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Biomedical subjects

L Wang

Publications and source records attributed to L Wang.

At least 55 records · Page 3Linked to original sources
PubMed2006

HTPAP gene on chromosome 8p is a candidate metastasis suppressor for human hepatocellular carcinoma.

Our previous studies suggested that chromosome 8p deletion is associated with metastasis of hepatocellular carcinoma (HCC), in which some novel metastasis suppressor genes might be harbored. The present study aimed to identify the metastatic suppressor gene(s). A cDNA chip was constructed with the expressed sequence tags (ESTs) from chromosome 8p and used to compare the difference of expression profiling between the MHCC97-H and MHCC97-L cell lines with different metastatic potentials and similar genetic backgrounds. In all, 10 ESTs were significantly downregulated in MHCC97-H cell line with higher metastatic potential. One full-length gene, HTPAP (phosphatidic acid phosphatase type 2 domain containing 1B), was identified at chromosome 8p12. Sequencing and bioinformatic analyses revealed that HTPAP has 826 bp and encodes a putative protein of 175 amino acids with a transmembrane segment at the NH2 terminus, two protein kinase C phosphorylation site and one tyrosine kinase phosphorylation site. Its expression level in metastatic tumor tissues was much lower than that of primary HCC tissues. Both in vitro and in vivo assays suggested that HTPAP could suppress the invasion and metastasis of HCC. These suggested that HTPAP is a novel metastatic suppressor gene for HCC. The mechanism of the effect of HTPAP on HCC metastasis is not clear yet and deserves further investigation.

Amino Acid Sequence↗
PubMed2006

Polyunsaturated fatty acids and anthropometric indices of children in rural China.

OBJECTIVE: To define fatty acid and macronutrient intakes in a rural Chinese preschool population, and relate these intakes to anthropometric indices. DESIGN: Cross-sectional survey of anthropometry and diet (three 24-h recalls). National Centers for Health Statistics/World Health Organization growth reference charts were used to determine the prevalence of malnutrition (z-scores less than -2 standard deviation (s.d.) below the mean): height-for-age (stunted), weight-for-age (underweight), weight-for-height (wasted) and mid-upper-arm-circumference-for-age (low fat/muscle). SUBJECTS AND SETTING: A total of 196 children aged 1-5 years old were volunteered by their families to participate in the survey, located in Heqing County, Yunnan Province, China. RESULTS: The respective prevalence of stunting, underweight, wasting and low fat/muscle was: 38, 21, 2 and 8%. Daily intakes of linoleic acid (LA; 18:2n-6), alpha-linolenic acid (LNA; 18:3n-3), arachidonic acid (AA; 20:4n-6) and docosahexaenoic acid (DHA; 22:6n-3), averaged for all children, were 2 100+/-1200, 300+/-250, 55+/-35 and 30+/-140 mg/day, respectively. As percent of total fat intake, LA contributed 11.9%, LNA 1.8%, AA 0.3% and DHA 0.2%. Height-for-age and weight-for-age z-scores were negatively correlated with g/kg/day intake of LA and AA (P<0.05). Weight-for-height z-score was negatively correlated with AA g/kg/day intake (P<0.05). CONCLUSIONS: This study provided polyunsaturated fatty acids (PUFA) intakes in rural preschool children in a developing country. The associations of PUFA intake with early childhood growth suggest that growth in preschool-aged children could be significantly and specifically related to n-6 fatty acid intakes.

Anthropometry↗
PubMed2006

Thiopurine S-methyltransferase pharmacogenetics: insights, challenges and future directions.

The thiopurine S-methyltransferase (TPMT) genetic polymorphism is one of the most 'mature' examples in pharmacogenetics. That is true because of its importance clinically for the individualization of thiopurine drug therapy and also because TPMT has provided novel insights into molecular mechanisms responsible for the functional effects of common genetic polymorphisms. This review will summarize the development of our understanding of the role of inheritance in the regulation of TPMT as well as the clinical implications of that genetic regulation. It will also summarize recent studies in which TPMT pharmacogenetics has enhanced our understanding of molecular mechanisms by which common polymorphisms influence or alter function. TPMT pharmacogenetics highlights the potential clinical importance of the translation of pharmacogenetics from bench to bedside, the potential for basic pharmacogenetic research to provide insight into mechanisms by which genetic polymorphisms can alter function, and the challenges associated with the achievement of both of those goals.

