Association between activation of the renin-angiotensin system and secondary erythrocytosis in patients with chronic obstructive pulmonary disease

Vlahakos, Demetrios; Kosmas, Epaminondas; Dimopoulou, Ioanna; Ikonomou, Ekaterini; Jullien, G; Vassilakos, Pavlos; Marathias, Katerina

doi:10.1016/s0002-9343(98)00390-8

Cited by 70 publications

(33 citation statements)

References 26 publications

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“…The results were clear: restitution of angiotensin II elevated both systolic blood pressure and hematocrit to near normal levels. Although we have not eliminated the possibility that blood pressure itself played a role in erythrocyte formation, these studies compliment a host of clinical investigations suggesting a direct role of the RAS in erythropoiesis (16,19,33,55). It is well known that erythropoietin is dependent on the intracellular signaling of the Jak-STAT system for efficacy.…”

Section: Angiotensin II and Erythropoiesissupporting

confidence: 59%

New approaches to genetic manipulation of mice: tissue-specific expression of ACE

Cole

Xiao

Adams

et al. 2003

American Journal of Physiology-Renal Physiology

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. New approaches to genetic manipulation of mice: tissue-specific expression of ACE. Am J Physiol Renal Physiol 284: F599-F607, 2003; 10.1152/ajprenal.00308. 2002The renin-angiotensin system (RAS) plays a central role in body physiology, controlling blood pressure and blood electrolyte composition. ACE.1 (null) mice are null for all expression of angiotensin-converting enzyme (ACE). These mice have low blood pressure, the inability to concentrate urine, and a maldevelopment of the kidney. In contrast, ACE.2 (tissue null) mice produce one-third normal plasma ACE but no tissue ACE. They also have low blood pressure and cannot concentrate urine, but they have normal indices of renal function. These mice, while very informative, show that the null approach to creating knockout mice has intrinsic limitations given the many different physiological systems that no longer operate in an animal without a functioning RAS. To investigate the fine control of body physiology by the RAS, we developed a novel promoter swapping approach to generate a more selective tissue knockout of ACE expression. We used this to create ACE.3 (liver ACE) mice that selectively express ACE in the liver but lack all ACE within the vasculature. Evaluation of these mice shows that endothelial expression of ACE is not required for blood pressure control or normal renal function. Targeted homologous recombination has the power to create new strains of mice expressing the RAS in selected subsets of tissues. Not only will these new genetic models be useful for studying blood pressure regulation but also they show great promise for the investigation of the function of the RAS in complicated disease models.angiotensin-converting enzyme; blood pressure; angiotensin II; liver; renin-angiotensin system ROUGHLY ONE-HALF OF ALL AMERICANS die from cardiovascular disease. Put differently, more Americans die of cardiovascular disease than the next seven leading causes of death combined (1). To understand cardiovascular disease, one must understand how the body regulates blood pressure, a complex process governed by many different components, including multiple vasoconstrictors and vasodilators. Among these is the renin-angiotensin system (RAS), which produces the vasoconstrictor angiotensin II. The basic physiology by which angiotensinogen is degraded to angiotensin II has been known for many years, with the importance of this system underscored by the enormous clinical utility of pharmaceuticals that interrupt angiotensin II formation or action. So with all that is known about the RAS, what could conceivably be new? In fact, the use of targeted homologous recombination in mouse embryonic stem (ES) cells has produced a startling series of insights into the operation and functional importance of the RAS. This progress has been so rapid and dramatic as to implicate the RAS as easily the most important regulator of cardiovascular function as measured through blood pressure control.The use of homologous recombination to modify genes relies on the properties of cul...

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Section: Angiotensin II and Erythropoiesissupporting

confidence: 59%

New approaches to genetic manipulation of mice: tissue-specific expression of ACE

Cole

Xiao

Adams

et al. 2003

American Journal of Physiology-Renal Physiology

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“…Further, losartan alone retarded the formation of CFU erythroid. It should be noted that a variety of clinical reports have observed an association between activation of the renin-angiotensin system and increased erythropoiesis (Jensen et al, 1993;Julian et al, 1994;Vlahakos et al, 1999;Cole et al, 2000). These studies come from analyses of patients with a variety of chronic diseases, including chronic obstructive pulmonary disease, heart failure, and renal transplantation.…”

Section: G Erythropoiesismentioning

confidence: 99%

A Modern Understanding of the Traditional and Nontraditional Biological Functions of Angiotensin-Converting Enzyme

et al. 2012

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“…Particularly, these studies have shown a possible involvement of the renin angiotensin system in the genesis of erythrocytosis observed following a kidney transplant 191 or in association with congestive heart failure, 192 chronic obstructive pulmonary disease, 193,194 essential, malignant, or renovascular hypertension [195][196][197] or with chronic hemodialysis. 198,199 The pathogenesis of erythrocytosis observed in these conditions is complex in that erythropoietin, angiotensin II and insulin-like growth factor I are all involved.…”

Section: Apoptotic Mechanisms In the Genesis Of Erythrocytosis Associmentioning

confidence: 99%

Apoptotic mechanisms in the control of erythropoiesis

2004

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Erythropoiesis is a complex multistep process encompassing the differentiation of hemopoietic stem cells to mature erythrocytes. The steps involved in this complex differentiation process are numerous and involve first the differentiation to early erythoid progenitors (burst-forming units-erythroid, BFU-E), then to late erythroid progenitors (colony-forming unitserythroid) and finally to morphologically recognizable erythroid precursors. A key event of late stages of erythropoiesis is nuclear condensation, followed by extrusion of the nucleus to produce enucleated reticulocytes and finally mature erythrocytes. During the differentiation process, the cells became progressively sensitive to erythropoietin that controls both the survival and proliferation of erythroid cells.A normal homeostasis of the erythropoietic system requires an appropriate balance between the rate of erythroid cell production and red blood cell destruction. Growing evidences outlined in the present review indicate that apoptotic mechanism play a relevant role in the control of erythropoiesis under physiologic and pathologic conditions. Withdrawal of erythropoietin or stimulation of death receptors such as Fas or TRAIL-Rs leads to activation of a subset of caspases-3, -7 and -8, which then cleave the transcription factors GATA-1 and TAL-1 and trigger apoptosis. In addition, there is evidence that a number of caspases are physiologically activated during erythroid differentiation and are functionally required for erythroid maturation. Several caspase substrates are cleaved in differentiating cells, including the protein acinus whose activation by cleavage is required for chromatin condensation.The studies on normal erythropoiesis have clearly indicated that immature erythroid precursors are sensitive to apoptotic triggering mediated by activation of the intrinsic and extrinsic apoptotic pathways. These apoptotic mechanisms are frequently exacerbated in some pathologic conditions, associated with the development of anemia (ie, thalassemias, multiple myeloma, myelodysplasia, aplastic anemia).The considerable progress in our understanding of the apoptotic mechanisms underlying normal and pathologic erythropoiesis may offer the way to improve the treatment of several pathologic conditions associated with the development of anemia.

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Association between activation of the renin-angiotensin system and secondary erythrocytosis in patients with chronic obstructive pulmonary disease

Cited by 70 publications

References 26 publications

New approaches to genetic manipulation of mice: tissue-specific expression of ACE

New approaches to genetic manipulation of mice: tissue-specific expression of ACE

A Modern Understanding of the Traditional and Nontraditional Biological Functions of Angiotensin-Converting Enzyme

Apoptotic mechanisms in the control of erythropoiesis

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