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Jie Xu

Publications and source records attributed to Jie Xu.

At least 91 records · Page 5Linked to original sources
PubMed2004

Transcription factor Egr-1 in calcific aortic valve disease.

BACKGROUND AND AIM OF THE STUDY: Previous immunohistochemistry studies have shown that the transcription factor, Egr-1, is increased in human atherosclerotic lesions but is absent from the normal adjacent aortic wall. The hypothesis was investigated that Egr-1 is also increased in calcified heart valve cusps because of the unique presence in these tissues of proteins known to be regulated by Egr-1, such as tenascin C (TN-C). METHODS: Non-calcified and calcified human aortic valves were obtained at autopsy or from cardiac surgery. Egr-1 immunohistochemical studies were performed. The effects of Egr-1 on cellular proliferation and on mechanisms of calcification were also investigated using sheep aortic valve interstitial cell (SAVIC) cultures. Signal transduction pathways involving Egr-1 were studied with specific inhibitors. RESULTS: Immunohistochemical studies revealed that calcific aortic stenosis cusps contained a significantly higher level of Egr-1 in the spindle-shaped interstitial cells of calcified human aortic valves, but not white blood cells. By comparison, Egr-1 was detected at very low levels in the interstitial cells of non-calcified human aortic valve cusps. SAVIC cultivated on denatured versus native collagen substrates demonstrated a marked increase in Egr-1 levels (by Western blotting), and an absence of calcification in these cultures, compared to SAVIC grown on native collagen which calcified severely with little Egr-1 expression. Parallel increases in TN-C and osteopontin (OPN), both of which are proteins associated with heart valve calcification, were observed (by Western blotting) in SAVIC grown on denatured collagen. Furthermore, a protein kinase-C (PKC) inhibitor blocked the up-regulation of Egr-1 and TN-C, implicating PKC-dependent signaling control of Egr-1 and TN-C up-regulation. CONCLUSION: Egr-1 is up-regulated in human calcific aortic stenosis cusps compared to non-calcified normal cusps. Egr-1 up-regulation involves a PKC-dependent signaling pathway. TN-C and OPN appear to be co-regulated with Egr-1. Furthermore, in SAVIC cultures on denatured collagen, Egr-1 up-regulation was associated with inhibition of calcification. Taken together, these results suggest that complex Egr-1 mechanisms may be operative in calcific aortic stenosis.

Aged↗
PubMed2003

SLC26A7: a basolateral Cl-/HCO3- exchanger specific to intercalated cells of the outer medullary collecting duct.

The outer medullary collecting duct (OMCD) plays an important role in bicarbonate reabsorption and acid-base regulation. An apical V-type H+-ATPase and a basolateral Cl-/HCO3- exchanger, located in intercalated cells of OMCD, mediate the bicarbonate reabsorption. Here we report the identification of a new basolateral Cl-/HCO3- exchanger in OMCD intercalated cells in rat kidney. Northern hybridizations demonstrated the predominant expression of this transporter, also known as SLC26A7, in the outer medulla, with lower expression levels in the inner medulla. SLC26A7 was recognized as a approximately 90-kDa band in the outer medulla by immunoblot analysis and was localized on the basolateral membrane of a subset of OMCD cells by immunocytochemical staining. No labeling was detected in the cortex. Double-immunofluorescence labeling with the aquaporin-2 and SLC26A7 antibodies or anion exchanger-1 and SLC26A7 antibodies identified the SLC26A7-expressing cells as alpha-intercalated cells. Functional studies in oocytes demonstrated that increasing the osmolality of the media (to simulate the physiological milieu in the medulla) increased the Cl-/HCO3- exchanger activity mediated via SLC26A7 by about threefold (P < 0.02 vs. normal condition). We propose that SLC26A7 is a basolateral Cl-/HCO3- exchanger in intercalated cells of the OMCD and may play an important role in bicarbonate reabsorption in medullary collecting duct.

Animals↗
PubMed2003

Prevention of postlaminectomy epidural fibrosis using bioelastic materials.

