Liu; Yanyan Zhao
A transgenic mouse model in which cytochrome P450 4F2 (CYP4F2) was expressed in multiple organs was expected to clarify the role of 20-hydroxyeicosatetraenoic acid (20-HETE) in the regulation of blood pressure, compared with our previously established kidney androgen-regulated protein (KAP) promoter CYP4F2 transgenic mouse model which predominantly showed renal overexpression of CYP4F2. A novel CYP4F2 transgenic mouse model driven by the cyto-megalovirus (CMV) promoter was generated and identified by PCR and subsequent sequencing. Extensive study of CMV-CYP4F2 transgenic mice demonstrated that CYP4F2 was exclusively expressed in the liver, while 20-HETE levels in the urine, kidney and blood were not affected, and there was no resulting change in the systolic blood pressure. This was in contrast to KAP-CYP4F2 transgenic mice which exerted prohypertensive action of 20-HETE resulting from the renal overexpression of CYP4F2. In addition, CYP4F2 overwhelmed the endogenous renal Cyp4a family mRNA levels in the KAP-CYP4F2 but not in the CMV-CYP4F2 transgenic mice. These results support the idea that overexpression of renal CYP4F2, leading to high 20-HETE in the urine and blood, may account for the elevated blood pressure. The CMV promoter did not direct CYP4F2 expression into extensive tissues and organs in an attempt to clarify the action of 20-HETE.
International Journal of Molecular Sciences | 2014
Shujuan Jiang; Jiubin Zhang; Dan Huang; Yuanyuan Zhang; Xiaoliang Liu; Yinzhao Wang; Rong He; Yanyan Zhao
Nail patella syndrome (NPS) is an autosomal dominant disorder characterized by nail malformations, patellar apoplasia, or patellar hypoplasia. Mutations within the LMX1B gene are found in 85% of families with NPS; thus, this gene has been characterized as the causative gene of NPS. In this study, we identified a heterozygous microdeletion of the entire LMX1B gene using multiplex ligation-dependent probe amplification (MLPA) in a Chinese family with NPS. The determination of the deletion breakpoints by Illumina genome-wide DNA analysis beadchip showed that the deletion was located in chromosome 9q33.3 and spanned about 0.66 Mb in size. This heterozygous deletion provides strong evidence for haploinsufficiency as the pathogenic mechanism of NPS.
Gene | 2018
Song Bai; Qiang Du; Xiaoliang Liu; Yuxin Tong; Bin Wu
OBJECTIVE Mutations in the cystic fibrosis transmembrane conductance regulator gene (CFTR) gene can be involved in the development of congenital bilateral absence of the vas deferens (CBAVD). This study was aimed at investigating mutations in the promoter region of the CFTR gene and its associated effects on CFTR transcription in Chinese patients with CBAVD. METHODS To identify CFTR promoter region mutations in Chinese CBAVD patients, fragments 1.4 kb upstream of the ATG start codon of the CFTR gene were sequenced in 66 Chinese patients with CBAVD and compared to the corresponding sequences from 60 healthy subjects and sequence data present in the NCBI database. The relationship between the mutations and gene regulation was explored using Transfac analysis and a phylogenetic footprint method. Plasmids were constructed by incorporating statistically significant variant sequences. The effects of the mutations on CFTR transcription were investigated using a dual luciferase reporter gene assay. RESULTS a total of six point mutations, which included c.-150G > T, c.-205 T > C, c.-245C > T, c.-871G > T, c.-966 T > G and c.-1062G > C, and one deletion mutation, namely c.-861delT, were identified in the promoter region of the CFTR gene in Chinese CBAVD patients. Among them, c.-966 T > G had the highest frequency and presented in either a homozygous or heterozygous mutation state. The frequency of G/G genotype in the CBAVD group was 33/66 (50.00%), while the T/G and T/T genotypes had frequencies of 18/66 (27.27%) and 15/66 (22.73%), respectively. A significant difference was found between the CBAVD and control group (P < 0.01). The locus for this variant was found in a conserved sequence. The Transfac tool showed that transcription factors EHF and STAT3, which are closely associated with reproduction, can bind to the sequence containing the variant locus. Two types of plasmid vectors, one carrying the G/G variant and the other the wild type T/T sequences, were constructed and respectively transfected into human cervical cancer cells (HeLa), human renal epithelial cells (HEK-293), and human colon cancer cells (SW480). It was found that the homozygous c.-966 T > G mutation significantly reduced CFTR transcription efficiency by 18.75%-35.50%. CONCLUSION Mutations in the promoter region of the CFTR gene in Chinese CBAVD patients are different from those found in comparable Caucasian patients. The homozygous c.-966 T > G mutation state had the highest frequency, which reduced the CFTR transcriptional level and showed significant tissue-specificity.
Molecular Endocrinology | 2012
Guangrui Lai; Jingjing Wu; Xiaoliang Liu; Yanyan Zhao
Human Genetics | 2013
Jingjing Wu; Xiaoliang Liu; Guangrui Lai; Xianghong Yang; Luzeng Wang; Yanyan Zhao
Molecular Medicine Reports | 2016
Bijun Zhang; Guangrui Lai; Xiaoliang Liu; Yanyan Zhao