Biomedical subjects

L Bao

Publications and source records attributed to L Bao.

At least 37 records · Page 2Linked to original sources

PubMed1999

[PCR amplification and cloning of the specific region of the gene encoding 83kd antigen from Borrelia burgdorferi].

According to the published gene sequence coding the 83 kd antigen from B31 strain of Borrelia Burgdorferi, we selected the region from 1419 bp to 1896 bp as the target sequence to design a pair of oligonucleotide primers, obtained the gene fragment by using PCR, and recombinant expression vector pBX1 by cloning the gene fragment into plasmid vector pBK-CMV. The recombinant plasmid can be made into nucleic acid probe for the classification of Borrelia burgdorferi. The gene fragment product expressed by pBX1 can be used as antigen in the serological diagnosis of Lyme disease.

Antigens, Bacterial↗

PubMed1998

Regulation of expression of galanin and galanin receptors in dorsal root ganglia and spinal cord after axotomy and inflammation.

Galanin can normally be detected only in a few dorsal root ganglion (DRG) neurons, but it is dramatically upregulated after peripheral nerve injury in both rat and monkey. Galanin is stored in large dense core vesicles, which after axotomy are often found close to the membrane of afferent nerve endings in the dorsal horn. In the monkey there is an increase in galanin in many nerve terminals in the superficial dorsal horn after axotomy, but such an increase is more difficult to detect in the rat. Galanin is also present in local dorsal horn neurons, where it is upregulated by peripheral inflammation. Both galanin-R1 and galanin-R2 receptor mRNAs are expressed in rat DRGs, mainly in, respectively, large and small DRG neurons. Galanin-R1 receptor mRNA is downregulated in DRG neurons after axotomy, and a small decrease in galanin-R2 receptor mRNA levels can also be seen. After peripheral tissue inflammation galanin-R1 receptor mRNA levels decrease and galanin-R2 receptor mRNA levels increase. The present results show that galanin and galanin receptors are present in sensory and local dorsal horn neurons and are regulated by nerve injury and inflammation. Galanin may therefore be involved in processing of pain information, primarily exerting analgesic effects. Whereas local dorsal horn neurons represent a defense system against inflammatory pain, we have proposed that a second defense system, against neuropathic pain, is intrinsic to DRG neurons.

Animals↗

PubMed1998

The human cystathionine beta-synthase (CBS) gene: complete sequence, alternative splicing, and polymorphisms.

Cystathionine beta-synthase [CBS; l-serine hydro-lyase (adding homocysteine), EC 4.2.1.22] catalyzes the first committed step of transsulfuration and is the enzyme deficient in classical homocystinuria. In this report, we describe the molecular cloning and the complete nucleotide sequence of the human CBS gene. We report a total of 28,046 nucleotides of sequence, which, in addition to the CBS gene, contains approximately 5 kb of the 5' flanking region. The human CBS gene contains 23 exons ranging from 42 to 209 bp. The 5' UTR is formed by 1 of 5 alternatively used exons and 1 invariably present exon, while the 3' UTR is encoded by exons 16 and 17. We also describe the identification of two alternatively used promoter regions that are GC rich (approximately 80%) and contain numerous putative binding sites for Sp1, Ap1, Ap2, and c-myb, but lack the classical TATA box. The CBS locus contains an unusually high number of Alu repeats, which may predispose this gene to deleterious rearrangements. Additionally, we report on a number of DNA sequence repeats that are polymorphic in North American and European Caucasians.

Alternative Splicing↗

PubMed1998

Identification and tissue distribution of human cystathionine beta-synthase mRNA isoforms.

