Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.7.7.49 (reverse transcriptase)
 31,746 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In the present study, we observed the expression of toll-like receptor 4 (TLR4) and its downstream signal pathway in peripheral blood monocytes (PBMs) from patients with acute cerebral infarct (ACI). The expression of TLR4 and MyD88 by PBMs was determined by flow cytometry and reverse transcriptase-polymerase chain reaction, and nuclear factor-kappaB (NF-kappaB) activity was detected by electrophoretic mobility shift assay. Ischemia/reperfusion injury-induced cerebral edema, infarction area, and neurologic impairment scores were determined in MyD88 gene knockout mice. The results indicated a significant increase in circulating TLR4(+) monocytes in ACI patients as compared with the control group and the transient ischemia attack (TIA) group. This change paralleled an elevation in TLR4mRNA transcription and serum tumor necrosis factor-alpha (TNF-alpha) and interleukin (IL)-6 in the ACI and TIA groups. Correlation analysis showed TLR4 expression to significantly correlate with cytokine levels and stroke severity. MyD88mRNA differed insignificantly among the three groups. Compared with wild-type mice, 6 h of cerebral ischemia followed by 24 h of reperfusion did not significantly change cerebral edema, cerebral infarction area, and neurologic impairment scores in MyD88 gene knockout mice. Compared with the control group, serum heat shock protein (HSP) 60 increased significantly in the ACI and TIA groups, leading to NF-kappaB activation in TLR4/CD14-transfected HEK293 cells. It is suggested that upregulated TLR4 expression on PMBs may act as one of the peripheral mechanisms of inflammatory injury after ACI. Moreover, circulating HSP60 may be a ligand for TLR4, which is involved in the peripheral mechanism of inflammatory injury after ACI, possibly through an MyD88-independent signal pathway.
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PMID:Upregulated expression of toll-like receptor 4 in monocytes correlates with severity of acute cerebral infarction. 1852 39

Nogo-A and its Nogo receptor (NgR) have been shown to inhibit plasticity after central nervous system lesions. Therefore, we hypothesized that Nogo-A and its receptor NgR will be upregulated and will activate RhoA, and thus, they play a role in the damage in the infarction developed. To test this hypothesis, a focal cerebral infarction model was created by coagulation of the right middle cerebral artery (MCA) and ipsilateral common carotid artery (CCA), as well as the simultaneous transient occlusion of the contralateral CCA for 30 min in 60 adult Sprague-Dawley rats. The rat brains were treated at 6 h, 12 h, 24 h, 48 h, 96 h, and 7 d after cerebral infarction. Sham controls were collected to determine histopathologic damage and Nogo-A, NgR, and RhoA expression using hematoxylin-eosin, immunohistochemical staining, Western blot analysis, and fluorimeter-based quantitive reverse transcriptase-polymerase chain reaction. The results indicate that cerebral infarction produced damage and edema on nerve cells in the infarction area, becoming most prominent at 24h after modeling. Meanwhile, a marked increase of Nogo-A, NgR, and RhoA expression was found at 6h in model groups compared with the sham controls, which peaked at 24 h after the operation. Immunohistochemical staining and Western blot analysis also showed upregulated Nogo-A located in the myelin sheath of the infarction area, NgR expressed on the surface of neurons and their processes, and RhoA expressed inside the cytoplasm of neurons in infarction brain. In conclusion, the upregulation of Nogo-A, NgR, and RhoA in the infarction area may be an important feature of cerebral infarction and may play a role in the pathologic progression of this lesion.
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PMID:Patterns of Nogo-A, NgR, and RhoA expression in the brain tissues of rats with focal cerebral infarction. 1952 73

Ischemic cerebral infarction is a leading cause of death and disability, but the key inflammatory cytokines were not fully understood and no successful therapy has been established. We have used the methods of reverse transcriptase-polymerase chain reaction (RT-PCR), enzyme-linked immunosorbent assay (ELISA), western blot, and immunohistochemical staining to detect the dynamic changes of IL-23/IL-17 axis in brain infarction and BMSC treatment on the sixth day. BMSC transplantation could reduce the infarct size (P<0.05) and improve functional deficits (P<0.001) in brain infarction. The level of IL-23/IL-17 axis expression is higher (P<0.05) in pMCAO-operated group than that in sham operated group. BMSC treatment could reduce IL-23 expression (P<0.05) and attenuate IL-17 expression (P<0.01) both in serum and around infarct lesion. So we have drawn the conclusion that IL-23/IL-17 axis induces inflammation in the pathophysiological process of cerebral infarction. BMSC treatment plays therapeutic role by immunomodulating the expression of IL-23/IL-17 axis. These findings may help to understand the cytokines in cerebral infarction and open up a possible new way of immunological treatment.
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PMID:The immunomodulatory effect of bone marrow stromal cells (BMSCs) on interleukin (IL)-23/IL-17-mediated ischemic stroke in mice. 2341 22