A major role of TGF-β1 in the homing capacities of murine hematopoietic stem cell/progenitors

被引：32

作者：

Capron, Claude ^{[1
,2
,3
]}

Lacout, Catherine ^{[1
]}

Lecluse, Yann ^{[1
,4
]}

Jalbert, Valerie ^{[3
]}

Chagraoui, Hedia ^{[1
]}

Charrier, Sabine ^{[1
,5
]}

Galy, Anne ^{[1
,5
]}

Bennaceur-Griscelli, Annelise ^{[6
]}

Cramer-Borde, Elisabeth ^{[2
,3
]}

Vainchenker, William ^{[1
,5
]}

机构：

[1] Univ Paris 11, INSERM, U1009, Inst Gustave Roussy,Fac Med Paris 11, F-94805 Villejuif, France

[2] Hop Cochin, INSERM, U1016, Dept Hematol, F-75674 Paris, France

[3] Fac Med Versailles Paris Ouest, Garches, France

[4] Inst Gustave Roussy, IFR 54, Villejuif, France

[5] INSERM, U951, Evry, France

[6] Hop Paul Brousse, Inserm 935, Fac Med Paris 11, Villejuif, France

来源：

BLOOD | 2010年 / 116卷 / 08期

关键词：

GROWTH-FACTOR-BETA; BONE MORPHOGENETIC PROTEIN-4; REGULATORY T-CELLS; TRANSFORMING GROWTH-FACTOR-BETA-1; TGF-BETA; SELF-RENEWAL; MICE CAUSES; RECEPTOR; PROGENITOR; GENE;

D O I：

10.1182/blood-2009-05-221093

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

Transforming growth factor-beta 1 (TGF-beta 1) is a pleiotropic cytokine with major in vitro effects on hematopoietic stem cells (HSCs) and lymphocyte development. Little is known about hematopoiesis from mice with constitutive TGF-beta 1 inactivation largely because of important embryonic lethality and development of a lethal inflammatory disorder in TGF-beta 1(-/-) pups, making these studies difficult. Here, we show that no sign of the inflammatory disorder was detectable in 8- to 10-day-old TGF-beta 1(-/-) neonates as judged by both the number of T-activated and T-regulator cells in secondary lymphoid organs and the level of inflammatory cytokines in sera. After T-cell depletion, the inflammatory disease was not transplantable in recipient mice. Bone marrow cells from 8- to 10-day-old TGF-beta 1(-/-) neonates showed strikingly impaired short-and long-term reconstitutive activity associated with a parallel decreased in vivo homing capacity of lineage negative (Lin(-)) cells. In addition an in vitro-reduced survival of immature progenitors (Lin(-) Kit(+) Sca(+)) was observed. Similar defects were found in liver cells from TGF-beta 1(-/-) embryos on day 14 after vaginal plug. These data indicate that TGF-beta 1 is a critical regulator for in vivo homeostasis of the HSCs, especially for their homing potential. (Blood. 2010; 116(8): 1244-1253)

引用

页码：1244 / 1253

页数：10

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