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Biomedical subjects

Wei Jiang

Publications and source records attributed to Wei Jiang.

At least 109 records · Page 6Linked to original sources
PubMed2004

Connective tissue growth factor (CTGF) is regulated by Wnt and bone morphogenetic proteins signaling in osteoblast differentiation of mesenchymal stem cells.

Osteoblast lineage-specific differentiation of mesenchymal stem cells is a well regulated but poorly understood process. Both bone morphogenetic proteins (BMPs) and Wnt signaling are implicated in regulating osteoblast differentiation and bone formation. Here we analyzed the expression profiles of mesenchymal stem cells stimulated with Wnt3A and osteogenic BMPs, and we identified connective tissue growth factor (CTGF) as a potential target of Wnt and BMP signaling. We confirmed the microarray results, and we demonstrated that CTGF was up-regulated at the early stage of BMP-9 and Wnt3A stimulations and that Wnt3A-regulated CTGF expression was beta-catenin-dependent. RNA interference-mediated knockdown of CTGF expression significantly diminished BMP-9-induced, but not Wnt3A-induced, osteogenic differentiation, suggesting that Wnt3A may also regulate osteoblast differentiation in a CTGF-independent fashion. However, constitutive expression of CTGF was shown to inhibit both BMP-9- and Wnt3A-induced osteogenic differentiation. Exogenous expression of CTGF was shown to promote cell migration and recruitment of mesenchymal stem cells. Our findings demonstrate that CTGF is up-regulated by Wnt3A and BMP-9 at the early stage of osteogenic differentiation, which may regulate the proliferation and recruitment of osteoprogenitor cells; however, CTGF is down-regulated as the differentiation potential of committed pre-osteoblasts increases, strongly suggesting that tight regulation of CTGF expression may be essential for normal osteoblast differentiation of mesenchymal stem cells.

Adenoviridae↗
PubMed2004

DAL-1/4.1B tumor suppressor interacts with protein arginine N-methyltransferase 3 (PRMT3) and inhibits its ability to methylate substrates in vitro and in vivo.

DAL-1 (differentially expressed in adenocarcinoma of the lung)/4.1B is a tumor suppressor gene on human chromosome 18p11.3 whose expression is lost in >50% of primary non-small-cell lung carcinomas. Based on sequence similarity, DAL-1/4.1B has been assigned to the Protein 4.1 superfamily whose members interact with plasma membrane proteins through their N-terminal FERM (4.1/Ezrin/Radixin/Moesin) domain, and cytoskeletal components via their C-terminal SAB (spectrin-actin binding) region. Using the DAL-1/4.1B FERM domain as bait for yeast two-hybrid interaction cloning, we identified protein arginine N-methyltransferase 3 (PRMT3) as a specific DAL-1/4.1B-interacting protein. PRMT3 catalyses the post-translational transfer of methyl groups from S-adenosyl-L-methionine to arginine residues of proteins. Coimmunoprecipitation experiments using lung and breast cancer cell lines confirmed this interaction in mammalian cells in vivo. In vitro binding assays demonstrated that this was an interaction occurring via the C-terminal catalytic core domain of PRMT3. DAL-1/4.1B was determined not to be a substrate for PRMT3-mediated methylation but its presence inhibits the in vitro methylation of a glycine-rich and arginine-rich methyl-accepting protein, GST (glutathione-S-transferase-GAR (glycine- and arginine-rich), which contains 14 'RGG' consensus methylation sites. In addition, induced expression of DAL-1/4.1B in MCF-7 breast cancer cells showed that the DAL-1/4.1B protein significantly inhibits PRMT3 methylation of cellular substrates. These findings suggest that modulation of post-translational methylation may be an important mechanism through which DAL-1/4.1B affects tumor cell growth.

Breast Neoplasms↗
PubMed2004

Effects of adrenomedullin on cell proliferation in rat adventitia induced by lysophosphatidic acid.

