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The parasitic protozoan Trypanosoma cruzi employs multiple molecular strategies to invade a broad range of nonphagocytic cells. Here we demonstrate that the invasion of human primary umbilical vein endothelial cells (HUVECs) or Chinese hamster ovary (CHO) cells overexpressing the B(2) type of bradykinin receptor (CHO-B(2)R) by tissue culture trypomastigotes is subtly modulated by the combined activities of kininogens, kininogenases, and kinin-degrading peptidases. The presence of captopril, an inhibitor of bradykinin degradation by kininase II, drastically potentiated parasitic invasion of HUVECs and CHO-B(2)R, but not of mock-transfected CHO cells, whereas the B(2)R antagonist HOE 140 or monoclonal antibody MBK3 to bradykinin blocked these effects. Invasion competence correlated with the parasites' ability to liberate the short-lived kinins from cell-bound kininogen and to elicit vigorous intracellular free calcium ([Ca(2+)](i)) transients through B(2)R. Invasion was impaired by membrane-permeable cysteine proteinase inhibitors such as Z-(SBz)Cys-Phe-CHN(2) but not by the hydrophilic inhibitor 1-trans-epoxysuccinyl-l-leucyl-amido-(4-guanidino) butane or cystatin C, suggesting that kinin release is confined to secluded spaces formed by juxtaposition of host cell and parasite plasma membranes. Analysis of trypomastigote transfectants expressing various cysteine proteinase isoforms showed that invasion competence is linked to the kinin releasing activity of cruzipain, herein proposed as a factor of virulence in Chagas' disease.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11067878&dopt=Abstract
Physiol Genomics. 2000 Nov 9;4(1):75-81.
Expression of a renin/GFP transgene in mouse embryonic, extra-embryonic, and adult tissues.
Jones CA, Hurley MI, Black TA, Kane CM, Pan L, Pruitt SC, Gross KW.
Department of Molecular and Cellular Biology, Roswell Park Cancer Institute, Buffalo 14260, USA.
A reporter construct was assembled with 4-kb of renin 5'-flanking sequence fused to humanized green fluorescent protein (GFP) cDNA. Transgenic mice carrying this construct were produced and assayed for GFP expression. In the adult, expression was detected in juxtaglomerular (JG) cells of the kidney and granular convoluted tubular cells of the submandibular gland. Furthermore, treatment of mice with captopril induced GFP expression in renal vascular smooth muscle cells. During embryogenesis, GFP expression was first detected at embryonic day E13 in the adrenal gland and Wolffian duct. Expression was also seen in the developing renal vasculature as early as E14 and remained detectable through birth. Renal GFP expression became restricted to JG cells in adults. Fetal adrenal and gonadal arteries also expressed GFP. In the placenta, GFP was observed in giant cell trophoblasts, consistent with reports of renin expression in chorionic cells of both humans and mice. We conclude that 4 kb of renin 5' flank is sufficient to direct multiple known renin expression patterns. Furthermore, the renin-GFP construct characterized here will provide a useful vital reporter for renin expression.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11074016&dopt=Abstract
Am J Hypertens. 2000 Nov;13(11):1189-93.
What is critical renal artery stenosis? Implications for treatment.
Simon G.
Hypertension Clinic, VA Medical Center, Minneapolis, Minnesota 55417, USA.
Renovascular disease due to progressive atherosclerotic renal artery stenosis is being diagnosed with increasing frequency in the elderly. At what degree of renal artery stenosis should intervention be recommended is not clear. To answer this question, unilateral or bilateral activation of the renin-angiotensin system or its absence were detected by captopril-stimulated renal vein renin measurements in 49 hypertensive patients, aged 63 years, with normal or near-normal renal function (serum creatinine concentration < or =2.0 mg/dL), and the information was matched against radiographic measurements of the extent of renal artery stenosis. With few exceptions, unilateral or bilateral hypersecretion of renin was associated with 80% or greater reduction of renal artery lumen diameter. In contrast, normal secretion or suppression of renin production in a kidney contralateral to an ischemic one was associated with either normal caliber renal artery or renal artery stenosis less than 80%. These findings suggest that renal artery stenosis less than 80% should be monitored rather than treated because improvement of renal function and amelioration of hypertension are not expected unless the renin-angiotensin system has been activated in the affected kidney. Renoprotection by early intervention is uncertain because progression of renal artery stenosis is unpredictable. Normal captopril-stimulated renal vein renin measurements in hypertensive patients obviate the need for further work-up or interventional therapy of renovascular disease.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11078179&dopt=Abstract
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