Fahlbusch, F. B., Hartner, A., Menendez-Castro, C., Noegel, S. C., Marek, I., Beckmann, M. W., Schleussner, E., Ruebner, M., Huebner, H., Doerr, H. -G., Schild, R. L., Doetsch, J. and Rascher, W. (2015). The placental mTOR-pathway: correlation with early growth trajectories following intrauterine growth restriction? J. Dev. Orig. Health Dis., 6 (4). S. 317 - 327. CAMBRIDGE: CAMBRIDGE UNIV PRESS. ISSN 2040-1752

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Abstract

Idiopathic intrauterine growth restriction (IUGR) is a result of impaired placental nutrient supply. Newborns with IUGR exhibiting postnatal catch-up growth are of higher risk for cardiovascular and metabolic co-morbidities in adult life. Mammalian target of rapamycin (mTOR) was recently shown to function as a placental nutrient sensor. Thus, we determined possible correlations of members of the placental mTOR signaling cascade with auxologic parameters of postnatal growth. The protein expression and activity of mTOR-pathway signaling components, Akt, AMP-activated protein kinase alpha, mTOR, p70S6kinase1 and insulin receptor substrate-1 were analysed via western blotting in IUGR v. matched appropriate-for-gestational age (AGA) placentas. Moreover, mTOR was immunohistochemically stained in placental sections. Data from western blot analyses were correlated with retrospective auxological follow-up data at 1 year of age. We found significant catch-up growth in the 1st year of life in the IUGR group. MTOR and its activated form are immunohistochemically detected in multiple placental compartments. We identified correlations of placental mTOR-pathway signaling components to auxological data at birth and at 1 year of life in IUGR. Analysis of the protein expression and phosphorylation level of mTOR-pathway components in IUGR and AGA placentas postpartum, however, did not reveal pathognomonic changes. Our findings suggest that the level of activated mTOR correlates with early catch-up growth following IUGR. However, the complexity of signals converging at the mTOR nexus and its cellular distribution pattern seem to limit its potential as biomarker in this setting.

Item Type: Journal Article
Creators:
CreatorsEmailORCIDORCID Put Code
Fahlbusch, F. B.UNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Hartner, A.UNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Menendez-Castro, C.UNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Noegel, S. C.UNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Marek, I.UNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Beckmann, M. W.UNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Schleussner, E.UNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Ruebner, M.UNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Huebner, H.UNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Doerr, H. -G.UNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Schild, R. L.UNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Doetsch, J.UNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Rascher, W.UNSPECIFIEDUNSPECIFIEDUNSPECIFIED
URN: urn:nbn:de:hbz:38-398454
DOI: 10.1017/S2040174415001154
Journal or Publication Title: J. Dev. Orig. Health Dis.
Volume: 6
Number: 4
Page Range: S. 317 - 327
Date: 2015
Publisher: CAMBRIDGE UNIV PRESS
Place of Publication: CAMBRIDGE
ISSN: 2040-1752
Language: English
Faculty: Unspecified
Divisions: Unspecified
Subjects: no entry
Uncontrolled Keywords:
KeywordsLanguage
CATCH-UP GROWTH; ACTIVATED PROTEIN-KINASE; GESTATIONAL-AGE INFANTS; CORONARY-HEART-DISEASE; FETAL-GROWTH; INSULIN SENSITIVITY; MAMMALIAN TARGET; SKELETAL-MUSCLE; DOWN-REGULATION; BIRTH-WEIGHTMultiple languages
Public, Environmental & Occupational HealthMultiple languages
URI: http://kups.ub.uni-koeln.de/id/eprint/39845

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