Lysophosphatidic acid (LPA) is a bioactive phospholipid having growth factor-like activity on fibroblasts and is involved in cardiovascular diseases such as hypertension and heart failure by inducing vascular remodeling, characterized by fibroblast proliferation and migration in adventitia. Among various bioactive factors that LPA works with, adrenomedullin (ADM) is a multiple functional peptide with an important cytoprotective effect against cardiovascular damage. We studied rat aortic adventitia to explore the possible paracrine/autocrine interaction between endogenous ADM and LPA. LPA stimulation of the adventitia to secrete ADM and express its mRNA was concentration dependent. ADM inhibited LPA-induced proliferation in adventitial cells and attenuated the activity of mitogen-activated protein kinase (MAPK) stimulated by LPA. In contrast, treatment with specific antagonists of the ADM receptor potentiated the LPA-induced proliferation in adventitial cells. We concluded that LPA stimulates the adventitia to produce and secrete ADM, which in turn regulates the vascular biological effects of LPA.

Adrenomedullin↗
PubMed2004

[Alterations of adrenomedullin and its receptor system in calcified myocardium and aorta of rats].

OBJECTIVE: To explore the production of ADM, changes and significance of adrenomedullin (ADM) mRNA and ADM receptor system-calcitonin receptor-like receptor (CRLR) and receptor activity modifying proteins (RAMPs) mRNA in calcified myocardium and aorta of rats. METHODS: Contents of ADM in plasma, myocardium and vessel were measured by radioimmunoassay (RIA). The amount of ADM, CRLR and RAMPs mRNA was determined by semi-quantitative RT-PCR. RESULTS: The contents of calcium in calcified myocardium and aorta were increased by 342% and 606% (all P<0.01), respectively, and alkaline phosphatase activities in calcified myocardium and vessel were increased by 66.5% and 82.7% (all P<0.01), respectively, compared with the control. Contents of ADM in plasma, myocardium and aorta were increased by 58 % (P<0.01), 14.3%(P<0.01) and 27.8%(P<0.05). Furthermore, it was found that the levels of ADM, CRLR and RAMP2 mRNA in calcified myocardium were elevated by 90.6% 157.5% and 119.6%(all P<0.01), respectively, but RAMP3 mRNA was decreased by 14.1 %(P<0.01). The levels of ADM, CRLR, RAMP2 and RAMP3 mRNA in calcified aorta were elevated by 37.7%(P<0.01), 41.4%(P<0.01),60.1%(P<0.05) and 13%(P<0.01) respectively, compared with the control. The elevated levels of CRLR, RAMP2 or RAMP3 mRNA were positively correlated with up regulations of ADM mRNA in calcified myocardium and aorta. CONCLUSION: Calcified myocardium and aorta may generate an increased amount of ADM, different alterations of gene expressions of ADM and its receptor system. These RESULTS suggest that ADM and its receptor system might participate in the regulation of calcification in heart and vessel.

Adrenomedullin↗
PubMed2004

Blockage of transforming growth factor beta receptors prevents progression of pig serum-induced rat liver fibrosis.

