An autocrine function for transforming growth factor (TGF)-beta3 in the transformation of atrioventricular canal endocardium into mesenchyme during chick heart development.
An autocrine function for transforming growth factor (TGF)-beta3 in the transformation of atrioventricular canal endocardium into mesenchyme during chick heart development.
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转化生长因子（TGF）-β3在鸡心脏发育过程中房室管心内膜向间充质转化中的自分泌功能。
DOI：
10.1006/dbio.1997.8807
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发表时间：
1998
期刊：
影响因子：
--
通讯作者：
Krug,EL
中科院分区：
文献类型：
--
作者：
Nakajima,Y;Yamagishi,T;Nakamura,H;Markwald,RR;Krug,EL
房室管心内膜向侵袭性间质转化是心隔和瓣膜形成的重要前提。Pottset等人之前的研究。国家的。学会科学。USA88, 1510-1520, 1991)表明，用tgf - β3反义寡脱氧核苷酸处理房室管心内膜和心肌共培养可阻断间质形成。基于这一观察结果，我们试图：(i)在转化生物测定中确定tgf - β3反义寡核苷酸的靶组织，（ii）更清楚地定义tgf - β3在房室管间质形成中的作用机制。原位杂交和免疫组化显示，在间质形成之前，房室管心肌或心内膜中很少或没有tgf - β3 mRNA或蛋白（第14期；多聚甲醛固定）。然而，到18期转化房室管心内膜细胞和间质以及心肌中tgf - β3 mRNA和蛋白均呈阳性。在培养生物测定中，经反义硫代寡脱氧核苷酸预处理的房室管心内膜单层tgf - β3在心肌条件培养基中不会转化为侵袭性间质：随后添加外源性tgf - β3蛋白可缓解这种抑制。未经预处理的对照培养物或接受错义寡核苷酸的对照培养物在心肌条件培养基中产生相似数量的侵袭性间质。在没有心肌条件培养基的情况下，将TGFβ3蛋白直接添加到房室管心内膜中，导致细胞关联丧失，并刺激细胞肥大，但在培养24小时后，不产生侵袭性间质形成或改变心内膜增殖。tgf - β2蛋白单独或与tgf - β3联合也获得了类似的结果。本研究结果表明：(1)房室管心内膜响应于非TGFβ3的心肌源性信号表达TGFβ3，(2)房室管心内膜TGFβ3以自分泌方式发挥作用，引发缓冲组织形成所需的选择特征，(3)TGFβ3单独或与TGFβ2联合不足以在培养中将房室管心内膜转化为侵袭性间质。
Transformation of atrioventricular canal endocardium into invasive mesenchyme is a critical antecedent of cardiac septation and valvulogenesis. Previous studies by Pottset al.(Proc. Natl. Acad. Sci. USA88, 1510–1520, 1991) showed that treatment of atrioventricular canal endocardial and myocardial cocultures with TGFβ3 antisense oligodeoxynucleotides blocked mesenchyme formation. Based on this observation, we sought to: (i) identify the target tissue of TGFβ3 antisense oligos in this transformation bioassay, and (ii) more clearly define the mechanism of TGFβ3 function in atrioventricular canal mesenchyme formation.In situhybridization and immunohistochemistry showed little or no TGFβ3 mRNA or protein in the atrioventricular canal myocardium or endocardium prior to mesenchyme formation (stage 14; paraformaldehyde fixation). However, by stage 18 transforming atrioventricular canal endocardial cells and mesenchyme as well as myocardium were positive for both TGFβ3 mRNA and protein. In culture bioassays, atrioventricular canal endocardial monolayers pretreated with antisense phosphorothioate oligodeoxynucleotides to TGFβ3 did not transform into invasive mesenchyme in response to cardiocyte conditioned medium: the subsequent addition of exogenous TGFβ3 protein relieved this inhibition. Control cultures without pretreatment or those receiving missense oligos generated similar numbers of invasive mesenchyme in response to cardiocyte conditioned medium. Direct addition of TGFβ3 protein to atrioventricular canal endocardial monolayers in the absence of cardiocyte conditioned medium resulted in loss of cell:cell associations and stimulated cellular hypertrophy, but did not engender invasive mesenchyme formation or alter endocardial proliferation after 24 h of culture. Similar results were obtained with TGFβ2 protein, either alone or in combination with TGFβ3. The results of this study indicate that: (i) atrioventricular canal endocardium expresses TGFβ3 in response to a myocardially derived signal other than TGFβ3, (ii) atrioventricular canal endocardial TGFβ3 functions in an autocrine fashion to elicit selected characteristics necessary for cushion tissue formation, and (iii) TGFβ3 alone or in combination with TGFβ2 is insufficient to transform atrioventricular canal endocardium into invasive mesenchyme in culture.
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影响因子：
20.1
作者：
A. Wessels;Marry W. M. Markman;J. Vermeulen;R. Anderson;A. Moorman;W. Lamers
通讯作者：
W. Lamers
DOI：
--
发表时间：
1986-03
期刊：
The Journal of biological chemistry
影响因子：
--
作者：
R. Ignotz;J. Massagué
通讯作者：
R. Ignotz;J. Massagué
影响因子：
2.7
作者：
BERNANKE, DH;MARKWALD, RR
通讯作者：
MARKWALD, RR
影响因子：
4.6
作者：
M. Dickson;H. Slager;E. Duffie;C. Mummery;R. Akhurst
通讯作者：
M. Dickson;H. Slager;E. Duffie;C. Mummery;R. Akhurst
心脏内皮向垫间充质的转化依赖于 ES/130：早期鸡胚的时间、空间和功能研究。
DOI：
--
发表时间：
1995
期刊：
Cellular & molecular biology research.
影响因子：
--
作者：
Krug,EL;Rezaee,M;Isokawa,K;Turner,DK;Litke,LL;Wunsch,AM;Bain,JL;Riley,DA;Capehart,AA;Markwald,RR
通讯作者：
Markwald,RR