Antineoplastic Agents↗
PubMed2006

Biochemical and functional characterization of Epstein-Barr virus-encoded BARF1 protein: interaction with human hTid1 protein facilitates its maturation and secretion.

EBV BARF1 gene encodes a secretory protein with transforming and mitogenic activities. In this report, the post-translational modification, folding, maturation and secretion of BARF1 are systematically studied by site-directed mutagenesis and overexpression of the protein in mammalian cells using the vaccinia/T7 system. The protein was shown to be post-translationally modified by N-linked glycosylation on the asparagine 95 residue. This modification was confirmed to be essential for the maturation and secretion of the protein. Analysis of the four cysteine residues by site-directed mutagenesis demonstrated that cysteine 146 and 201 were essential for proper folding and secretion of the protein. To search for human proteins involved in the maturation process of the protein, a yeast two-hybrid screening was carried out using the BARF1 sequence from amino acids 21-221 (BARF1Delta) as bait, leading to the identification of human hTid1 protein as a potential interacting protein. This interaction was subsequently confirmed by coimmunoprecipitation and dual immunofluorescent labeling of cells coexpressing BARF1 and hTid1, and the interaction domain in hTid1 was mapped to amino acids 149-320. Interestingly, coexpression of BARF1 with hTid1 demonstrated that hTid1 could promote secretion of BARF1, suggesting that hTid1 may act as a chaperone to facilitate the folding, processing and maturation of BARF1.

HSP40 Heat-Shock Proteins↗
PubMed2006

Epidural cooling for selective brain hypothermia in porcine model.

BACKGROUND: Hypothermia has been shown to be neuroprotective in many animal models and several human trials of brain ischemic and trauma. However systemic hypothermia may result in fatal complications. This study was undertaken to test epidural cooling as a new method of inducing selective brain hypothermia. METHOD: Six adult swine (mean mass, 33.8+/-3.6 kg) were studied. Anesthesia was maintained with pentobarbital sodium (25 mg kg-1, i.v.) and pancuronium bromide (0.5 mg kg-1 h-1, i.v.). Five probes were placed in the rectum, deep brain, brain surface, epidural space, and room air for temperature monitoring respectively. Epidural cooling was performed using cold-saline (4 degrees C) perfusion into the epidural space through a flexible double-lumen catheter. The dripping speed of cold saline was controlled to maintain the target temperature. The changes of the epidural space pressure, complete blood counts, basic metabolic panels, tests for fibrinolysis and coagulation status were monitored to assess hypothermia-induced changes. FINDINGS: Following the epidural cooling perfused with cold-saline (4 degrees C) at mean dripping speed of 720 ml per hour, the local brain surface temperature could decrease rapidly to 17.3-21.6 degrees C within one minute, and deep brain temperature decreased to 27.2-29.7 degrees C within 5 minutes. The target temperatures were easily controlled by the dripping speed of cold saline (from mild to deep hypothermia). The rectal temperature was maintained at normal range within 6 perfusion hours. No arrhythmia was observed, and all hematological variables were within the normal range for swine. No increased intracranial pressure was induced by the cooling method. CONCLUSIONS: The data demonstrate that epidural space cooling was technically feasible and useful for selective brain hypothermia, and the target temperatures are easily controlled. The induction of hypothermia was rapid and maintained for a long period of time, whereas the body temperature was maintained within the normal range and without hemodynamic instability.

Animals↗
PubMed2006

Oncolysis and suppression of tumor growth by a GFP-expressing oncolytic adenovirus controlled by an hTERT and CMV hybrid promoter.