Cystathionine beta-synthase (CBS) catalyzes the irreversible, serine-dependent conversion of homocysteine to cystathionine via a transsulfuration pathway. CBS deficiency not only is the leading cause of homocystinuria, an inherited genetic disorder, but may contribute to cardiovascular disease as well. We isolated three new isoforms of human CBS mRNA from a human liver cDNA library. We designate these CBS mRNAs as CBS 3, CBS 4, and CBS 5, and the CBS mRNAs reported previously by Kraus et al. (1993) (Hum. Mol. Genet. 2, 1933-1938) and Kruger and Cox (1994) (Proc. Natl. Acad. Sci. USA 91, 6614-6618) as CBS 1 and CBS 2, respectively. Sequence analyses show that the only difference among the five CBS mRNAs is at the beginning of the 5'-untranslated region. Tissue distribution studies reveal that liver and pancreas have the highest amounts of CBS mRNAs. CBS mRNA is present in all regions of the brain tested. We also report the differential distribution of CBS mRNA isoforms in tissues, showing that pancreas contains all five CBS isoforms and the liver has four CBS mRNA isoforms, CBS 1-4. The kidney contains only CBS 1 and CBS 2. In human fetal tissues, CBS 2 is present in the liver and kidney. PCR-based quantitative analyses of CBS mRNA isoforms in human liver demonstrate that CBS 1 and CBS 2 are the major species, with CBS 2 being more abundant, while CBS 3-5 are the minor species. Furthermore, results from our human liver cDNA screening and primer extension experiments show that each of the five CBS transcripts begins with a different exon, suggesting that CBS gene transcription might be regulated by more than one promoter.

Alternative Splicing↗

PubMed1998

Neuropeptide Y: some viewpoints on a multifaceted peptide in the normal and diseased nervous system.

Using immunohistochemical and in situ hybridization methodologies the localization of neuropeptide tyrosine (NPY) and two of its receptors, the Y1- and the Y2-receptor (R), has been analysed in various tissues in normal animals and animals subjected to different experimental procedures as well as animals with a genetic and an acquired disease. (1) Dorsal root ganglion (DRG) neurons are discussed with special focus on the effect of peripheral nerve injury. In normal DRG neurons NPY cannot be detected, whereas Y1-R mRNA and Y1-R-like immunoreactivity (LI) are strongly expressed. The Y1-Rs decorate the membrane of the cell soma and are not transported peripherally into the axonal branches. Y2-R mRNA levels are low. After axotomy there is a marked increase in NPY, a decrease in Y1-Rs and an increase in Y2-Rs. The Y2-R is transported centrifugally. These findings suggest that NPY-ergic mechanisms participate in the adaptive changes of sensory neurons in response to injury. (2) Using specific antibodies the cellular and subcellular localization of the Y1-R protein have been analysed in cerebral blood vessels. The results demonstrate high concentrations of receptors in smooth muscle cells around pial arterioles with lower numbers in large vessels on the basal surface of the brain. In many regions the receptors 'disappear' after the arterioles have entered the brain tissue. At the ultrastructural level the receptors are found both on the endothelial and peripheral side of the muscle cells as well as laterally, where muscle cells oppose each other. The receptor protein is often associated with small vesicles. No NPY-positive nerve fibers were found around the Y1-R-rich arterioles, but they were only seen around the arteries with low Y1-R levels. The Y1-R-rich arterioles were, however, seen close to numerous NPY-positive fibers originating from central interneurons. These findings raise the possibility that centrally originating NPY can influence cerebral blood flow, possibly by stimulating NPY-Rs on the peripheral side of the muscle cells. However, also blood borne NPY, released under special conditions, such as stress from sympathetic nerves and the adrenal medulla and transported with blood, may stimulate receptors on the endothelial side of the smooth muscle cells. (3) In the arcuate nucleus Y1- and Y2-Rs are found, whereby the Y1-Rs are located in its ventro-medial portion and co-localized with POMC peptides, and the Y2-R in its ventromedial part, partly co-localized with NPY. NPY nerve endings makes synaptic contact with the POMC/Y1-R-positive neurons. In a mouse model for genetic anorexia very high levels of NPY were observed in arcuate neurons as compared to control mice. However, NPY mRNA levels were not different between the two groups. Taken together these findings are in good agreement with the view that NPY in the arcuate nucleus plays an important role in regulating feeding behaviour. (4) After intracerebral prion inoculation in mice an upregulation of NPY mRNA levels was observed in CA3 pyramidal neurons, and this effect was seen at a time point just before the first behavioural symptoms were manifested. At approximately the same time there was a dramatic decrease in Y2-R binding in strata oriens and radiatum of the CA1 region of the hippocampus, whereas in other regions no changes or much smaller changes were observed. Also, there was only a very slight decrease in Y2-R mRNA levels in CA3 neurons. It thus appears as if the prion disease prevents ligand binding to the Y2-R, perhaps by influencing traffic of receptor proteins, possibly at the level of cell membrane-associated caveolae, which have been implicated in the conversion of normal protein to scrapie protein. It is possible that these changes in NPY-ergic mechanisms may underlie some of the central symptoms associated with the prion disease. (ABSTRACT TRUNCATED)

