pl Bl5: A cDNA Clone of the Rat mRNA Encoding Cyclophilin

Pe, Danielson; Forss‐Petter, Sonja; Ma, Brow; Calavetta, L; Douglass, James; Milner, Robert J.; Jg, Sutcliffe

doi:10.1089/dna.1988.7.261

Cited by 1,043 publications

(448 citation statements)

References 31 publications

Supporting

Mentioning

435

Contrasting

Order By: Relevance

“…Equal loading of the samples was checked by reprobing the blots with were performed for 30 minutes in a moist chamber. The reaction, which resulted in a brown staining of cytoplasmic reac-the 900-bp BamHI-BamHI complementary DNA of p1B15 coding for cyclophilin 55 after the hybridization procedure. Filtive sites, was visualized by incubation for 10 minutes in Trisbuffered saline containing 0.06% diaminobenzidine (Fluka, ters were then washed to a maximal stringency of 0.11 sodium saline citrate/0.1% sodium dodecyl sulfate at 65ЊC and Italy) and 0.01% H 2 O 2 added just before use.…”

Section: Methodsmentioning

confidence: 99%

Interferon gamma decreases hepatic stellate cell activation and extracellular matrix deposition in rat liver fibrosis

et al. 1996

View full text Add to dashboard Cite

Hepatic fibrosis is a common response to chronic liver early response to cell injury. Rats were killed after 1 or injury of variable origin (viral, metabolic, or toxic). Re-3 weeks of treatment with DMN, IFN-g, DMN / IFN-g, gardless of the etiologic factor, liver fibrosis is characor saline. Immunohistochemistry was used to iden-terized by increased production of extracellular matrix tify proliferating (desmin-positive/bromodeoxyuridine components that form the hepatic scars and consists of factor is the most potent proliferative cytokine forFrom the

show abstract

Section: Methodsmentioning

confidence: 99%

Interferon gamma decreases hepatic stellate cell activation and extracellular matrix deposition in rat liver fibrosis

et al. 1996

View full text Add to dashboard Cite

show abstract

“…The relative amount of MSP or tPA mRNA hybridization in each Northern blot was normalized for any differences in sample RNA loading by rehybridizing stripped membranes to one or more cDNA control probes. The control cDNAs used were EcoRI-digested cyclophilin (pML -20) (Danielson et al, 1988) and a human ␤-actin cDNA or a cDNA probe to the glycolytic enzyme glyceraldehyde-3-phosphate dehydrogenase (GAPDH), obtained from C lontech.…”

Section: Msp R Na E Xpression In Brain and Peripheral Tissuesmentioning

confidence: 99%

Nervous System-Specific Expression of a Novel Serine Protease: Regulation in the Adult Rat Spinal Cord by Excitotoxic Injury

1997

View full text Add to dashboard Cite

A full-length cDNA clone of a previously unidentified serine protease, myelencephalon-specific protease (MSP), has been isolated by using a PCR cloning strategy and has been shown to be expressed in a nervous system and spinal cord-specific pattern. Sequence analysis demonstrated that MSP is most similar in sequence to neuropsin, trypsin, and tissue kallikrein and is predicted to have trypsin-like substrate specificity. MSP mRNA was found to be ϳ10-fold greater in the CNS of the rat and human, as compared with most peripheral tissues, and within the CNS was found to be highest by a factor of four in the medulla oblongata and spinal cord. Levels of mRNA encoding tissue plasminogen activator (tPA) also were elevated in the spinal cord but were more widespread in peripheral tissues as compared with MSP.In the adult rat lumbosacral spinal cord, in situ localization of MSP mRNA demonstrated 2-fold higher levels in the white, as compared with the gray, matter. MSP mRNA expression was shown to increase 3-fold in the white matter and 1.5-fold in the gray laminae at 72 hr after intraperitoneal injection of the AMPA/ kainate glutamate receptor-specific agonist, kainic acid (KA). MSP mRNA remained elevated in the ventral gray matter, including expression associated with the motor neurons of lamina IX, at 7 d after the initial excitotoxic insult. Together, these observations indicate that MSP is in a position to play a fundamental role in normal homeostasis and in the response of the spinal cord to injury.

