Differential Regulation in the Expression of Hepatic Genes in Nephrotic and Pair-Fed Rats

Ibarra-Rubio, María Elena; Pedraza‐Chaverrí, José; Panduro, Arturo

doi:10.1159/000187452

Cited by 10 publications

(4 citation statements)

References 29 publications

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“…No changes were found in the mRNA level or transcription rate for this protein. Results similar to these have also been found in PAN nephrosis (23). Therefore, nephrosis does not increase the hepatic synthesis of all secretory proteins to the same extent, and the acute phase response, if involved at all, is not operative after the establishment of proteinuria.…”

Section: Hy Poalbuminemiasupporting

confidence: 81%

Lipoprotein Metabolism in Experimental Nephrosis

Marsh

1996

Experimental Biology and Medicine

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In experimental nephrosis, a decrease in plasma albumin resulting from proteinuria causes a decreased in the plasma oncotic pressure. The existence of an osmoreceptor, which responds to the low oncotic pressure and produces a factor(s) that signals the liver to increase the secretion of plasma proteins, is postulated. The hyperlipidemia characteristic of the nephrotic syndrome results primarily from increased hepatic secretion of apolipoproteins and lipoproteins representing the entire density spectrum from VLDL, IDL, and LDL to HDL. Not all plasma proteins and apolipoproteins are affected to the same extent. Increased mRNA levels due to increased transcription have been shown for albumin and apolipoprotein A-1 (apoA-1). The increased secretion of VLDL, the major vehicle for triglyceride transport from the liver, appears to be due mainly to posttranscriptional events possibly related to increased lipogenesis. Once proteinuria begins, the demand for amino acids for albumin and apolipoprotein synthesis by the liver is increased. To meet this demand, protein catabolism in the peripheral tissues is increased. One manifestation of this process is a decrease in lipoprotein lipase which reduces VLDL catabolism, contributing to the sustained elevation of plasma VLDL. The spectacular overproduction of apoA-1 in nephrosis in the rat is accompanied by a decreased fractional catabolic rate (FCR), contributing to the maintenance of high levels of HDL. Urinary loss of HDL and its renal catabolism does not account for the decreased FCR. The reason for the decreased FCR is not known. Work with nephrotic rats overexpressing transgenic human apoA-1 has shown that human A-1 forms smaller HDL3-sized particles, rather than the larger HDL2 of the rat. This may contribute to the failure of HDL levels to increase in the human nephrotic syndrome. High plasma VLDL and LDL with normal or low HDL probably account for the increased incidence of coronary artery disease in the nephrotic syndrome.

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Section: Hy Poalbuminemiasupporting

confidence: 81%

Lipoprotein Metabolism in Experimental Nephrosis

Marsh

1996

Experimental Biology and Medicine

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“…Tile ACE activity lneasurements for testis and epididymis were performed using the linear segments of the plots of HA production vs tissue extract volume and incubation time. The ACE activities of the testis and epididymis were inhibited by HHL at concentrations above 5 mM just as is the ACE of human heart muscle (15), testis (7) and sheep serum (16). Eventhough the K values and HA concentrations obtained were different for each tissue, the inhibition by HHL occurred at concentrations above 5 raM.…”

Section: Discussionmentioning

confidence: 92%

Sheep testicular and epididymal angiotensin converting enzyme: inhibitions by captopril, lisinopril and enalapril

Udupa

Rao

1997

IUBMB Life

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Inhibition of angiotensin converting enzyme(ACE) in presence of captopril(C), lisinopril(L) and enalapril(E) were investigated in testis and epididymis of sheep using Hip‐His‐Leu as substrate. Captopril, lisinopril and enalapril were competitive inhibitors of the enzyme from both tissues. Differences in the I50 and Ki values using these three inhibitors reflects the affinities of these inhibitors for the, ACE. In addition, the relative potencies of captopril, lisinopril and enalapril were different for testicular ACE(C > L > E) and epididymal ACE(L>C >E). This observation suggests differences between the active sites of the testicular and epididymal ACE which may reflect on their functions in vivo.

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“…Although protein C and AT have similar small molecular size, protein C has a negative charge that markedly reduces its relative renal loss. More importantly, increased hepatic synthesis of protein C and other vitamin K ‐dependent zymogens has been documented in a rat model of nephrotic syndrome 63 . Protein C shares common transcription regulatory sites with the other vitamin K ‐dependent coagulation proteins, including at least 3 liver‐specific regulatory elements 64 .…”

Section: Discussionmentioning

confidence: 99%

Examination of hemostatic parameters to detect hypercoagulability in dogs with severe protein‐losing nephropathy

Donahue

Brooks

Otto

2011

J Vet Emergen Crit Care

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Hemostatic abnormalities consistent with systemic hypercoagulability are common in dogs with RF and PLN, however, no prothrombotic factors unique to PLN were identified in our study. The thrombotic tendency of PLN may therefore involve parameters we did not directly assess such as platelet reactivity, fibrinolysis, perturbations in blood flow, and/or endothelial dysfunction. High protein C is a novel finding in PLN dogs of unknown clinical relevance.

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Differential Regulation in the Expression of Hepatic Genes in Nephrotic and Pair-Fed Rats

Cited by 10 publications

References 29 publications

Lipoprotein Metabolism in Experimental Nephrosis

Lipoprotein Metabolism in Experimental Nephrosis

Sheep testicular and epididymal angiotensin converting enzyme: inhibitions by captopril, lisinopril and enalapril

Examination of hemostatic parameters to detect hypercoagulability in dogs with severe protein‐losing nephropathy

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