STUDY DESIGN: The use of elastic protein-based polymers for the prevention of epidural fibrosis following lumbar spine laminectomy was investigated in a rabbit model. OBJECTIVES: To determine the safety and efficacy of two bioelastic polymers in matrix and gel forms as interpositional materials in preventing postlaminectomy epidural fibrosis. SUMMARY OF BACKGROUND DATA: Postlaminectomy epidural fibrosis complicates revision spine surgery and is implicated in cases of "failed back syndrome." Materials employed as mechanical barriers to limit tethering of neural elements by the fibrosis tissue have met with little success. A recent family of protein-based polymers, previously reported to prevent postoperative scarring and adhesions, may hold promise in treating this condition. METHODS: Sixteen female New Zealand White rabbits underwent laminectomy at L4 and L6. Two polymer compositions, each in membrane and gel forms, were implanted at a randomly assigned level in four rabbits each, with the remaining level serving as an internal control. The animals were killed at 8 weeks, and qualitative and quantitative histology and gross pathologic examination were performed for both the control and the experimental sites to assess the polymers' efficacy in preventing dorsal epidural fibrosis. RESULTS: The use of the polymers caused no adverse effects. Compared to the control sites, both polymers in either gel or membrane form significantly reduced the formation of epidural fibrosis and its area of contact with the dura postlaminectomy. However, no significant difference in efficacy was detected between either the polymers or their respective forms in preventing epidural fibrosis. CONCLUSIONS: The selected compositions of biosynthetic, bioelastic polymers were safe and effective in the limiting the direct contact and consequent tethering of the underlying neural elements by the postlaminectomy epidural fibrosis in rabbits.

Animals↗
PubMed2003

Identification of an apical Cl-/HCO3- exchanger in gastric surface mucous and duodenal villus cells.

The molecular identity of the apical HCO3(-)-secreting transporter in gastric mucous cells remains unknown despite its essential role in preventing injury and ulcer by gastric acid. Here we report the identification of a Cl-/HCO3- exchanger that is located on apical membranes of gastric surface epithelial cells. RT-PCR studies of mouse gastrointestinal tract mRNAs demonstrated that this transporter, known as anion exchanger isoform 4 (AE4), is expressed in both stomach and duodenum. Northern blot analysis of RNA from purified stomach epithelial cells indicated that AE4 is expressed at higher levels in mucous cells than in parietal cells. Immunoblotting experiments identified AE4 as a approximately 110- to 120-kDa protein in membranes from stomach epithelium and apical membranes from duodenum. Immunocytochemical staining demonstrated that AE4 is expressed in apical membranes of surface cells in both mouse and rabbit stomach and duodenum. Functional studies in oocytes indicated that AE4 functions as a Cl-/HCO3- exchanger. These data show that AE4 is an apical Cl-/HCO3- exchanger in gastric mucous cells and duodenal villus cells. On the basis of its function and location, we propose that AE4 may play an important role in mucosal protection.

Animals↗
PubMed2003

De novo 1q32q44 duplication and distal 1q trisomy syndrome.

We report on an infant with minor anomalies and a de novo 1q duplication. The chromosomal abnormality was diagnosed prenatally after sonographic detection of cerebral ventriculomegaly and bilateral choroid plexus cysts in the fetus. The amniocentesis showed an abnormal male karyotype, 46,XY,dup(1)(q32q44), subsequently confirmed by fluorescence in situ hybridization using whole chromosome paint 1 and comparative genomic hybridization. The baby, born at 37 weeks of gestation, had wide cranial sutures and large fontanelles, sloping forehead, hypertelorism, short and downward-slanting palpebral fissures, a high-arched and narrow palate, malformed ears, and long feet with overriding second and third toes. This is the sixth case of known duplication involving the 1q32q44 segment; the physical findings in the case reported herein are similar to those of other patients reported previously, providing further evidence of the existence of the "distal 1q trisomy" phenotype.

Abnormalities, Multiple↗
PubMed2003

Advances in molecular cytogenetics for the evaluation of mental retardation.

Recent years have witnessed rapid advances in molecular cytogenetics and its impact in studying mental retardation (MR). We review new molecular cytogenetic methods, including interphase fluorescence in situ hyrbridization (FISH), comparative genomic hybridization (CGH), multicolor karyotyping, telomere FISH, primed in situ labeling (PRINS), genotyping, microdissection, and microarray for the evaluation of MR. These new methods are very useful in two major aspects: further characterization of chromosome abnormalities as detected with routine banding analysis, including additions, duplications, deletions, translocations, markers, or complex aberrations; and screening for "hidden" chromosome aberrations in patients with an apparently normal karyotype. These new methods have great diagnostic potential in prenatal, postnatal, and preimplantational settings. Although powerful, at this point, they are primarily research tools in nature. It is essential that these new methods be used in conjunction with standard methods in order to maximize obtainable information for better management of patients with MR.

Chromosome Aberrations↗
PubMed2003

Expression of connective tissue growth factor in bone: its role in osteoblast proliferation and differentiation in vitro and bone formation in vivo.

