Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.1.26.9 (ribonuclease)
 6,589 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Transforming growth factor alpha (TGF-alpha) is expressed in the brain and affects cells by binding to the epidermal growth factor receptor (EGF-R). Using a ribonuclease protection assay, we found that TGF-alpha steady state mRNA levels in the mouse striatum peak during the first week of postnatal life. Temporally this peak correlates with the height of gliogenesis in the subependymal layer (SEL), which lies along the striatal border of the lateral ventricle. In vitro studies demonstrate that TGF-alpha can stimulate the proliferation of astrocytes, so glial fibrillary acidic protein (GFAP) mRNA levels were measured as well and it was observed that the peak of GFAP expression followed that of TGF-alpha by 1 week. Furthermore, in a TGF-alpha deficient mouse, waved-1 (wa-1), a significant reduction of GFAP mRNA levels and immunostaining for GFAP was found in the striatum. Bromodeoxyuridine labeling combined with immunohistochemistry of normal postnatal day 6 brain showed that the proliferating cells in the SEL are EGF-R immunoreactive. In the waved-1 SEL, there were fewer BrdU positive cells and there was a reduced level of [3H]thymidine incorporation. EGF-R immunoreactive cells were found in the SEL of the adult mouse brain. Taken together, our data suggest that the TGF-alpha/EGF-R signaling pathway is involved in postnatal mitogenic events in the brain.
 ...
PMID:Striatal TGF-alpha: postnatal developmental expression and evidence for a role in the proliferation of subependymal cells. 765 13

Acute hepatic injury initiates known cellular and molecular events for regeneration. In contrast, the molecular mechanisms of repair following chronic liver injuries have not been defined. Transforming growth factor alpha (TGF alpha) and hepatocyte growth factor (HGF) are hepatocyte mitogens whose in vivo expression in liver is central to the regulation of regeneration. To study the role of TGF alpha and HGF in liver injury and repair, we used a model of reversible biliary obstruction without a bilioenteric anastomosis. In rats, the common bile duct was obstructed either by a vessel loop suspended from the abdominal wall (LOOP) or by ligation and division (DLD). After 7 days of obstruction, animals were autopsied or were decompressed by subcutaneous release of the loop and then autopsied at 1, 2, 4, 7, or 10 days of postdecompression. Serum bilirubin (mg/dl) increased to 14.8 +/- 2.9 (DLD) and 10.3 +/- 3.0 (LOOP) (+/- SEM, NS, ANOVA) at 7 days of obstruction. Liver sections demonstrated equal ductal hyperplasia and collagen deposition after LOOP and DLD. Biliary decompression reversed bile duct proliferation and normalized bilirubin. Analysis of injured and repairing liver mRNA by ribonuclease protection assay showed that TGF alpha mRNA levels were not significantly altered by injury or during repair. HGF mRNA was elevated following obstruction and showed increased expression 1 day after decompression, peaking at 2 days of repair. This evidence of modulation of HGF during liver repair following chronic cholestatic injury suggests that HGF may have a role in cellular proliferation during repair or act as a compensatory growth factor during injury.
 ...
PMID:The expression of regenerative growth factors in chronic liver injury and repair. 799 51