| Kaur, C., Hao, A.J., Wu, C.H. and Ling, E.A. |
------>authors3_c=None ------>paper_class1=1 ------>Impact_Factor=None ------>paper_class3=2 ------>paper_class2=3 ------>vol=54 ------>confirm_bywho=thfong ------>insert_bywho=chw0204 ------>Jurnal_Rank=None ------>authors4_c=None ------>comm_author= ------>patent_EDate=None ------>authors5_c=None ------>publish_day=None ------>paper_class2Letter=None ------>page2=9 ------>medlineContent= ------>unit=E0107 ------>insert_date=20010724 ------>iam=3 ------>update_date= ------>author=??? ------>change_event=5 ------>ISSN=None ------>authors_c=None ------>score=-13 ------>journal_name=Microscopy Research and Techniques ------>paper_name=Origin of microglia ------>confirm_date=20010726 ------>tch_id=083004 ------>pmid=19815726 ------>page1=2 ------>fullAbstract=PURPOSE. To use a laser-induced ocular hypertension (LIOH) mouse model to examine the optic nerve head (ONH) expression of EphB/ephrin-B, previously shown to be upregulated in glaucomatous DBA/2J mice. To relate ephrin-B reverse signaling with states of axonal response to disease. METHODS. LIOH was induced unilaterally in CD-1 mice by laser photocoagulation of limbal and episcleral veins. Intraocular pressure (IOP) was measured with Tonolab. EphB/ephrin-B mRNA expression was assessed by in situ hybridization on eye cup cryosections and real-time PCR. Cell specific markers were used to identify the cellular origin of EphB/ephrin-B expression. Activation of ephrin-B signaling was investigated with a phospho-specific antibody on cryosections and retinal whole-mounts. RESULTS. Upregulation of EphB/ephrin-B expression occurred early within a day of IOP elevation. A transient increase of phosphorylation-dependent ephrin-B (pEB) reverse signaling was observed in ONH axons, microglia, and some astrocytes. Morphologically unaffected RGC axons differed from axons with reactive aberrant trajectories by exhibiting increased pEB activation, while pEB levels in morphologically affected axons were comparable to controls. CONCLUSIONS. An Eph-ephrin signaling network is activated at the ONH after LIOH in CD-1 mice, either prior to or coincident with the initial morphological signs of RGC axon damage reported previously. Of note, ephrin-B reverse signaling was transiently up-regulated in RGC axons at the ONH early in their response to IOP elevation but was down-regulated in axons that had succumbed to glaucomatous injury and exhibited aberrant trajectories. Ephrin-B reverse signaling may mark RGC axons for damage or confer a protective advantage against injury. ------>tmu_sno=None ------>sno=3907 ------>authors2=None ------>authors3=None ------>authors4=None ------>authors5=None ------>authors6=None ------>authors6_c=None ------>authors=Kaur, C., Hao, A.J., Wu, C.H. and Ling, E.A. ------>delete_flag=0 ------>SCI_JNo=None ------>authors2_c=None ------>publish_area=None ------>updateTitle=Axonal/Glial Upregulation of EphB/ephrin-B Signaling in Mouse Experimental Ocular Hypertension. ------>language=2 ------>check_flag= ------>submit_date= ------>country=None ------>no= ------>patent_SDate=None ------>update_bywho= ------>publish_year=2001 ------>submit_flag= ------>publish_month=None |