One of the challenges of oncolytic virotherapy is the inability to easily track or monitor virus activity during treatment. Here we describe the construction and functional characterization of Ad/hTC-GFP-E1, an oncolytic virus whose transgenes GFP and E1A are both under the control of a synthetic promoter (hTC). This promoter consists of sequences from the human telomorase reverse transcriptase promoter and a minimal cytomegalovirus (CMV) early promoter. The tumor-specific expression of E1A and GFP was demonstrated by Western blot and fluorescent microscope analyses, and the tumor-specific cytotoxicity by crystal-violet staining and cell viability assays. Viral replication and tumor cell lysis occurred at multiplicities of infection (MOI) as low as 100 viral particles per cell in sensitive cell lines. No overt cytotoxic effect was observed in normal human fibroblasts, even at MOIs over 2000 vp. The presence of oncolytic vector was easily visualized and quantitated in vitro and in vivo, in correlation with viral replication. Intralesional administration of the virus into subcutaneous H1299 (NSCLC) tumor xenografts significantly suppressed tumor growth and provided a survival benefit. Together, these results demonstrate that an hTERT-specific oncolytic adenovirus expressing an hTERT-specific transgene is applicable for cancer therapy.

Adenoviridae↗
PubMed2006

Oncogenic Vav1 induces Rac-dependent apoptosis via inhibition of Bcl-2 family proteins and collaborates with p53 deficiency to promote hematopoietic progenitor cell proliferation.

Vav1 is an hematopoietic-specific Rho guanine nucleotide exchange factor coupling tyrosine kinase receptors and Rac GTPases, and has been implicated in transformation of fibroblasts and pancreas. To determine the biologic effect and oncogenic potential of Vav1 in hematopoietic lineages, we stably express oncogenic mutant of Vav1 in primary bone marrow cells using retrovirus-mediated gene transfer. Contrary to the growth stimulatory effects observed in fibroblasts, oncogenic Vav1 inhibits hematopoietic stem cell/progenitor engraftment in vivo and progenitor cell expansion in vitro via inducing apoptosis. The oncogenic Vav1-induced apoptosis is associated with reduced expression of Bcl-2 and Bcl-xL proteins and effectively suppressed by transgenic overexpression of Bcl-2, suggesting Vav1-mediated signaling via Bcl-2 in apoptosis. Also, oncogenic Vav1 stimulates sustained activation of Rac GTPases and the biologic effects of oncogenic Vav1 are Rac-dependent. Further, when expressed in the p53-deficient cells, which express elevated Bcl-2 and Bcl-xL and are resistant to the apoptosis, oncogenic Vav1 enhances both proliferation and self-renewal of hematopoietic progenitor cells. These results demonstrate clear phenotypic differences between wild-type and p53(-/-) hematopoietic cells expressing oncogenic Vav1, and suggest oncogenic potential of Vav1-mediated pathways in primary hematopoietic cell when they collaborate with additional genetic hits that affect the p53 pathway.

Animals↗
PubMed2006

Homotypic FADD interactions through a conserved RXDLL motif are required for death receptor-induced apoptosis.

Death receptors in the TNF receptor superfamily signal for apoptosis via the ordered recruitment of FADD and caspase-8 to a death-inducing signaling complex (DISC). However, the nature of the protein-protein interactions in the signaling complex is not well defined. Here we show that FADD self-associates through a conserved RXDLL motif in the death effector domain (DED). Despite exhibiting similar binding to both Fas and caspase-8 and preserved overall secondary structure, FADD RDXLL motif mutants cannot reconstitute FasL- or TRAIL-induced apoptosis and fail to recruit caspase-8 into the DISC of reconstituted FADD-deficient cells. Abolishing self-association can transform FADD into a dominant-negative mutant that interferes with Fas-induced apoptosis and formation of microscopically visible receptor oligomers. These findings suggest that lateral interactions among adapter molecules are required for death receptor apoptosis signaling and implicate self-association into oligomeric assemblies as a key function of death receptor adapter proteins in initiating apoptosis.

Adaptor Proteins, Signal Transducing↗
PubMed2006

Genetic analysis and fine mapping of a rice brown planthopper (Nilaparvata lugens Stål) resistance gene bph19(t).