Connective tissue growth factor (CTGF) is a secreted, extracellular matrix-associated signaling protein that regulates diverse cellular functions. In vivo, CTGF is expressed in many tissues with highest levels in the kidney and brain. The purpose of this study was twofold; first, to localize CTGF in normal bone in vivo during growth and repair, and second, to examine CTGF expression and function in primary osteoblast cultures in vitro and test its effect on bone formation in vivo. Northern and Western blot analyses confirmed that CTGF is expressed in normal long bones during the period of growth or modeling. In situ hybridization and immunohistochemical analysis demonstrated intense staining for CTGF mRNA and protein in osteoblasts lining metaphyseal trabeculae. Examination of CTGF expression in the fracture callus demonstrated that it was primarily localized in osteoblasts lining active, osteogenic surfaces. In primary osteoblast cultures, CTGF mRNA levels demonstrated a bimodal pattern of expression, being high during the peak of the proliferative period, abating as the cells became confluent, and increasing to peak levels and remaining high during mineralization. This pattern suggests that CTGF may play a role in osteoblast proliferation and differentiation as previously demonstrated for fibroblasts and chondrocytes. Treatment of primary osteoblast cultures with anti-CTGF neutralizing antibody caused a dose-dependent inhibition of nodule formation and mineralization. Treatment of primary osteoblast cultures with recombinant CTGF (rCTGF) caused an increase in cell proliferation, alkaline phosphatase activity, and calcium deposition, thereby establishing a functional connection between CTGF and osteoblast differentiation. In vivo delivery of rCTGF into the femoral marrow cavity induced osteogenesis that was associated with increased angiogenesis. This study clearly shows that CTGF is important for osteoblast development and function both in vitro and in vivo.

Animals↗
PubMed2003

[Effect of salvianolate on migration of human vascular endothelial cells].

OBJECTIVE: To study the effect of salvianolate on the migration of endothelial cells induced by monocytes. METHODS: Transwell-boydom system was used to test the migration of endothelial cells induced by monocytes. Enzyme-linked immunosorbent assay (ELISA) and RT-polymerase chain reaction (RT-PCR) method were used to determine the effect of salvianolate on the expression of vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF) and their mRNA of monocytes. RESULTS: The migration of endothelial cells induced by monocytes was facilitated by salvianolate, compared with the control. After the monocytes were treated by salvianolate for 24 hours, the expression of mRNA of VEGF and bFGF was significantly up-regulated, and the expression of VEGF and bFGF was increased. CONCLUSION: The facilitation of salvianolate on the migration of endothelial cells induced by monocytes was observed. Salvianolate stimulates the expression of VEGF and bFGF and their mRNA of monocytes, and salvianolate may have the role of inducing migration of endothelial cells by working on these two factors.

Cell Line↗
PubMed2003

[Clinical study of treatment with continuous renal replacement therapy on severe hepatitis with hepatic encephalopathy].

OBJECTIVE: To evaluate clinical significance and the therapeutic mechanisms of the treatment with continuous renal replacement therapy on severe hepatitis with hepatic encephalopathy. METHODS: Forty-seven cases were randomly divided into three groups: continuous renal replacement therapy (CRRT) group, plasma exchange (PE)+CRRT group and basic treatment group. The former two groups were respectively operated by CRRT and PE+CRRT with basic treatment. Serum biochemical tests, amino, tumor necrosis factor-alpha(TNF-alpha) and interleukin-6 (IL-6) were performed before and after treatment with CRRT. RESULTS: 75.0% patients in CRRT group and 86.7% patients in PE+CRRT group regained normal consciousness, but in basic treatment group 31.3%, achieved a normal neurologic recovery (all P<0.05). The survival rate of patients in CRRT group, PE+CRRT group and basic treatment group were respectively 25.0%, 46.7%, 6.25% (all P<0.05). It was showed that renal function and serum amino were markedly improved after treatment with CRRT, serum TNF-alpha and IL-6 decreased (all P<0.05). There were no changes in levels of serum bilirubin and total bile acid. The hemodynamic function was kept stable and there were no complications during the CRRT therapy. The survival rate of patients was associated with the degree of hepatic encephalopathy in CRRT group, PE+CRRT group(P<0.05). CONCLUSION: Our results show that CRRT is an effective mean in treating severe hepatitis with hepatic encephalopathy and obviously increase the survival rate combined with PE in early hepatic encephalopathy.

Adult↗
PubMed2003

[Clinical analysis of patients with severe acute respiratory syndrome in Beijing area].

