| Lin H |
------>authors3_c= ------>paper_class1=1 ------>Impact_Factor=7.371 ------>paper_class3=2 ------>paper_class2=1 ------>vol=19 ------>confirm_bywho=jschu ------>insert_bywho=cjcheng ------>Jurnal_Rank=1.8 ------>authors4_c= ------>comm_author= ------>patent_EDate=None ------>authors5_c= ------>publish_day=1 ------>paper_class2Letter=None ------>page2=348 ------>medlineContent= ------>unit=E0102 ------>insert_date=20080321 ------>iam=7 ------>update_date=None ------>author=??? ------>change_event=4 ------>ISSN=1046-6673 ------>authors_c= ------>score=500 ------>journal_name=J Am Soc Nephrol ------>paper_name=Disruption of guanylyl cyclase-G protects against acute renal injury. ------>confirm_date=20080321 ------>tch_id=087010 ------>pmid=18199799 ------>page1=339 ------>fullAbstract=The membrane forms of guanylyl cyclase (GC) serve as cell-surface receptors that synthesize the second messenger cGMP, which mediates diverse cellular processes. Rat kidney contains mRNA for the GC-G isoform, but the role of this receptor in health and disease has not been characterized. It was found that mouse kidney also contains GC-G mRNA, and immunohistochemistry identified GC-G protein in the epithelial cells of the proximal tubule and collecting ducts. Six hours after ischemia-reperfusion (I/R) injury, GC-G mRNA and protein expression increased three-fold and remained upregulated at 24 h. For determination of whether GC-G mediates I/R injury, a mutant mouse with a targeted disruption of the GC-G gene (Gucy2g) was created. At baseline, no histologic abnormalities were observed in GC-G(-/-) mice. After I/R injury, elevations in serum creatinine and urea were attenuated in GC-G(-/-) mice compared with wild-type controls, and this correlated with less tubular disruption, less tubular cell apoptosis, and less caspase-3 activation. Measures of inflammation (number of infiltrating neutrophils, myeloperoxidase activity, and induction of IL-6 and P-selectin) and activation of NF-kappaB were lower in GC-G(-/-) mice compared with wild-type mice. Direct transfer of a GC-G expression plasmid to the kidneys of GC-G(-/-) mice resulted in a dramatically higher mortality after renal I/R injury, further supporting a role for GC-G in mediating injury. In summary, GC-G may act as an early signaling molecule that promotes apoptotic and inflammatory responses in I/R-induced acute renal injury. ------>tmu_sno=None ------>sno=17041 ------>authors2=Cheng CF ------>authors3=Hou HH ------>authors4=Lian WS ------>authors5=Chao YC ------>authors6=Ciou YY, Djoko B, Tsai MT, Cheng CJ, Yang RB ------>authors6_c= ------>authors=Lin H ------>delete_flag=0 ------>SCI_JNo=None ------>authors2_c= ------>publish_area=0 ------>updateTitle=Disruption of guanylyl cyclase-G protects against acute renal injury. ------>language=2 ------>check_flag=None ------>submit_date=None ------>country=None ------>no=2 ------>patent_SDate=None ------>update_bywho=None ------>publish_year=2008 ------>submit_flag=None ------>publish_month=2 |