Inhibition of angiotensin I–converting enzyme induces radioprotection by preserving murine hematopoietic short-term reconstituting cells

Charrier, Sabine; Michaud, Annie; Badaoui, Sabrina; Giroux, Sébastien; Ezan, Éric; Sainteny, Françoise; Corvol, Pierre; Vainchenker, William

doi:10.1182/blood-2003-11-3828

Cited by 61 publications

(63 citation statements)

References 28 publications

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“…Short-term ACE inhibition (2 days) suppressed the G0 to G1 transition of Lin 2 cells (i.e., bone marrow progenitor cells) (Davis et al, 2010). This effect of short-term ACE inhibition reduces the potential shortterm injury to stem cells, and is what was seen in the irradiation experiments described earlier that resulted in enhanced stem-cell survival (Charrier et al, 2004). In contrast, longer-term treatment with ACE inhibitors (greater than 7 days) appeared to increase the proliferation of bone marrow progenitors (Davis et al, 2010).…”

Section: Sca1supporting

confidence: 49%

“…Acute ACE inhibitor administration in mice prevented potential colony-forming cells from entering the cell cycle, and thus protected these cells from the lethal effects of chemotherapy or irradiation (Chisi et al, 2000). Further in vivo analysis of an irradiation model showed that ACE inhibitors preserved stem cells and bone marrow multilineage hematopoietic progenitors, including colony-forming unit (CFU) granulocyte/ macrophage, burst-forming unit erythroid, and CFU megakaryocyte (Charrier et al, 2004). The protective effect appeared due to the loss of angiotensin II--mediated AT1 signaling.…”

Section: Acementioning

confidence: 99%

See 1 more Smart Citation

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

Bernstein

Ong

Blackwell

et al. 2013

Pharmacological Reviews

273

263

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Section: Sca1supporting

confidence: 49%

Section: Acementioning

confidence: 99%

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

Bernstein

Ong

Blackwell

et al. 2013

Pharmacological Reviews

273

263

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“…Unlike brain and testis, circulation within the BM reflects both a elevate levels of Ac-SDKP. 76 This effect of Ang II may in part be due to BM stroma because in a strict single-cell recruitment assay, ACE inhibition did not alter the recruitment of primitive core blood (CD34 + CD38 -) into cell division. 73 Recent studies have revealed that ACE-regulated hematopoiesis is quite complex.…”

Section: Discussionmentioning

confidence: 98%

The peptide network regulated by angiotensin converting enzyme (ACE) in hematopoiesis

Shen

Bernstein

2011

Cell Cycle

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T he concept of a local bone marrow renin-angiotensin system (RAS) has been introduced and accumulating evidence suggests that the local RAS is actively involved in hematopoiesis. Angiotensin converting enzyme (ACE) is a key player in the RAS and makes the final effector angiotensin II. Besides angiotensin II, ACE also regulates a panel of bioactive peptides, such as substance P, Ac-SDKP and angiotensin 1-7. These peptides have also been individually reported in the regulation of pathways of hematopoiesis. In this setting, an ACE-regulated peptide network orchestrating hematopoiesis has emerged. Here, we focus on this peptide network and discuss the roles of ACE and its peptides in aspects of hematopoiesis. Special attention is given to the recent revelation that ACE is a bona fide marker of hematopoietic stem cells.

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“…12,13 More recently, pre-treatment of myeloablated mice with telmisartan, another AT 1 -receptor antagonist, increased survival rate and protected bone marrow haematopoietic stem cells (HSC) from radiotoxicity. 14 The mechanisms accounting for the in vivo actions of Ang II may be due to the direct effects of Ang II on HSC, since blockade of CD34 + cell AT 1 -receptor-mediated activity resulted in suppression of erythroid and myeloid precursor development. 15,16 These studies suggest that Ang II directly influences bone marrow dynamics through AT 1 -receptor stimulation by influencing haematopoietic events as early as HSC entry into the cell cycle.…”

Section: Introductionmentioning

confidence: 99%

Angiotensin II stimulates arachidonic acid release from bone marrow stromal cells

Richmond

Tallant

Gallagher

et al. 2004

J Renin Angiotensin Aldosterone Syst

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Introduction Angiotensin II (Ang II) is recognised as a regulator of haematopoiesis, but its actions within the bone marrow are not fully understood. Support of haematopoiesis by bone marrow stromal cells (MSC) is dependent on factors that include arachidonic acid and macrophage colony stimulating factor (MCSF), both of which are increased by Ang II stimulation in other tissues. To further elucidate the mechanisms of Ang II-regulated haematopoiesis, we determined whether Ang II-stimulation alters arachidonic acid release and MCSF secretion from MSC. Methods Cynomolgus monkey MSC isolated from bone marrow aspirates and the human HS-5 stromal cell line were studied for Ang II-mediated arachidonic acid (AA) release, while secretion of MCSF in response to Ang II was studied in HS-5 cells. Cells were labelled overnight with 3H-AA and the release of 3H-AA was measured in culture medium following 20 minutes stimulation with Ang II, alone or in combination with the AT1- or AT 2-receptor antagonists, losartan and PD 123319, respectively. MCSF secretion into culture medium was measured using an enzyme immunoassay following 24 hours of treatment with Ang II alone or in combination with losartan or PD 123319. Phorbol-myristate-acetate, known to stimulate release of AA and MCSF, was used as a positive control in both experiments. Results In response to Ang II, release of 3H-AA from monkey and human MSC was increased (p<0.05) to 147±4% and 124±3% of control, respectively. The AT1- and AT2-receptor antagonists, losartan and PD 123319, individually reduced Ang II-stimulated 3H-AA release. In contrast, Ang II had no effect on secretion of MCSF from HS-5 cells. Conclusions These results provide mechanistic evidence for Ang II-mediated haematopoiesis through AA release that may, in part, explain Ang II-facilitated recovery of haematopoiesis in experimental myelosuppression and the anaemias associated with Ang II receptor blockade.

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Inhibition of angiotensin I–converting enzyme induces radioprotection by preserving murine hematopoietic short-term reconstituting cells

Cited by 61 publications

References 28 publications

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

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

The peptide network regulated by angiotensin converting enzyme (ACE) in hematopoiesis

Angiotensin II stimulates arachidonic acid release from bone marrow stromal cells

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