Animals↗

PubMed1998

Down-regulation of mu-opioid receptors in rat and monkey dorsal root ganglion neurons and spinal cord after peripheral axotomy.

To understand the role of opioids and their receptors in chronic pain following peripheral nerve injury, we have studied the mu-opioid receptor in rat and monkey lumbar 4 and 5 dorsal root ganglion neurons and the superficial dorsal horn of the spinal cord under normal circumstances and after peripheral axotomy. Our results show that many small neurons in rat and monkey dorsal root ganglia, and some medium-sized and large neurons in rat dorsal root ganglia, express mu-opioid receptor-like immunoreactivity. Most of these neurons contain calcitonin gene-related peptide. The mu-opioid receptor was closely associated with the somatic plasmalemma of the dorsal root ganglion neurons. Both mu-opioid receptor-immunoreactive nerve fibers and cell bodies were observed in lamina II of the dorsal horn. The highest intensity of mu-opioid receptor-like immunoreactivity was observed in the deep part of lamina II. Most mu-opioid receptor-like immunoreactivity in the dorsal horn originated from spinal neurons. A few mu-opioid receptor-positive peripheral afferent terminals in the rat and monkey dorsal horn were calcitonin gene-related peptide-immunoreactive. In addition to pre- and post-junctional receptors in rat and monkey dorsal horn neurons, mu-opioid receptors were localized on the presynaptic membrane of some synapses of primary afferent terminals in the monkey dorsal horn. Peripheral axotomy caused a reduction in the number and intensity of mu-opioid receptor-positive neurons in the rat and monkey dorsal root ganglia, and of mu-opioid receptor-like immunoreactivity in the dorsal horn of the spinal cord. The decrease in mu-opioid receptor-like immunoreactivity was more pronounced in the monkey than in the rat dorsal root ganglia and spinal cord. It is probable that there was a parallel trans-synaptic down-regulation of mu-opioid-like immunoreactivity in local dorsal horn neurons of the monkey. These data suggest that one factor underlying the well known insensitivity of neuropathic pain to opioid analgesics could be due to a marked reduction in the number of mu-opioid receptors in the axotomized sensory neurons and in interneurons in the dorsal horn of the spinal cord.

Animals↗

PubMed1998

Localization and regulation of the delta-opioid receptor in dorsal root ganglia and spinal cord of the rat and monkey: evidence for association with the membrane of large dense-core vesicles.