Genetic analysis and fine mapping of a resistance gene against brown planthopper (BPH) biotype 2 in rice was performed using two F(2) populations derived from two crosses between a resistant indica cultivar (cv.), AS20-1, and two susceptible japonica cvs., Aichi Asahi and Lijiangxintuanheigu. Insect resistance was evaluated using F(1) plants and the two F(2) populations. The results showed that a single recessive gene, tentatively designated as bph19(t), conditioned the resistance in AS20-1. A linkage analysis, mainly employing microsatellite markers, was carried out in the two F(2) populations through bulked segregant analysis and recessive class analysis (RCA), in combination with bioinformatics analysis (BIA). The resistance gene locus bph19(t) was finely mapped to a region of about 1.0 cM on the short arm of chromosome 3, flanked by markers RM6308 and RM3134, where one known marker RM1022, and four new markers, b1, b2, b3 and b4, developed in the present study were co-segregating with the locus. To physically map this locus, the bph19(t)-linked markers were landed on bacterial artificial chromosome or P1 artificial chromosome clones of the reference cv., Nipponbare, released by the International Rice Genome Sequencing Project. Sequence information of these clones was used to construct a physical map of the bph19(t) locus, in silico, by BIA. The bph19(t) locus was physically defined to an interval of about 60 kb. The detailed genetic and physical maps of the bph19(t) locus will facilitate marker-assisted gene pyramiding and cloning.

Animals↗
PubMed2006

Randomized clinical trial of the effects of abdominal drainage after elective hepatectomy using the crushing clamp method.

BACKGROUND: Abdominal drainage is a standard procedure after hepatectomy, but this practice has been challenged recently. METHODS: Between September 2004 and March 2005, 120 consecutive patients who had undergone hepatic resection by the same surgical team were randomly allocated into drainage and no drainage groups (60 in each group). Patient characteristics, preoperative liver function, presence of cirrhosis, resection-related factors and postoperative complications were compared between the two groups. RESULTS: The groups were comparable in terms of demographics, indications for surgery, preoperative liver function test results, presence of cirrhosis, extent of hepatectomy, intraoperative blood loss and requirement for blood transfusion. Symptomatic subphrenic collection and pleural effusion occurred in four patients (7 per cent) who had abdominal drainage and three (5 per cent) who did not. Local wound complications occurred in 17 (28 per cent) and two (3 per cent) patients respectively (P < 0.001). The postoperative hospital stay was similar in the two groups. Multivariate analysis indicated that the presence of cirrhosis and abdominal drainage were independently related to the development of postoperative wound complications. CONCLUSION: Routine abdominal drainage is unnecessary after elective hepatectomy using the crushing clamp method.

Blood Loss, Surgical↗
PubMed2006

Contrasting behaviors of mutant cystathionine beta-synthase enzymes associated with pyridoxine response.

Cystathionine beta-synthase (CBS) deficiency is a recessive genetic disorder characterized by extremely elevated levels in plasma homocysteine. Patients homozygous for the I278T or R266K mutations respond clinically to pharmacologic doses of pyridoxine, the precursor of a cofactor for the enzyme, 5'-pyridoxal phosphate (PLP). Here we test the hypothesis that these mutations are pyridoxine responsive because they lower the affinity of the enzyme for PLP. We show that recombinant R266K has 30 to 100% of the specific activity of the wild-type enzyme, while I278T only has only 1 to 5% activity. Kinetic studies show that the decreased activity in both enzymes is due to reduced turnover rate and not substrate binding. Neither I278T nor R266K appear to greatly affect multimer status of the enzyme. The R266K enzyme has reduced affinity for PLP compared to the wild-type enzyme, providing a mechanism for the pyridoxine response observed in patients. Surprisingly, the I278T enzyme does not have altered affinity for PLP. To confirm that this was not an in vitro artifact, we examined pyridoxine response in mice that stably express human I278T as their sole source of CBS activity. These mice have extremely elevated plasma homocysteine levels and do not respond significantly to large doses of pyridoxine. Our findings suggest that there may be multiple mechanisms involved in response to pyridoxine.

Alleles↗
PubMed2006

Gene expression profile of transgenic mouse kidney reveals pathogenesis of hepatitis B virus associated nephropathy.

