Activin Subunit and Receptor Expression in Normal and Cleft Human Fetal Palate Tissues

  title={Activin Subunit and Receptor Expression in Normal and Cleft Human Fetal Palate Tissues},
  author={Geralyn M Lambert-Messerlian and Elizabeth E. Eklund and Halit Pinar and Umadevi Tantravahi and Alan L. Schneyer},
  journal={Pediatric and Developmental Pathology},
  pages={436 - 445}
Craniofacial malformations, such as cleft palate, present serious complications in the newborn and are often of unknown etiology. Activin BA subunit deletion leads to cleft palate in mice, but the expression of this protein in the human palate has not been explored. Our goal was to determine the spatial and temporal expression of inhibin/activin subunits; the binding protein, follistatin; and activin receptors in the human fetal palate. Residual human fetal palate tissues, with or without cleft… Expand
Biological Mechanisms in Palatogenesis and Cleft Palate
Normalization of the biological mechanisms regulating palatogenesis in susceptible fetuses is expected to contribute to cleft prevention and the role of specific genes in cleft formation is discussed. Expand
MORN5 Expression during Craniofacial Development and Its Interaction with the BMP and TGFβ Pathways
The restricted expression of MORN5 in the lip fusion zone shown here supports the human genetic data in which Morn5 variants were associated with increased risk of non-syndromic cleft lip with or without cleft palate and is both regulated by and required for BMP signaling. Expand
Genomic analyses in African populations identify novel risk loci for cleft palate
Novel loci for CPO at or near genome-wide significance on chromosomes 2 and 19 are identified and in situ hybridization of Sult2a1 in mice showed expression of SULT2A1 in mesenchymal cells in palate, palatal rugae and palatal epithelium in the fused palate. Expand


Inhibins and activins in human fetal abnormalities
Investigation of the potential role of activin in human craniofacial development by examining the spatial and temporal expression of inhibin/activin subunits, follistatin and the activin receptors in the fetal palate finds expression of theactivin A subunit and its receptors are consistent with a developmental role. Expand
Multiple defects and perinatal death in mice deficient in follistatin
Follistatin-deficient mice are retarded in then* growth, have decreased mass of the diaphragm and intercostal muscles, shiny taut skin, skeletal defects of the hard palate and the thirteenth pair of ribs, their whisker and tooth development is abnormal, they fail to breathe, and die within hours of birth, indicating that follistatin may modulate the actions of several members of the transforming growth factor-β family. Expand
Expression of messenger ribonucleic acids encoding the inhibin/activin system during mid- and late-gestation rat embryogenesis.
The data suggest that inhibin and activin regulate aspects of the fetal reproductive system, whereas activin A may regulate the growth and differentiation of many embryonic tissues and follistatin is in a position to modulate the effects of activin during postimplantation rat embryogenesis. Expand
The tissue distribution of activin beta A- and beta B-subunit and follistatin messenger ribonucleic acids suggests multiple sites of action for the activin-follistatin system during human development.
The results suggest that the activin-follistatin system regulates the development of several organ systems in the mid-gestational human fetus. Expand
Testicular expression of inhibin and activin subunits and follistatin in the rat and human fetus and neonate and during postnatal development in the rat.
In the rat testis, the majority of inhibin alpha-sub unit and inhibin/activin betaB-subunit is immunolocalized to the fetal-type Leydig cells during fetal/neonatal life but, following birth, immunoexpression in the Sertoli cells of both subunits increases markedly while follistatin is immunodetectable only postnatally. Expand
Expression of inhibin/activin subunit messenger ribonucleic acids during rat embryogenesis.
In situ hybridization techniques were utilized to examine the localization of the mRNAs encoding the inhibin/activin subunits in rat embryos, suggesting that inhibin and activin may be produced in the gonads and possibly play a hormonal role in the embryonic rat during the last trimester of pregnancy and aspects of the embryonic development of the heart, skin, hair and whiskers. Expand
Expression of activin subunits, activin receptors and follistatin in postimplantation mouse embryos suggests specific developmental functions for different activins.
The present data suggest that follistatin, but not one of the known activin forms (A,B,AB) is involved in early postimplantation development. Expand
Different phenotypes for mice deficient in either activins or activin receptor type II
A role of ActRcII in activin signalling in pituitary gonadotrophs is confirmed and the striking lack of overlap between phenotypes of ActCcII- deficient and activin-deficient mice suggests that the ligands that signal through ActRCII during embryonic development are not activins. Expand
Immunohistochemical detection of activin A in osteoclasts.
It is suggested that osteoclast produce activin in the bone tissues and that activin may play some roles by autocrine and/or paracrine manner in bone metabolisms. Expand
Immunohistochemical localization of activin A and follistatin in human tissues.
Findings indicated that activin A and follistatin are widely distributed in human tissues, suggesting thatactivin plays important roles as a common regulator in various tissues under the control of co-existing follistin. Expand