Using immunohistochemistry and immunoelectron microscopy, the localization and regulation of delta-opioid receptor-like immunoreactivity were studied in dorsal root ganglia and spinal cord of normal rat and monkey, and after peripheral axotomy. Delta-opioid receptor-like immunoreactivity was observed in many small dorsal root ganglion neurons, and in the rat most of them contained substance P and calcitonin gene-related peptide. At the ultrastructural level, delta-opioid receptor-like immunoreactivity was localized in the Golgi complex, on the membrane of the large dense-core vesicles and on the membrane of and/or inside a type of large vesicle with an interior of low electron density. The latter vesicles were often in contact with multivesicular bodies. In the superficial dorsal horn of the spinal cord, most delta-opioid receptor-positive nerve fibers contain substance P and/or calcitonin gene-related peptide, both in rat and monkey. Also, in these nerve endings delta-opioid receptor-like immunoreactivity was found on the membrane of large dense-core vesicles and on the membrane of, or in, the lucent vesicles. Occasionally, delta-opioid receptor-like immunoreactivity was observed on the plasmalemma of the terminals, particularly when the vesicles were in exocytotic contact with the plasmalemma. Peripheral axotomy induced a decrease in delta-opioid receptor-like immunoreactivity both in cell bodies in the dorsal root ganglia and in terminals in the dorsal horn. These data suggest that the delta-opioid receptor may be a constituent of the membrane of large dense-core vesicles storing and releasing neuropeptides. It is suggested that upon exocytotic release of substance P and calcitonin gene-related peptide from large dense-core vesicles, there is a transient modification of the surface of the primary afferent terminals which leads to exposure of the receptor protein so that enkephalin released from adjacent terminals can activate the receptor. The decrease in delta-opioid receptors after axotomy indicates that delta-opioid receptor-mediated inhibitory effects are attenuated at the spinal level both in the rat and monkey.

Animals↗

PubMed1998

Thymosin beta15 expression in tumor cell lines with varying metastatic potential.

We previously isolated thymosin beta15 from highly metastatic Dunning rat prostatic carcinoma cells. Immunohistochemical study of human prostate cancer specimens revealed a general correlation between Gleason grade and thymosin beta15 expression, with high-grade (more malignant) tumors showing increased staining compared to low-grade tumors. To determine whether thymosin beta15 may be differentially expressed in cancer cells with different metastatic potential other than in the prostatic carcinoma cells, we examined thymosin beta15 mRNA levels in tumor cell lines from different species. We also examined thymosin beta15 protein levels in human breast cancer samples. Thymosin beta15 was upregulated in the highly metastatic mouse lung and human breast cancer cell lines in comparison to the nonmetastatic counterparts. Immunohistochemical staining showed the evidence of upregulation of thymosin beta15 in malignant human breast carcinomas as compared to benign breast tumors. The expression of thymosin beta15 was correlated with the metastatic potential of the mouse lung carcinoma and human breast carcinoma cells in addition to the prostatic carcinomas. Thymosin beta15 may be a useful marker to predict metastatic potential of certain human cancers.

Animals↗

PubMed1998

Localization of autoepitopes on the PCM-1 autoantigen using scleroderma sera with autoantibodies against the centrosome.

Characterization of epitope domains of autoantigens is important for deducing the cellular functions of autoantigens and may be important for understanding the autoimmune response. In the reported studies, epitope analysis of the centrosome autoantigen PCM-1 was performed. For these investigations, portion of the PCM-1 cDNA were subcloned into the pMAL expression plasmid, fusion proteins were induced, and aliquots of the extracts were probed by immunoblot analysis using two human autoimmune anticentrosome autoantisera. Immunoblotting identified three individual autoepitopes of 26-40 amino acid residues, amino acids 506-545, 1434-1465, and 1661-1686, within the PCM-1 protein. ELISA assays using non-denatured proteins did not identity any additional autoepitopes in the remainder of the PCM-1 molecule. To analyze the identified autoepitopes further, synthetic peptides were generated that covered each of the three autoepitopes and the synthetic peptides then were probed using the scleroderma sera. Peptides that covered the antigenic regions from amino acids 506-545 and 1434-1465 failed to react with the anticentrosome autoantisera suggesting that overall protein conformation may be important for the formation of those two autoepitopes. Peptides derived from the sequence of the third autoepitope were recognized by autoantibodies present in the anticentrosome autoantisera allowing the identification of the tripeptide KDC as the autoepitope in this region of the PCM-1 molecule. These studies lay the foundation for future investigations of the autoimmune response in scleroderma patients that are producing anticentrosome autoantibodies and should allow an investigation of the cellular role of the PCM-1 protein.