Hepatitis B virus (HBV)-associated nephritis has been reported worldwide. Immune complex deposition has been accepted as its pathogenesis, although the association between the presence of local HBV DNA and viral antigen and the development of nephritis remains controversial. To understand better the roles played by HBV protein expression in the kidney, the global gene expression profile was studied in the kidney tissue of a lineage of HBV transgenic mouse (#59). The mice expressed HBsAg in serum, and HBsAg and HBcAg in liver and kidney, but without virus replication. Full-length HBV genome (adr subtype, C genotype) isolated from a chronic HBV carrier was used to establish the transgenic mice #59. Similarly manipulated mice that did not express HBV viral antigens served as controls. Southern blotting, hybridization with HBV probe, and immuno-histochemical staining were used to study HBV gene expression. mRNA extracted from the kidney tissue was analyzed using Affymetrix microarrays. HBsAg and HBcAg were located mainly in the cytoplasm of tubular epithelium. Altogether 520 genes were "up-regulated" more than twofold and 76 genes "down-regulated" more than twofold in the kidney. The complement activation, blood coagulation, and acute-phase response genes were markedly "up-regulated". Compared to the controls, the level of serum C3 protein was decreased in #59 mice, while the level of C3 protein from kidney extract was increased. Results indicate that expression of HBsAg and HBcAg in tubular epithelial cells of the kidney per se can up-regulate complement-mediated inflammatory gene pathways, in addition to immune complex formation.

Animals↗
PubMed2006

The diversity of the DnaJ/Hsp40 family, the crucial partners for Hsp70 chaperones.

DnaJ/Hsp40 (heat shock protein 40) proteins have been preserved throughout evolution and are important for protein translation, folding, unfolding, translocation, and degradation, primarily by stimulating the ATPase activity of chaperone proteins, Hsp70s. Because the ATP hydrolysis is essential for the activity of Hsp70s, DnaJ/Hsp40 proteins actually determine the activity of Hsp70s by stabilizing their interaction with substrate proteins. DnaJ/Hsp40 proteins all contain the J domain through which they bind to Hsp70s and can be categorized into three groups, depending on the presence of other domains. Six DnaJ homologs have been identified in Escherichia coli and 22 in Saccharomyces cerevisiae. Genome-wide analysis has revealed 41 DnaJ/Hsp40 family members (or putative members) in humans. While 34 contain the typical J domains, 7 bear partially conserved J-like domains, but are still suggested to function as DnaJ/ Hsp40 proteins. DnaJA2b, DnaJB1b, DnaJC2, DnaJC20, and DnaJC21 are named for the first time in this review; all other human DnaJ proteins were dubbed according to their gene names, e.g. DnaJA1 is the human protein named after its gene DNAJA1. This review highlights the progress in studying the domains in DnaJ/Hsp40 proteins, introduces the mechanisms by which they interact with Hsp70s, and stresses their functional diversity.

Amino Acid Sequence↗
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↗
PubMed2006

Long-term outcome and neuroradiological findings of 31 patients with 6-pyruvoyltetrahydropterin synthase deficiency.

Tetrahydrobiopterin (BH(4)) deficiency is an autosomal recessive disorder caused by enzyme defects in the biosynthesis or recycling of BH(4). Patients with BH(4) deficiency present with severe neurological signs and symptoms and require a different treatment from classical phenylketonuria. During the last 12 years, 31 cases of BH(4) deficiency were identified in our department. They were all classified as 6-pyruvoyl-tetrahydropterin synthase (PTPS) deficiency. They were diagnosed at the ages of 2.5-48 months and treated with BH(4), L-dopa and 5-hydroxytryptophan immediately after diagnosis. The average development quotients (DQ) at diagnosis and after treatment for more than 3 years were 53+/- 16, and 78+/- 15, respectively. A significant negative correlation was observed between the level of the DQ and the age at which treatment was commenced (r = -0.751, p = 0.002). Developmental profiles were uneven. Language, adaptability and at later age mathematics were particularly weak areas. Only two patients achieved a good performance in mathematics. Eleven patients who were treated with drugs from ages of 2.9-48 months had neuroradiological scanning. Computed tomography disclosed calcification in lentiform nuclei in one patient and magnetic resonance imaging disclosed delayed myelination and abnormal high intensity signal in cerebral white matter in all of them. Even though most of abnormalities were reversible, small patchy or spotted areas were still present on these regions after treatment for 10-46 months. In summary, our study supports the substantial efficacy of the current therapeutic approach in PTPS deficiency of normalizing amine neurotransmitters with three drugs as early as possible. For the first time, calcifications could be detected in patients with PTPS deficiency. Abnormalities in white matter on magnetic resonance imaging were not related to clinical manifestations and most were reversible.

