激素诱导干细胞的增殖和分化

qgjin

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- X" z/ @  |' u  J$ n9 o' |The pregnancy hormones human chorionic gonadotropin and progesterone induce human embryonic stem cell proliferation and differentiation into neuroectodermal rosettes。
  s: A% o% N( O! NMiguel J Gallego1†, Prashob Porayette1†, Maria M Kaltcheva1, Richard L Bowen2, Sivan Vadakkadath Meethal1,5,
/ q7 r0 u+ b, ~% j) }5 eCraig S Atwood1,3,4*
( x% v& z0 T$ _' h5 e2 Y& o# N( I) \3 d+ o/ B1 E1 L$ j( t
Abstract
+ F5 G! E1 U7 U7 {& t) W- AIntroduction: The physiological signals that direct the division and differentiation of the zygote to form a
! h) K+ `; w/ Qblastocyst, and subsequent embryonic stem cell division and differentiation during early embryogenesis, are
# h. }! ?9 M  q5 Munknown. Although a number of growth factors, including the pregnancy-associated hormone human chorionic
/ y; A8 h; p+ Ggonadotropin (hCG) are secreted by trophoblasts that lie adjacent to the embryoblast in the blastocyst, it is not- V. O2 O1 I3 [' p, F/ u' H
known whether these growth factors directly signal human embryonic stem cells (hESCs).
2 {0 a% F/ W! VMethods: Here we used hESCs as a model of inner cell mass differentiation to examine the hormonal requirements
/ n$ ~# c" z! T& i3 ]# Cfor the formation of embryoid bodies (EB’s; akin to blastulation) and neuroectodermal rosettes (akin to neurulation).' e8 c) K5 R1 z/ \# [9 i$ E9 J! y
Results: We found that hCG promotes the division of hESCs and their differentiation into EB’s and" f! Z$ r5 D- W4 G' y
neuroectodermal rosettes. Inhibition of luteinizing hormone/chorionic gonadotropin receptor (LHCGR) signaling
" ^$ Q& G. g7 b. x2 csuppresses hESC proliferation, an effect that is reversed by treatment with hCG. hCG treatment rapidly upregulates$ L1 ^" ^, x' n) J
steroidogenic acute regulatory protein (StAR)-mediated cholesterol transport and the synthesis of progesterone: H7 W9 f2 n4 |$ `
(P4). hESCs express P4 receptor A, and treatment of hESC colonies with P4 induces neurulation, as demonstrated by
% K6 l  \; q! x9 g, Zthe expression of nestin and the formation of columnar neuroectodermal cells that organize into neural tubelike# |; F0 R! ^' i
rosettes. Suppression of P4 signaling by withdrawing P4 or treating with the P4-receptor antagonist RU-486 inhibits4 F0 h( T. D& o; Q- B  B6 u4 P+ ?
the differentiation of hESC colonies into EB’s and rosettes.4 ^/ ]; @% E: t
Conclusions: Our findings indicate that hCG signaling via LHCGR on hESC promotes proliferation and
* i0 B1 E2 d6 z- D# j  I9 `  ldifferentiation during blastulation and neurulation. These findings suggest that trophoblastic hCG secretion and
; r" c5 z5 G/ y1 u( vsignaling to the adjacent embryoblast could be the commencement of trophic support by placental tissues in the2 Y0 V9 p; z* w$ ^. J! s- R" i3 `
growth and development of the human embryo.

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