Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P00750 (PLA)
 16,800 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The spontaneous capillary tube migration of metastatic MAT 13762 rat mammary adenocarcinoma cells has been measured and compared with that of a non-metastatic variant, TGR. MAT 13762 cells migrated to a greater extent in the presence than in the absence of serum, and in both cases migration areas were considerably greater than for TGR cells. Different clones of hybrids, formed by fusing metastatic and non-metastatic variants, showed migration areas ranging from those of the metastatic to those of the non-metastatic parent cells. Despite their differing migrations, all of these clones were either non or only slightly metastatic. Treatment of TGR cells with trypsin enhanced their migration to that of MAT 13762 cells, whereas trypsin-treated MAT 13762 cells showed a slightly decreased migration. Although MAT 13762 cells, unlike TGR cells, produced large amounts of plasminogen activator (PA), no evidence was obtained for the direct involvement of PA in the high migration rate of MAT 13762 cells.
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PMID:Spontaneous capillary tube migration of metastatic rat mammary adenocarcinoma cells. 653 58

Dual renin-angiotensin system (RAS) blockade in diabetic nephropathy is no longer feasible because of the profit/side effect imbalance. (Pro)renin receptor [(P)RR] blockade with handle region peptide (HRP) has been reported to exert beneficial effects in various diabetic models in a RAS-independent manner. To what degree (P)RR blockade adds benefits on top of RAS blockade is still unknown. In the present study, we treated diabetic TGR(mREN2)27 rats, a well-established nephropathy model with high prorenin levels [allowing continuous (P)RR stimulation in vivo], with HRP on top of renin inhibition with aliskiren. Aliskiren alone lowered blood pressure and exerted renoprotective effects, as evidenced by reduced glomerulosclerosis, diuresis, proteinuria, albuminuria, and urinary aldosterone levels as well as diminished renal (P)RR and ANG II type 1 receptor expression. It also suppressed plasma and tissue RAS activity and suppressed cardiac atrial natriuretic peptide and brain natriuretic peptide expression. HRP, when given on top of aliskiren, did not alter the effects of renin inhibition on blood pressure, RAS activity, or aldosterone. However, it counteracted the beneficial effects of aliskiren in the kidney, induced hyperkalemia, and increased plasma plasminogen activator-inhibitor 1, renal cyclooxygenase-2, and cardiac collagen content. All these effects have been linked to (P)RR stimulation, suggesting that HRP might, in fact, act as a partial agonist. Therefore, the use of HRP on top of RAS blockade in diabetic nephropathy is not advisable.
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PMID:Deterioration of kidney function by the (pro)renin receptor blocker handle region peptide in aliskiren-treated diabetic transgenic (mRen2)27 rats. 2469 88