AIM: To test the hypothesis that introduction of antisense T beta R I and T beta R II eukaryotic expressing plasmids into a rat model of immunologically induced liver fibrosis might block the action of TGF-beta (1) and halt the progression of liver fibrosis. METHODS: RT-Nest-PCR and gene recombination techniques were used to construct rat antisense T beta R I and T beta R II recombinant plasmids which could be expressed in eukaryotic cells. The recombinant plasmids and empty vector (pcDNA3) were encapsulated by glycosyl-poly-L-lysine and then transducted into rats of pig serum-induced liver fibrosis model. Expression of exogenously transfected gene was assessed by Northern blot, and hepatic expressions of T beta R I and T beta R II were evaluated by RT-PCR and Western blot. We also performed ELISA for serum TGF-beta(1), hydroxyproline of hepatic tissues, immunohistochemistry for collagen types I and III, and VG staining for pathological study of the liver tissues. RESULTS: The exogenous antisense T beta R I and T beta R II plasmids could be well expressed in vivo, and block mRNA and protein expression of T beta R I and T beta R II in the fibrotic liver at the level of mRNA respectively. These exogenous plasmid expressions reduced the level of TGF-beta(1) (antisense T beta R I group 23.998+/-3.045 ng/mL, antisense T beta R II group 23.156+/-3.131 ng/mL, disease control group 32.960+/-3.789 ng/mL; F=38.19, 36.73, P<0.01). Compared with disease control group, the contents of hepatic hydroxyproline (antisense T beta R I group 0.169+/-0.015 mg/g liver, antisense T beta R II group 0.167+/-0.009 mg/g liver, disease control group 0.296+/-0.026 mg/g liver; F=14.39, 15.48, P<0.01) and the deposition of collagen types I and III decreased in the two antisense treatment groups (antisense T beta R I group, collagen type I 669.90+/-50.67, collagen type III 657.29+/-49.48; antisense T beta R II group, collagen type I 650.26+/-51.51, collagen type III 661.58+/-55.28; disease control group, collagen type I 1209.44+/-116.60, collagen type III 1175.14+/-121.44; F=15.48 to 74.89, P<0.01). Their expression also improved the pathologic classification of liver fibrosis models (compared with disease control group, chi(2)=17.14, 17.24, P<0.01). No difference was found in the level of TGF-beta(1), the contents of hepatic hydroxyproline and collagen types I and III and pathologic grade between pcDNA3 control group and disease control group or between the two antisense treatment groups (F=0.11 to 1.06, chi(2)=0.13 to 0.16, P>0.05). CONCLUSION: Antisense T beta R I and T beta R II recombinant plasmids have certain reverse effects on liver fibrosis and can be used as possible candidates for gene therapy.

Activin Receptors, Type I↗
PubMed2004

Inhibitor of DNA binding/differentiation helix-loop-helix proteins mediate bone morphogenetic protein-induced osteoblast differentiation of mesenchymal stem cells.

Bone morphogenetic proteins (BMPs) belong to the TGF-beta superfamily and play an important role in development and in many cellular processes. We have found that BMP-2, BMP-6, and BMP-9 induce the most potent osteogenic differentiation of mesenchymal stem cells. Expression profiling analysis has revealed that the Inhibitors of DNA binding/differentiation (Id)-1, Id-2, and Id-3 are among the most significantly up-regulated genes upon BMP-2, BMP-6, or BMP-9 stimulation. Here, we sought to determine the functional role of these Id proteins in BMP-induced osteoblast differentiation. We demonstrated that the expression of Id-1, Id-2, and Id-3 genes was significantly induced at the early stage of BMP-9 stimulation and returned to basal levels at 3 days after stimulation. RNA interference-mediated knockdown of Id expression significantly diminished the BMP-9-induced osteogenic differentiation of mesenchymal progenitor cells. Surprisingly, a constitutive overexpression of these Id genes also inhibited osteoblast differentiation initiated by BMP-9. Furthermore, we demonstrated that BMP-9-regulated Id expression is Smad4-dependent. Overexpression of the three Id genes was shown to promote cell proliferation that was coupled with an inhibition of osteogenic differentiation. Thus, our findings suggest that the Id helix-loop-helix proteins may play an important role in promoting the proliferation of early osteoblast progenitor cells and that Id expression must be down-regulated during the terminal differentiation of committed osteoblasts, suggesting that a balanced regulation of Id expression may be critical to BMP-induced osteoblast lineage-specific differentiation of mesenchymal stem cells.

Adenoviridae↗
PubMed2004

Relationship between contents of adrenomedullin and distributions of neutral endopeptidase in blood and tissues of rats in septic shock.

