Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.15.1 (ACE)
 18,300 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Factor VIII-related antigen (F8) and Ulex europaeus lectin (UEL) are accepted markers for human blood vessel endothelium. However, disagreement exists as to whether lymphatic vessels stain for F8, and accordingly this study was undertaken to address this issue. Moreover, another vascular endothelial marker, angiotensin converting enzyme (ACE) was also examined in lymphatics. Segments of human thoracic duct and portions of small bowel containing lacteals with post-mortem intervals of less than 15 hours, were removed at autopsy and fixed in B5 or formalin. The specimens were processed routinely and sections examined by indirect immunohistochemical techniques for F8 (Dako Corp.), ACE and for UEL (EY Lab). F8, UEL, and ACE positivity was uniformly found in thoracic ducts and lacteals; however, the staining intensity was less in lymphatic vessels with F8 and UEL than with comparable arteries or veins. ACE staining intensity, on the other hand, was similar in blood vessels and lymphatics. Both formalin and B5 fixation preserved antigenicity; however, background staining was greater with B5 fixation whereas tissue staining was slightly more intense with formalin fixation.
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PMID:Vascular endothelial markers of the human thoracic duct and lacteal. 303 2

A functional renin-angiotensin system (RAS) is required for normal kidney development. Neonatal inhibition of the RAS in rats results in long-term pathological renal phenotype and causes hyaluronan (HA), which is involved in morphogenesis and inflammation, to accumulate. To elucidate the mechanisms, intrarenal HA content was followed during neonatal completion of nephrogenesis with or without angiotensin converting enzyme inhibition (ACEI) together with mRNA expression of hyaluronan synthases (HAS), hyaluronidases (Hyal), urinary hyaluronidase activity and cortical lymphatic vessels, which facilitate the drainage of HA from the tissue. In 6-8days old control rats cortical HA content was high and reduced by 93% on days 10-21, reaching adult low levels. Medullary HA content was high on days 6-8 and then reduced by 85% to 12-fold above cortical levels at day 21. In neonatally ACEI-treated rats the reduction in HA was abolished. Temporal expression of HAS2 corresponded with the reduction in HA content in the normal kidney. In ACEI-treated animals cortical HAS2 remained twice the expression of controls. Medullary Hyal1 increased in controls but decreased in ACEI-treated animals. Urine hyaluronidase activity decreased with time in control animals while in ACEI-treated animals it was initially 50% lower and did not change over time. Cells expressing the lymphatic endothelial mucoprotein podoplanin in ACEI-treated animals were increased 18-fold compared to controls suggesting compensation. In conclusion, the high renal HA content is rapidly reduced due to reduced HAS2 and increased Hyal1 mRNA expressions. Normal angiotensin II function is crucial for inducing these changes. Due to the extreme water-attracting and pro-inflammatory properties of HA, accumulation in the neonatally ACEI-treated kidneys may partly explain the pathological renal phenotype of the adult kidney, which include reduced urinary concentration ability and tubulointerstitial inflammation.
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PMID:Angiotensin converting enzyme inhibition blocks interstitial hyaluronan dissipation in the neonatal rat kidney via hyaluronan synthase 2 and hyaluronidase 1. 2093 85