Modulation of diabetes-induced palate defects by maternal immune stimulation.
Modulation of diabetes-induced palate defects by maternal immune stimulation.
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DOI：
10.1002/ar.20836
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发表时间：
2009-02
影响因子：
2
通讯作者：
Holladay, Steven D.
中科院分区：
文献类型：
--
作者：
Hrubec, Terry C.;Toops, Kimberly A.;Holladay, Steven D.
母体糖尿病可以在实验室动物和人类中诱发许多发育异常，包括面部和腭部的畸形。糖尿病妇女的新生儿出生缺陷的发生率比非糖尿病妇女高约3至5倍。在小鼠中，母体免疫系统的非特异性激活可以减少由各种病因（包括高血糖症）引起的胎儿异常。本研究旨在确定非特异性母体免疫刺激是否可以减少糖尿病引起的腭裂和口面裂。在诱导高血糖之前，用弗氏完全佐剂（FCA）、粒细胞-巨噬细胞集落刺激因子（GM-CSF）或干扰素-γ（IFNγ）免疫刺激雌性ICR小鼠。在繁殖前，使用链脲霉素诱导雌性动物的高血糖症（26-35 mmol血糖）。在妊娠第17天采集每个给药组12-18窝胎仔。测量腭的宽度和长度，并确定口面裂的发生率。母亲高血糖使腭的长度和宽度均下降。GM-CSF或FCA的母体免疫刺激限制了高血糖引起的腭缩短程度。三种免疫刺激剂中的每一种都减弱了腭的显著狭窄。治疗组之间的口面裂发生率无显著差异。腭发育是一个由细胞信号驱动的复杂过程，这些信号调节细胞的生长和凋亡。母体高血糖引起的细胞信号失调可导致胎儿畸形。母体免疫刺激可以防止这些信号通路的失调，从而减少胎儿畸形和正常化腭生长。
Maternal diabetes can induce a number of developmental abnormalities in both laboratory animals and humans, including deformities of the face and palate. The incidence of birth defects in newborns of diabetic women is approximately 3 to 5 times higher than among non-diabetics. In mice, non specific activation of the maternal immune system can reduce fetal abnormalities caused by various etiologies including hyperglycemia. This study was conducted to determine whether non-specific maternal immune stimulation could reduce diabetes induced palate defects and orofacial clefts. Female ICR mice were immune stimulated prior to induction of hyperglycemia with Freund’s complete adjuvant (FCA), granulocyte-macrophage colony-stimulating factor (GM-CSF) or interferon-γ (IFNγ). Streptozocin was used to induce hyperglycemia (26–35 mmol blood glucose) in females prior to breeding. Fetuses from 12–18 litters per treatment group were collected on day 17 of gestation. Palate width and length were measured and the incidence of orofacial clefts was determined. Palate length and width were both decreased by maternal hyperglycemia. Maternal immune stimulation with GM-CSF or FCA limited the degree of palate shortening from the hyperglycemia. Each of the three immune stimulants attenuated significant narrowing of the palate. Rates of orofacial clefts were not significantly different between treatment groups. Palatogenesis is a complex process driven by cellular signals which regulate cell growth and apoptosis. Dysregulation of cellular signals by maternal hyperglycemia can result in fetal malformations. Maternal immune stimulation may prevent dysregulation of these signaling pathways thus reducing fetal malformations and normalizing palate growth.
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影响因子：
1.3
作者：
Okano, Junko;Suzuki, Shigehiko;Shiota, Kohei
通讯作者：
Shiota, Kohei
DOI：
10.1002/bdrb.20062
发表时间：
2006-02-01
影响因子：
--
作者：
Hrubec, TC;Prater, MR;Holladay, SD
通讯作者：
Holladay, SD
影响因子：
7.6
作者：
BLAUSTEIN, FM;FELLER, R;ROSENZWEIG, S
通讯作者：
ROSENZWEIG, S
影响因子：
5.6
作者：
Punareewattana, K;Sharova, LV;Holladay, SD
通讯作者：
Holladay, SD
影响因子：
1.3
作者：
Sato, Toshio J.
通讯作者：
Sato, Toshio J.