Adrenomedullin (ADM), a multifunction peptide with important roles in regulating cardiovascular homeostasis, has the vasodilatory properties and is of particular interest in the pathophysiology of sepsis. ADM levels in plasma and tissues are regulated by the proteolysis of neutral endopeptidase (NEP), the major enzyme of ADM degradation. We observed the NEP activity in the plasma, the activity and distribution of NEP and its mRNA expression in the tissues of rats in septic shock to study the possible role of NEP in elevating tissue ADM concentration during sepsis. ADM level increases progressively during sepsis except in the jejunum. Rats in early phase of shock (ES) showed diverse changes in tissue NEP activity. Plasma NEP activity, tissue NEP activity and its protein and mRNA expression in the left ventricle, aorta, jejunum and lung in the late phase of shock (LS) rats were lower than those in ES and the control, but no statistical change of NEP activity in the kidney was observed. The level of ADM was inversely correlated with NEP activity in the plasma, ventricle and aorta and positively correlated with NEP activity in the jejunum. Thus, in sepsis, the local concentration and action of ADM in tissues may be differentially regulated by NEP.

Adrenomedullin↗
PubMed2004

[Effects of substance P on granulation tissue fibroblasts proliferation and expression of basic fibroblast growth factor mRNA].

OBJECTIVE: To explore the proliferation-promoting effect of sensory neuropeptide substance P (SP) on the cultured granulation tissue fibroblasts in vitro and its regulative effect on the gene expression of basic fibroblast growth factor (bFGF) mRNA. METHODS: The proliferation-promoting effect of cultured granulation tissue fibroblasts was observed by means of MTT; the regulative effect of SP on gene expression of fibroblast bFGF by RT-PCR. The time and dose-efficiency relations were also observed. RESULTS: There was a significant proliferation-promoting effect of SP on the cultured granulation tissue fibroblasts in vitro in a remarkable dose-dependent fashion. However, bFGF antibody only partly exerted its inhibitive effect. SP could induce the bFGF mRNA expression of the fibroblasts at the 3rd and 6th hour (P < 0.01). SP could promote the bFGF mRNA expression of the fibroblasts in the concentration of 10(-9) - 10(-5) mol/L and peaked in the concentration of 10(-7) mol/L. CONCLUSIONS: SP has a significant proliferation-promoting effect on the granulation tissue fibroblasts, which is correlated with SP inducing bFGF mRNA expression of fibroblasts.

Animals↗
PubMed2004

Epidemiology of Helicobacter infection in wild rodents in the Xinjiang-Uygur autonomous region of China.

Helicobacter species were detected in the feces of wild rodents captured in Qiemo and Ruoqiang in the Xinjiang-Uygur autonomous region of China by polymerase chain reaction and 16S rRNA partial sequence analysis. Forty-four wild rodents, including one Przewalski's gerbil (Brachiones przewalskii), three Northern three-toed jerboas (Dipus sagitta), one long-eared jerboa (Euchoreutes naso), 34 midday gerbils (Meriones meridianus), two short-tailed bandicoot rats (Nesokia indica) and three great gerbils (Rhombomys opimus), were examined. Epidemiological studies indicated that Helicobacter spp. were detected in all genera tested; that H. hepaticus, H. apodemus, H. canadensis, and H. winghamensis were widespread in wild rodents; and that the dominant Helicobacter species in rodents differed depending not only on the order or genus of the animal but also on the animal's habitat. H. bilis, H. pylori, H. rodentium and " H. suncus" were not detected in any animals. It appears that the wild rodents tested in this study are not a reservoir of H. pylori infection.

Animals↗
PubMed2004

Should selective serotonin reuptake inhibitors be prescribed to all patients with ischemic heart disease?

Recent studies have uncovered more and more evidence demonstrating the adverse relationship between depression and ischemic heart disease. One of the most significant mechanisms that may explain the adverse relationship is the increased platelet activity, otherwise known as aggregation, observed to occur in patients with depression or ischemic heart disease. Platelet activity is further elevated in patients with depression and ischemic heart disease. Selective serotonin reuptake inhibitors are antidepressants and also act like platelet inhibitors. The results of large-scale clinical trials suggest that the use of selective serotonin reuptake inhibitors may reduce cardiac events in post-myocardial infarction patients or in those with unstable angina that may be related to the effects of selective serotonin reuptake inhibitors on platelet aggregation.