show abstract

“…The levels found were normalized by using cyclophilin mRNA as a reference. Cyclophilin mRNA is constitutively expressed in brain (22) and was detected by hybridization of the blots to a 700-bp BamHI-Pst I fragment of the cDNA piB15 (23) (14) and double-stranded cDNAs (14,17) and for cRNA probes (14). In brief, hybridization to cDNA probes was carried out for 16-18 h at 65°C in a 15-ml solution containing 1 x 106 cpm of 32P-labeled probe per ml, 10x Denhardt's solution (0.2% Ficoll/0.2% polyvinylpyrrolidone/0.2% bovine serum albumin) 4x SSC (0.06 M sodium citrate/0.6 M sodium chloride, pH 7.0), poly(adenylic acid) at 10 ,g/ml, denatured salmon sperm DNA at 100 ,ug/ml, 1 mM EDTA, and 1% SDS.…”

mentioning

confidence: 99%

Involvement of transforming growth factor alpha in the release of luteinizing hormone-releasing hormone from the developing female hypothalamus.

Ojeda

Urbanski

Costa

et al. 1990

Proc. Natl. Acad. Sci. U.S.A.

157

121

View full text Add to dashboard Cite

Little is known about the presence of trophic factors in the hypothalamus and the role they may play in regulating the functional development of hypothalamic neurons. We have investigated the ability of epidermal growth factor (EGF) and transforming growth factor a (TGF-a) to affect the release of luteinizing hormone-releasing hormone (LHRH), the neuropeptide that controls reproductive development. We have also determined whether the genes encoding EGF and TGF-a are expressed in the prepubertal female hypothalamus. Northern blot analysis of poly(A)+ RNA utilizing a single-stranded EGF cDNA probe failed to reveal the presence of EGF mRNA in either the hypothalamus or the cerebral cortex at any age studied (fetal day 18 to postnatal day 36). In contrast, both a complementary RNA probe and a double-stranded TGF-a cDNA recognized in these regions a 4.5-kilobase (kb) mRNA species identical to TGF-a mRNA. The abundance of TGF-a mRNA was 3-4 times greater in the hypothalamus than in the cerebral cortex. Both EGF and TGF-a (2-100 ng/ml) elicited a dose-related increase in LHRH release from the median eminence ofjuvenile rats in vitro. They also enhanced prostaglandin E2 (PGE2) release. The transforming growth factors TGF-fi, and -P2 were ineffective. Only a high dose of basic fibroblast growth factor was able to increase LHRH and PGE2 release. Blockade of the EGF receptor transduction mechanism with RG 50864, a selective inhibitor of EGF receptor tyrosine kinase activity, prevented the effect of both EGF and TGF-a on LHRH and PGE2 release but failed to inhibit the stimulatory effect of PGE2 on LHRH release. Inhibition of prostaglandin synthesis abolished the effect of TGF-et on LHRH, indicating that PGE2 mediates TGF-ainduced LHRH release. The results indicate that the effect of EGF and TGF-a on LHRH release is mediated by the EGF/TGF-a receptor and suggest that TGF-a rather than EGF may be the physiological ligand for this interaction. Since in the central nervous system most EGF/TGF-a receptors are located on glial cells, the results also raise the possibility that-at the median eminence-TGF-a action may involve a glial-neuronal interaction, a mechanism by which the trophic factor first stimulates PGE2 release from glial cells, and then PGE2 elicits LHRH from the neuronal terminals.

show abstract

pl Bl5: A cDNA Clone of the Rat mRNA Encoding Cyclophilin

Cited by 1,043 publications

References 31 publications

Interferon gamma decreases hepatic stellate cell activation and extracellular matrix deposition in rat liver fibrosis

Interferon gamma decreases hepatic stellate cell activation and extracellular matrix deposition in rat liver fibrosis

Nervous System-Specific Expression of a Novel Serine Protease: Regulation in the Adult Rat Spinal Cord by Excitotoxic Injury

Involvement of transforming growth factor alpha in the release of luteinizing hormone-releasing hormone from the developing female hypothalamus.

Contact Info

Product

Resources

About