Human ?-fetoprotein purified from amniotic fluid enhances growth factor-mediated cell proliferation in vitro

1991 ◽  
Vol 30 (2) ◽  
pp. 112-118 ◽  
Author(s):  
Brooks A. Keel ◽  
Kevan B. Eddy ◽  
Sechin Cho ◽  
Jeffrey V. May
Keyword(s):  
Cell Proliferation ◽  
Growth Factor ◽  
Amniotic Fluid ◽  
Proliferation In Vitro

scholarly journals Immunocytochemical analysis of chromaffin cell proliferation in vitro.

1992 ◽  
Vol 40 (7) ◽  
pp. 1043-1045 ◽  
Author(s):  
A S Tischler ◽  
L A Ruzicka ◽  
J C Riseberg
Keyword(s):  
Cell Proliferation ◽  
Growth Factor ◽  
Chromaffin Cells ◽  
Chromaffin Cell ◽  
Adrenal Glands ◽  
Neonatal Rat ◽  
Brdu Incorporation ◽  
Incorporated Brdu ◽  
Proliferation In Vitro

The bromodeoxyuridine (BrdU) incorporation technique for immunocytochemical labeling of S-phase nuclei was optimized for the study of chromaffin cell proliferation. Sequential fixation in ethanol followed by paraformaldehyde, and the use of DNAse to render incorporated BrdU accessible to antibody, permitted permanent double staining for BrdU and tyrosine hydroxylase. The efficacy of the technique was demonstrated in microcultures of dissociated neonatal rat adrenal glands, in which chromaffin cells exhibited proliferative responses to nerve growth factor and fibroblast growth factor similar to those previously demonstrated by autoradiography. Growth factor responsiveness was observed in both serum-containing and serum-free medium.

Inducing Proliferation of Human Amniotic Epithelial (HAE) Cells for Cell Therapy

2000 ◽  
Vol 9 (5) ◽  
pp. 701-704 ◽  
Author(s):  
Satoshi Terada ◽  
Keiko Matsuura ◽  
Shin Enosawa ◽  
Masao Miki ◽  
Akinori Hoshika ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Growth Factor ◽  
Amniotic Fluid ◽  
Cell Population ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β ◽  
Inborn Errors ◽  
Maternal Immune System ◽  
Mother And Child

Probably because amnion is derived from the fetus and is exposed to the maternal immune system, human amniotic epithelial (HAE) cells do not express the HLA-A, -B, -C, or -DR antigens on their surfaces, suggesting that HAE cells do not induce rejection (immune reaction) after allotransplantation. And the amnion, like the placenta, is useless to the mother and child after birth. Therefore, HAE cells or tissues were expected to be suitable for allotransplantation. Because HAE cells produce large amounts of enzymes, amnion transplantation has been carried out in order to correct inborn errors of metabolism by supplementing lysosomal enzyme deficiencies. However, several problems remain before amnion allotransplantation can be accepted as effective. The HAE cell population is limited, because the maximum number of HAE cells obtainable from one donor is about 2 × 108 cells, and HAE cells proliferate poorly in in vitro culture. In this study, we aimed at increasing the HAE cell population in vitro. First, we investigated the effect of several cytokines on HAE cell proliferation and found that hepatocyte growth factor (HGF), epidermal growth factor (EGF), and transforming growth factor-β stimulated it, whereas IL-6 and LIF inhibited it. Second, we investigated the effects of amniotic fluid on HAE cell proliferation and observed that IL-6 in amniotic fluid inhibits it. Then, to inhibit the dying of cells, we attempted to inhibit apoptosis (one mode of cell death). Treatment with caspase III inhibitor increased the cell viability of HAE cells by 20%.

scholarly journals Epidermal growth factor receptor activity is necessary for mouse basal cell proliferation

2014 ◽  
Vol 307 (10) ◽  
pp. L800-L810 ◽  
Author(s):  
Heather M. Brechbuhl ◽  
Bilan Li ◽  
Russell W. Smith ◽  
Susan D. Reynolds
Keyword(s):  
Cell Proliferation ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Basal Cell ◽  
Basal Cells ◽  
Epithelial Repair ◽  
Epidermal Growth ◽  
Proliferation In Vitro

ERB family receptors (EGFR, ERB-B2, ERB-B3, and ERB-B4) regulate epithelial cell function in many tissue types. In the human airway epithelium, changes in ERB receptor expression are associated with epithelial repair defects. However, the specific role(s) played by ERB receptors in repair have not been determined. We aimed to determine whether ERB receptors regulate proliferation of the tracheobronchial progenitor, the basal cell. Receptor tyrosine kinase arrays were used to evaluate ERB activity in normal and naphthalene (NA)-injured mouse trachea and in air-liquid interface cultures. Roles for epidermal growth factor (EGF), EGFR, and ERB-B2 in basal cell proliferation were evaluated in vitro. NA injury and transgenic expression of an EGFR-dominant negative (DN) receptor were used to evaluate roles for EGFR signaling in vivo. EGFR and ERB-B2 were active in normal and NA-injured trachea and were the only active ERB receptors detected in proliferating basal cells in vitro. EGF was necessary for basal cell proliferation in vitro. The EGFR inhibitor, AG1478, decreased proliferation by 99, and the Erb-B2 inhibitor, AG825, decreased proliferation by ∼66%. In vivo, EGFR-DN expression in basal cells significantly decreased basal cell proliferation after NA injury. EGF and EGFR are necessary for basal cell proliferation. The EGFR/EGFR homo- and the EGFR/ERB-B2 heterodimer account for ∼34 and 66%, respectively, of basal cell proliferation in vitro. Active EGFR is necessary for basal cell proliferation after NA injury. We conclude that EGFR activation is necessary for mouse basal cell proliferation and normal epithelial repair.

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