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

被引:30
作者
Shen, Xiao Z. [1 ]
Bernstein, Kenneth E. [1 ,2 ]
机构
[1] Cedars Sinai Med Ctr, Dept Biomed Sci, Los Angeles, CA 90048 USA
[2] Cedars Sinai Med Ctr, Dept Pathol & Lab Med, Los Angeles, CA 90048 USA
基金
美国国家卫生研究院;
关键词
hematopoiesis; myelopoiesis; angiotensin converting enzyme (ACE); angiotensin II; AT1; receptor; renin-angiotensin system (RAS); substance P; Ac-SDKP; angiotensin; 1-7; BONE-MARROW STROMA; SUBSTANCE-P; IN-VITRO; MAS PROTOONCOGENE; PROGENITOR CELLS; THYMOSIN BETA-4; STEM-CELLS; EXPRESSION; SYSTEM; RECEPTOR;
D O I
10.4161/cc.10.9.15444
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
The 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.
引用
收藏
页码:1363 / 1369
页数:7
相关论文
共 77 条
[1]   Acute angiotensin-converting enzyme inhibition increases the plasma level of the natural stem cell regulator N-acetyl-seryl-aspartyl-lysyl-proline [J].
Azizi, M ;
Rousseau, A ;
Ezan, E ;
Guyene, TT ;
Michelet, S ;
Grognet, JM ;
Lenfant, M ;
Corvol, P ;
Menard, J .
JOURNAL OF CLINICAL INVESTIGATION, 1996, 97 (03) :839-844
[2]  
BERNSTEIN KE, 2010, CURR OPIN PHARM
[3]  
BONNET D, 1992, EXP HEMATOL, V20, P1165
[4]  
BONNET D, 1993, BLOOD, V82, P3307
[5]  
CALVO CF, 1992, J IMMUNOL, V148, P3498
[6]   Inhibition of angiotensin I-converting enzyme induces radioprotection by preserving murine hematopoietic short-term reconstituting cells [J].
Charrier, S ;
Michaud, A ;
Badaoui, S ;
Giroux, S ;
Ezan, E ;
Sainteny, F ;
Corvol, P ;
Vainchenker, W .
BLOOD, 2004, 104 (04) :978-985
[7]   Captopril inhibits in vitro and in vivo the proliferation of primitive haematopoietic cells induced into cell cycle by cytotoxic drug administration or irradiation but has no effect on myeloid leukaemia cell proliferation [J].
Chisi, JE ;
Briscoe, CV ;
Ezan, E ;
Genet, R ;
Riches, AC ;
Wdzieczak-Bakala, J .
BRITISH JOURNAL OF HAEMATOLOGY, 2000, 109 (03) :563-570
[8]  
CORVOL P, 1995, METHOD ENZYMOL, V248, P283
[9]  
COUTTON C, 1994, EXP HEMATOL, V22, P1076
[10]   DESIGN OF POTENT COMPETITIVE INHIBITORS OF ANGIOTENSIN-CONVERTING ENZYME - CARBOXYALKANOYL AND MERCAPTOALKANOYL AMINO-ACIDS [J].
CUSHMAN, DW ;
CHEUNG, HS ;
SABO, EF ;
ONDETTI, MA .
BIOCHEMISTRY, 1977, 16 (25) :5484-5491