Angina, Unstable↗
PubMed2004

Ecotoxicological evaluation of 4-aminobiphenyl using a test battery.

Experimental bioassays are currently used in ecotoxicology and environmental toxicology to provide information for risk assessment evaluation of new chemicals and to investigate their effects and mechanisms of action; in addition, ecotoxicological models are used for the detection, control, and monitoring of the presence of pollutants in the environment. As a single bioassay will never provide a full picture of the quality of the environment, a representative, cost-effective, and quantitative test battery should be developed. In this study, the effects of 4-aminobiphenyl (4-ABP) were investigated using a battery of ecotoxicological model systems, including immobilization of Daphnia magna, development of zebrafish embryos, and inhibition of mammalian cell proliferation. The growth inhibition effects of 4-ABP were assessed on mouse connective tissue fibroblast cells (L929 cells) and human hepatocelluar carcinoma cells (HepG2 cells) by using a 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-2H-trazolium bromide reduction assay. The results reveal that 4-aminobiphenyl is toxic for aquatic organisms and mammalian cells. The system most sensitive to 4-aminobiphenyl is D. magna immobilization, followed by development of zebrafish embryos, and inhibition of cell proliferation. L929 and HepG2 cell growth inhibition bioassays show low sensitivity. These findings indicate that a single model for the possible harmful effect of 4-ABP has its limitations; only a test battery, composed of bioassays on different species, can provide an accurate assessment of the action of 4-ABP in the whole environment.

Aminobiphenyl Compounds↗
PubMed2004

Urotensin-II activates L-arginine/nitric oxide pathway in isolated rat aortic adventitia.

Urotensin-II (U-II), a cyclic peptide widely expressed in blood vessels, has diverse vascular actions that range from potent vasoconstriction to vasodilation. Although, U-II-induced vasodilation has been shown to be partially dependent on nitric oxide (NO), the involvement of vascular adventitia-derived NO, remains unknown. The present study aimed to elucidate the activation of U-II on L-arginine/NO pathway in isolated rat aortic adventitia. In adventitia of thoracic and abdominal aortas, the l-arginine/NO pathway was similarly characterized: the uptake of l-[(3)H]arginine was Na(+)-independent, with the peak occurring over around 40 min incubation; the total NO synthase (NOS) activity was mostly calcium-independent (>90%), and significantly inhibited by a specific iNOS inhibitor AMT; the production of NO metabolites nitrate and nitrite (NO(x)) was stimulated by L-arginine but not by D-arginine. In aortic adventitia exposed to rat U-II (10(-9) and 10(-8)M) for 6 h, the V(max) of l-[(3)H]arginine uptake over 40 min incubation was significantly increased, while the K(m) of l-[(3)H]arginine uptake showed no significant change. Besides, the iNOS mRNA level was up-regulated, the total NOS activity, largely calcium-independent, was significantly induced, and the NO(x) production was significantly stimulated by U-II. According to the same protocol as U-II, the positive control lipopolysaccharide (LPS, 10 microg/ml), which had been established to activate adventitial L-arginine/NO pathway, increased l-[(3)H]arginine uptake, iNOS activity and NO(x) production to a greater extent than U-II. In addition, the total NOS activities induced by 3 and 6h incubation of U-II and LPS were significantly inhibited by a specific inhibitor of protein synthesis, actinomycin D. In conclusion, the results showed that rat U-II activated L-arginine/NOS/NO pathway in rat aortic adventitia, suggesting a potential contributive role of adventitia-derived NO in the vasodilator response of U-II.

Animals↗
PubMed2004

The association between depression and chronic kidney disease and mortality among patients hospitalized with congestive heart failure.