Autoantibodies↗

PubMed1998

[Cloning and expression of leptospiral protective antigen gene OmpL1 in BCG].

This study was intended to produce a new living vaccine against leptospirosis using BCG as vector. Leptospiral outer envelop antigen gene OmpL1 was amplified from the genome of pathogenic leptopira serova Lai 017 by PCR, and cloned in E. coli-BCG shuttle plasmid pY6002. Recombinant plasmids were isolated by dot blotting with Digoxigeninlabeled OmpL1 gene. After transforming the recombinant plasmids in BCG (Shanghai strain) by electroporation, the genomic DNA of all 21 transformants were prepared and hybridized with OmpL1. It showed that 6 of the 21 transformants were recombinants in which the OmpL1 gene had been integrated into the genome of BCG. By immunoblotting with OmpL1 infected rabbit antiserum, which was preabsorbed to remove antibody against E. coli and SPA-HRP, three recombinants, pLI1, pLI2 and pLI3, were detected to express OmpL1 protein. The ability of expression is in the order of pLI2 > pLI1 >> plI3. These studies provide the possibility of further research on the development of highly efficient recombinant vaccines against leptospirosis.

Cloning, Molecular↗

PubMed1997

Localization of neuropeptide Y Y1 receptors in cerebral blood vessels.

The localization of neuropeptide Y (NPY) Y1 receptor (R) -like immunoreactivity (LI) has been studied in cerebral arteries and arterioles of the rat by immunohistochemistry using fluorescence, confocal, and electron microscopy. High levels of Y1-R-LI were observed in smooth muscle cells (SMCs) in the small arterioles of the pial arterial network, especially on the basal surface of the brain, and low levels in the major basal cerebral arteries. The levels of Y1-R-LI varied strongly between adjacent SMCs. Y1-R-LI was associated with small endocytosis vesicles, mainly on the outer surface of the SMCs, but also on their endothelial side and often laterally at the interface between two SMCs. NPY-immunoreactive (Ir) nerve fibers could not be detected in association with the Y1-R-rich small arterioles but only around arteries with low Y1-R levels. A dense network of central NPY-Ir nerve fibers in the superficial layers of the brain was lying close to the strongly Y1-R-Ir small arterioles. The results indicate that NPY has a profound effect on small arterioles of the brain acting on Y1-Rs, both on the peripheral and luminal side of the SMCs. However, the source of the endogenous ligand, NPY, remains unclear. NPY released from central neurons may play a role, in addition to blood-borne NPY.

Animals↗

PubMed1997

[Characterication of reference strains of L. interrogans in China by ISSP-PCR].

The gene polymorphism of the DNAs extracted from reference strains of L. interrogans in China was characterized by LSSP-PCR primered by G1 or G2, which were a pair of specific primers for L. interrogans. The fingerprinting produced by LSSP-PCR showed that serovar lai, serovar canicola, serovar pyrogens, serovar autumnalis, serovar australis, serovar linhai, serovar wolffi and serovar haemolytic have similar patterns, but serovar hebdomadis, serovar javanica, serovar ballum, serovar pomona, serovar spaidjin, serovar tarassov and serovar manahao I have different profiles. This result agreed with the classification of genetic species by Yasuda. The utilization of LSSP-PCR banding patterns in the identification of leptospries in blood samples also gained encouraging results. Compared with the routine methods in genetic species classification, LSSP-PCR has the advantages of rapidity, simplicity and low-cost. It appears to be a promising tool in studying such slowly growing bacteria as leptospires. Further exploration of LSSP-PCR in classification and identification of Leptospires is worthwhile.