Brain↗
PubMed2006

Conversion from cyclosporine to mycophenolate mofetil improves expression of A20 in the rat kidney allografts undergoing chronic rejection.

AIMS: Cytoprotective genes have shown to display potent anti-inflammatory and antiapoptotic functions in endothelial and smooth muscle cells. We investigated whether cytoprotective genes, especially A20, were involved in mycophenolate mofetil (MMF)'s ability to ameliorate transplant arteriosclerosis in an experimental chronic rejection model. METHODS: Sprague-Dawley rat renal grafts were orthotopically transplanted into Wistar rats following the procedure of Kamada with our modification. The recipients were divided into three oral treatment groups: (1) vehicle group (cyclosporine [CsA] 10 mg/kg.d x 10 d followed by vehicle), (2) CsA group (CsA 10 mg/kg.d x 10 d followed by CsA 6 mg/kg.d), (3) MMF group (converted from CsA 10 mg/kg.d x 10 d to MMF 20 mg/kg.d on day 11). At the same time points after transplantation, the rats were sacrificed to harvest the renal allografts. The expression of four cytoprotective genes, A20, heme oxygenase (HO)-1, Bcl-2, and Bcl-XL, was analyzed by quantitative reverse-transcriptase polymerase chain reaction and immunohistochemistry. RESULTS: The four-cytoprotective genes were all detected in rat kidney allografts undergoing chronic allograft nephropathy. The expression of A20 in grafted kidneys was significantly higher in the MMF than in the CsA or the vehicle group (P < .01). There was no significant difference between the CsA and the MMF groups in the expression of HO-1, Bcl-2, and Bcl-XL. CONCLUSIONS: We demonstrated that MMF improved the expression of A20 in rat kidney allografts undergoing chronic allograft nephropathy. The correlation between MMF and A20 provide an explanation for the mechanism by which MMF ameliorates transplant arteriosclerosis in an experimental animal model of chronic rejection.

Animals↗
PubMed2006

Comparison of rapamycin versus FK506 on expression of cytoprotective genes in the rat kidney allografts undergoing chronic allograft nephropathy.

AIMS: It is increasingly recognized that expression of cytoprotective genes in grafts can affect the progress of chronic allograft nephropathy (CAN). Little is known about the influence of different immunosuppressive regimens on expression of cytoprotective genes in allografts undergoing CAN. We investigate whether there is difference between rapamycin (Rapa) and FK506 in the expression of cytoprotective genes in rat kidney allografts undergoing CAN. METHODS: Sprague-Dawley rat renal grafts were orthotopically transplanted into Wistar rats following the procedure of Kamada with our modification. The recipients were divided into three oral treatment groups: group 1: vehicle group (cyclosporine [CsA] 10 mg/kg.dx 10 days followed by vehicle); group 2: Rapa group (CsA 10 mg/kg.d x 10 d followed by Rapa 0.8 mg/kg.d); group 3: FK506 group (CsA 10 mg/kg.d x 10 d followed by FK506 0.15 mg/kg.d). At the same times after transplantation, the rats were sacrificed to harvest the renal allografts. The expression of four cytoprotective genes, A20, heme oxygenase (HO)-1, Bcl-2, and Bcl-X/L were analyzed in these grafted kidneys by quantitative reverse transcriptase polymerase chain reaction and immunohistochemistry. RESULTS: Four cytoprotective genes were all detected in rat kidney allografts undergoing CAN. The expression of A20 in the Rapa group was significantly higher than that in the FK506 or the vehicle group (P < .05). There was no significant difference between the Rapa group and FK506 group in the expressions of HO-1, Bcl-2, and Bcl-X/L. CONCLUSIONS: We demonstrate that various immunosuppressive agents have different effects on the expression of cytoprotective genes.

Animals↗