OBJECTIVE: To study the epidemiological, clinical and laboratory characteristics, treatment and prognosis of patients with severe acute respiratory syndrome (SARS). METHODS: Clinical data from 250 patients with SARS were retrospectively analyzed. RESULTS: The age of the patients were 36 +/- 16, 44.0% (n = 110) were male, and 56.0% (n = 140) were female. The incubation period was 8 +/- 7 days. The most common symptom were fever (100. 0%), cough (72.8%), and fatigue (70.0%). 27.2% of the patients had decreased white blood cell counts. 64.2% of the patients had decreased lymphocytes. 91.4% and 80.6% of the patients had decreased CD(4)(+) and CD(8)(+) cell counts, respectively. 162 patients (64.8%) had decreased SaO(2). Serum ALT, AST, LDH and CK were elevated in 45.2%, 29.4%, 42.1%, and 18.3% of the patients respectively. Serum IgG to SARS virus was positive in 69.9% of the patients at recovery stage. General combination therapy including antibiotics, anti-viral agents, glucocorticoids and immunity-enhancing agents, was used. Artificial ventilation was used in 196 patients including 8 for whom invasive mechanical ventilation was used Eighty-one (32.4%) were diagnosed as having severe type of SARS. 25 patients died of SARS. CONCLUSIONS: SARS is a highly communicable disease and mostly affects youth and people in their prime of life. It has characteristic clinical manifestations. Combination therapy can be very effective for most patients.

Adolescent↗
PubMed2002

A protease-activated pathway underlying Th cell type 2 activation and allergic lung disease.

The respiratory allergens that induce experimental Th cell type 2-dependent allergic lung inflammation may be grouped into two functional classes. One class of allergens, in this study termed type I, requires priming with adjuvants remote from the lung to overcome airway tolerogenic mechanisms that ordinarily preclude allergic responses to inhaled Ags. In contrast, the other, or type II, allergen class requires neither remote priming nor additional adjuvants to overcome airway tolerance and elicit robust allergic lung disease. In this study, we show in an experimental model that diverse type II allergens share in common proteolytic activity that is both necessary and sufficient for overcoming airway tolerance and induction of pulmonary allergic disease. Inactivated protease and protease-free Ag fragments showed no allergenic potency, demonstrating that only active protease acting on endogenous substrates was essential. Furthermore, induction of airway tolerance could be aborted and allergic lung disease established by simply adding purified protease to a type I allergen. Thus, exogenous proteases are common to type II allergens and may be generally required to overcome the innate resistance of the airway to Th cell type 2 activation and allergic inflammation, raising concern for their potential contribution to diseases such as asthma.

Allergens↗
PubMed2002

Expression of the Na+-HCO-3 cotransporter NBC4 in rat kidney and characterization of a novel NBC4 variant.

The purpose of the present studies was to examine the renal distribution and functional properties of Na(+)-HCO(3)(-) cotransporter type 4 (NBC4), the latest NBC isoform to be identified. Zonal distribution studies in rat kidney by Northern blot hybridization and RT-PCR demonstrated that NBC4 is highly abundant in the outer medulla and cortex but is low in the inner medulla. Nephron segment distribution studies indicated that NBC4 is predominantly expressed in the medullary and cortical thick ascending limb of the loop of Henle. Using specific primers on the basis of the published sequence (GenBank accession no. AF-207661), a full-length NBC4 variant was cloned from human liver and examined. The sequence of this variant (called NBC4e) is shorter by 86 amino acids vs. the published sequence. Xenopus laevis oocytes injected with the full-length NBC4e cRNA were compared with NBC1-expressing oocytes. Although exposure of NBC1-expressing oocytes to CO(2)/HCO(3)(-) resulted in immediate hyperpolarization, the NBC4-expressing oocytes did not show any alteration in membrane potential. NBC activity in oocytes, assayed as the Na(+)-dependent, HCO(3)(-)-mediated intracellular pH recovery from acidosis, indicated that NBC4 is a DIDS-inhibitable NBC. We propose that NBC4 is expressed in the thick ascending limb of the loop of Henle and mediates cellular HCO(3)(-) uptake in this segment.

Animals↗
PubMed2002

Decreased allergic lung inflammatory cell egression and increased susceptibility to asphyxiation in MMP2-deficiency.

Clearance of recruited immune cells is necessary to resolve inflammatory reactions. We show here that matrix metalloproteinase 2 (MMP2), as part of an interleukin 13 (IL-13)-dependent regulatory loop, dampens inflammation by promoting the egress of inflammatory cells into the airway lumen. MMP2-/- mice showed a robust asthma phenotype and increased susceptibility to asphyxiation induced by allergens. However, whereas the lack of MMP2 reduced the influx of cells into bronchoalveolar lavage (BAL), numerous inflammatory cells accumulated in the lung parenchyma. BAL of MMP2-/- mice lacked normal chemotactic activity, whereas lung inflammatory cells from the same mice showed appropriate chemotactic responses. Thus, MMP2 establishes the chemotactic gradient required for egression of lung inflammatory cells and prevention of lethal asphyxiation.

Animals↗