DNA, Bacterial↗

PubMed1997

[Analysis on speciems of serum and urine in 66 cases of early leptospirosis by PCR and biotin-AMPPD hybridization].

We used polymerase chain reaction (PCR) and Biotin-AMPPD hybridization to detect leptospiral DNA in blood and urine samples in 66 patients at the early stage of leptospirosis. The results showed that PCR and Biotin-AMPPD hybridization not only ruled out the non-specific PCR amplification and increased the reliability for clinical specineus of leptospirosis but also raised the detecting sensibility (from 71.3% to 86.1%). The positive rates of PCR resulted from serum and urine showed no statistical difference; therefore urine sample is worthy of application and dissemination for detecting leptospires at the early stage of leptospirosis. Urine sample is easier for one to collect, preserve and has less intervention. The primers G1, G2 are optimal opplication of PCR in epdemic areas in China.

Biotin↗

PubMed1997

Localization and quantitation of expression of the cell motility-related protein thymosin beta15 in human breast tissue.

Thymosin beta15 is a newly discovered 5300-Da protein that binds actin monomers and inhibits actin polymerization and might thus increase cellular motility. Thymosin beta15 is upregulated at both the mRNA and protein levels in prostate cell lines in a manner directly related to their capacity to metastasize. We hypothesize that because this protein is upregulated in cells with a propensity to metastasize, it might be a useful prognostic marker in breast cancer. Because this is a newly described protein, neither the subcellular localization of thymosin beta15 or its expression in breast cancer has been examined. We describe the use of an affinity-purified polyclonal antibody to show that within breast epithelium, thymosin beta15 is localized diffusely throughout the cytoplasm and that thymosin beta15 is upregulated in malignant (compared with benign) breast tissue. In contrast to the prostate model, thymosin beta15 is upregulated in nonmetastatic breast cancer and even ductal carcinoma in situ (compared with benign breast tissue), and, consequently, it might represent a potential early marker for breast malignancy. Additional studies are needed to evaluate the precise role and prognostic value of thymosin beta15 in breast cancer.

Adolescent↗

PubMed1997

[Clinical and experimental study for allergic rhinitis with treatment of biminkang mixture].

OBJECTIVE: To observe the efficacy of Biminkang in treating allergic rhinitis. METHODS: One hundred and sixty-four cases of allergic rhinitis were treated with the Chinese medicine Biminkang mixture mainly consisted of the Kazak folk herb Artemisia rupestis L. and in 52 cases of allergic rhinitis were treated as the control with the patent medicine Biyankang. RESULTS: The total effective rates in both groups are 93.9% and 69.2% respectively. After stopping the medications, the recurrence rates were 46.8% and 87.1%. Biminkang was better than Biyankang in short or long term of effectiveness (P < 0.01). Pharmacological study demonstrated Biminkang played a significant role of resisting histamine, inhibiting allergic reaction I and stabilizing cell membrane of mastocyte. CONCLUSION: Biminkang mixture is an effective drug in treating allergic rhinitis.

Adolescent↗

PubMed1996

Intracellular signaling pathway of substance P-induced superoxide production in human neutrophils.