BACKGROUND: The point prevalence of depression and its relationship to poor outcomes among patients with chronic kidney disease (CKD) has not been fully characterized. METHODS: We performed a secondary analysis of a prospective cohort of 374 patients admitted with congestive heart failure between March 1, 1997 and June 30, 1998, to investigate the point prevalence of depression among patients with CKD and its association with mortality. The Beck Depression Inventory (BDI) was administered to all patients. Those who scored 10 or higher were administered the National Institute of Mental Health Diagnostic Interview Schedule (DIS). Logistic regression was used to examine the association between severe CKD, corresponding to a creatinine clearance less than 30 mL/min/72 kg (<0.50 mL/s/72 kg), depression, and mortality at 1 year. RESULTS: Point prevalences of depressive symptoms by BDI and major depression by DIS were 54.8% and 21.6% if severe CKD was present and 32.8% and 13.0% if severe CKD was absent, respectively. After controlling for important clinical factors, severe CKD was associated with depressive symptoms by BDI (odds ratio, 2.89; 95% confidence interval, 1.39 to 5.99). Both depression by DIS and severe CKD were significant predictors of mortality. The increased mortality risk associated with depression did not decline with decreasing kidney function. CONCLUSION: Depression was more prevalent among patients with than without severe CKD and had at least as strong an association with mortality as compared with depression in patients with no or less severe CKD. The point prevalence of depression decreased when the DIS interview was used, perhaps related to the presence of somatic measures on the BDI reflecting uremia. Studies assessing the efficacy of antidepressants among patients with CKD are needed to determine whether, in addition to treating depression, pharmacotherapy impacts mortality.

Adult↗
PubMed2004

Effects of adrenomedullin on cell proliferation in rat adventitia induced by aldosterone.

OBJECTIVE: Aldosterone is involved in cardiovascular diseases such as hypertension and heart failure by inducing sodium retention and vascular remodeling, which is characterized by fibroblast proliferation and migration in adventitia. It is well known that aldosterone stimulates vascular smooth muscle cells and fibroblasts to produce and secrete adrenomedullin (ADM), a multiple functional peptide with an important cytoprotective effect against cardiovascular damage. We examined the effect of aldosterone on ADM production and secretion and its mRNA expression in rat aortic adventitia to study the paracrine/autocrine interaction between endogenous ADM and aldosterone. METHODS: ADM produced and secreted from adventitia stimulated by aldosterone in the absence or presence of spironolactone, RU486 or spironolactone together with RU486 were detected by radioimmunoassay, proliferation in adventitia cells was evaluated by the level of [H]-thymine incorporation, and preproADM gene expression was measured by semi-quantitative reverse transcriptase polymerase chain reaction. RESULTS: Adventitial ADM secretion and mRNA expression stimulated by aldosterone were concentration-dependent as was the inhibitive effect of ADM on aldosterone-induced proliferation. The induction of aldosterone in ADM secretion was mediated by mineralocorticoid receptor. Antagonists of specific receptors of calcitonin gene-related peptide (CGRP) receptor type 1 and ADM both potentiated the proliferation effect induced by aldosterone; and thiorphan, an inhibitor of the enzyme for ADM degradation, inhibited the adventitial [H]-thymine incorporation induced by aldosterone. ADM inhibited the activity of extracellular signal related kinase (ERK) stimulated by aldosterone. CONCLUSION: Aldosterone stimulates adventitia to produce and secrete ADM, which in turn, antagonizes the aldosterone-induced proliferation in adventitia.

Adrenomedullin↗
PubMed2004

Identification of a novel mutation and a de novo mutation in DKC1 in two Chinese pedigrees with Dyskeratosis congenita.