We examined the intracellular mechanisms of substance P-induced superoxide anion (O2-) production in human neutrophils. Addition of substance P (30 microM) caused O2- production and biphasic increases in intracellular Ca2+ concentrations ([Ca2+]i) (early transient and subsequent sustained components) associated with the formation of inositol 1,4,5-trisphosphate (IP3). O2- and [Ca2+]i were assayed by using ferricytochrome C and fura 2-AM, respectively. These responses were abolished by tachykinin NK1 receptor antagonists, [D- Pro9[spiro-gamma-lactam],Leu10,Trp11]physalaemin-(1-11) (GR82334) or [D-Arg1,D-Trp7,9,Leu11]substance P (spantide), and an intracellular Ca2+ chelator, 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid (BAPTA-AM). Inhibition of IP3 formation by GTP-binding protein (G-protein) inactivators such as guanosine 5'-O-(2-thiodiphosphate) (GDP beta S) and islet-activating protein (IAP), or a phospholipase C inhibitor, 1-[6-[[17 beta-3-methoxyestra-1,3,5(10)- trien-17-yl]amino]hexyl]1 H-pyrrole-2,5-dione (U-73122), blocked the substance P-induced O2- production and biphasic increases in [Ca2+]i. An IP3 receptor antagonist, heparin, reduced both the substance P-induced O2- production and the transient increase in [Ca2+]i without any significant effects on the sustained increase in [Ca2+]i. Protein kinase C inhibitors, 1-(5-isoquinolinesulfonyl)-2-methylpiperazine dihydrochloride (H-7) and calphostin C, only slightly suppressed O2- production, and abolished the sustained increase in [Ca2+]i without any significant effects on the transient increase in [Ca2+]i. A Ca2+ entry blocker, nicardipine, completely inhibited the sustained increase in [Ca2+]i without affecting O2- production and the transient increase in [Ca2+]i. These results suggest that the tachykinin NK1 receptor/G-protein-linked IP3 formation with the resulting IP3-induced transient increase in [Ca2+]i is the main signal transduction pathway for substance P-stimulated O2- production in neutrophils.

Calcium↗

PubMed1996

Peripheral axotomy induces increased expression of neurotensin in large neurons in rat lumbar dorsal root ganglia.

In normal rat lumbar 4 and 5 dorsal root ganglia (DRGs) a few large neurons expressed neurotensin-like immunoreactivity (LI). Twenty hours after crushing the lumbar 4 and 5 dorsal roots or the sciatic nerve, accumulations of neurotensin-LI were seen in many nerve fibers on the ganglionic side of both crushes, indicating a significant centrifugal transport of neurotensin under normal circumstances. A distinct increase in expression of neurotensin (peptide and mRNA) was observed in many large neuron profiles in the ipsilateral lumbar 4 and 5 DRGs two days after unilateral sciatic nerve transection. Two weeks after axotomy the number of neurotensin-positive neuron profiles was reduced and had almost reached normal levels. In the superficial dorsal horn of the lesion side the number of neurotensin immunoreactive fibers in laminae I-II was markedly reduced 7 days after peripheral axotomy. There was no detectable increase in neurotensin-L1 in laminae III-IV of spinal dorsal horn, in the dorsal column nuclei or in the peripheral neuroma (2-28 days after axotomy), suggesting that the amounts of neurotensin transported centrifugally from DRG neurons after axotomy are low. Neurotensin-LI only sometimes colocalized with neuropeptide Y-LI, another peptide known to be upregulated in large DRG neurons. These two peptides may therefore partly be localized in different populations of large DRG neurons. The present results show that, in contrast to the nerve injury-induced general downregulation of neurotensin systems in the superficial dorsal horn and of neurotensin receptor mRNA expression in DRGs as shown in previous studies, axotomy causes upregulation of expression of neurotensin peptide in some large DRG neurons.

Animals↗

PubMed1996

Thymosin beta 15: a novel regulator of tumor cell motility upregulated in metastatic prostate cancer.

The Dunning rat prostatic carcinoma is a model system where cell motility closely correlates with the metastatic phenotype. We have identified a novel gene, upregulated in the highly motile and metastatic Dunning cancer cell lines, that represents a new member of the thymosin-beta family, thymosin beta 15. Transfection of antisense thymosin beta 15 constructs into rat prostatic carcinoma cells demonstrates that this molecule positively regulates cell motility, a critical component of the metastatic pathway. Thymosin beta 15 levels are elevated in human prostate cancer and correlate positively with the Gleason tumor grade. Thymosin beta 15 may represent a potential new biochemical marker for human prostate cancer progression.

Actins↗