Dyskeratosis congenita (DKC) is a rare and fatal congenital syndrome characterized by the triad of reticular skin pigmentation, nail dystrophy and mucosal leukoplakia, and the predisposition to bone marrow failure and malignancies. Mutations in DKC1 gene encoding dyskerin are responsible for the X-linked dyskeratosis congenita. Here we report mutation analysis of two Chinese pedigrees with dyskeratosis congenita. The 15 coding exons of DKC1 and their flanking regions were amplified from genomic DNA by PCR. DNA sequencing and restriction endonuclease digestion were used for mutation detection. Transition mutation of 1226C-->T (P409L) found in the first pedigree is a novel mutation. In the second pedigree, the proband's mother phenotypically normal carried a de novo transition mutation of 1058C-->T (A353 V) in one allele, and transmitted the mutant allele to her two sons who had typical manifestations of dyskeratosis congenita.

Adult↗
PubMed2004

Effects of taurine and homocysteine on calcium homeostasis and hydrogen peroxide and superoxide anions in rat myocardial mitochondria.

1. Taurine and homocysteine are metabolites of methionine. Hyperhomocysteinaemia is one of the risk factors for cardiovascular disease. Although taurine may be a cardiovascular cytoprotective substance, we hypothesized that it may antagonize the effects of homocysteine on myocardial mitochondrial function. 2. We studied the effects of taurine and homocysteine on [(45)Ca] uptake, Ca(2+)-ATPase activity and generation of hydrogen peroxide and superoxide anions in vitro in rat isolated myocardial mitochondria. 3. Results showed that the inhibition of mitochondrial [(45)Ca] uptake by homocysteine (0.1, 0.5 and 1.0 mmol/L) was concentration dependent. Taurine (5, 10 and 20 mmol/L) promoted [(45)Ca] uptake in a concentration-dependent manner, as well as concentration dependently reducing the homocysteine (0.5 mmol/L)-induced inhibition of mitochondrial [(45)Ca] uptake. 4. Homocysteine significantly inhibited mitochondrial Ca(2+)-ATPase activity, whereas taurine had a diphasic action on this activity. Taurine, at 5 and 10 mmol/L, increased Ca(2+)-ATPase activity (P < 0.01), but 20 mmol/L taurine inhibited Ca(2+)-ATPase activity (P < 0.05). Taurine attenuated the inhibitory effect of homocysteine on Ca(2+)-ATPase activity. 5. Homocysteine stimulated the generation of hydrogen peroxide and superoxide anions. Taurine had no effect on the generation of the anions, but inhibited their homocysteine-stimulated generation. 6. These results indicate that taurine and homocysteine have opposite effects in myocardial mitochondria with regard to [(45)Ca] uptake, Ca(2+)-ATPase activity and the generation of hydrogen peroxide and superoxide anions. Our results may show an important mechanism for the cardiovascular protective effects of taurine.

Animals↗
PubMed2004

Relationship between the contents of adrenomedullin and distributions of neutral endopeptidase in blood and tissues of spontaneously hypertensive rats.

Adrenomedullin (ADM) is a multifunctional peptide with important roles in the cardiovascular system, especially in the adjustment of cardiovascular and renal homeostasis. ADM is present in plasma, organs and tissues, and its activity increases during hypertension. It remains unknown whether the clearance of this peptide is altered during hypertension. Neutral endopeptidase (NEP) is the major enzyme in ADM's degradation. We observed the activity and distribution of NEP and the expression of its mRNA in the plasma, cardiac ventricle, aorta, jejunum and kidney of spontaneously hypertensive rats (SHRs) in order to study the possible role of NEP in elevating tissue ADM concentrations during hypertension. ADM and NEP were diffuse in all tissues studied. The level of tissue ADM was generally higher in SHR tissues than in control tissues, except in the renal medulla, and its mRNA expression was higher in all tissues. Plasma NEP activity, general NEP activity and the expression of NEP mRNA in the left ventricle, aorta and jejunum in SHRs was lower than that of controls, and the level of ADM was inversely correlated with NEP activity. NEP activity and mRNA and protein expression in SHR kidneys were higher than in control kidneys; moreover, the ADM content was positively correlated with NEP activity in the renal cortex. NEP activity in the lung of SHRs did not differ from that of controls. Thus, in SHRs, the local concentration and action of ADM in the tissues may be differentially regulated by NEP.

Adrenomedullin↗