Glucocorticoids have pleiotropic effects on small intestinal crypt cells

Glucocorticoids have long been known to accelerate maturation of the intestinal tract, but the molecular mechanisms that account for their physiological function in the epithelium remain poorly characterized. Using rat intestinal epithelial cell lines (IEC-6, IEC-17, and IEC-18) as models, we have characterized glucocorticoid receptors in crypt cells and documented striking morphological, ultrastructural, and functional alterations induced by these hormones in intestinal cells. They include arrest of growth, formation of tight junctions, appearance of long, slender microvilli, reorganization of the endoplasmic reticulum and trans-Golgi network, and downregulation of the cell cycle regulatory proteins cyclin-dependent kinase 6 and p27(Kip1). These effects are consistent with the activation or modulation of multiple genes important in the physiological function of absorptive villous cells but are probably not directly involved in the induction of cell differentiation.

Medienart:

E-Artikel

Erscheinungsjahr:

1999

Erschienen:

1999

Enthalten in:

Zur Gesamtaufnahme - volume:277

Enthalten in:

The American journal of physiology - 277(1999), 5 vom: 16. Nov., Seite G1027-40

Sprache:

Englisch

Beteiligte Personen:

Quaroni, A [VerfasserIn]
Tian, J Q [VerfasserIn]
Göke, M [VerfasserIn]
Podolsky, D K [VerfasserIn]

Links:

Volltext

Themen:

10028-17-8
147604-94-2
4G7DS2Q64Y
7S5I7G3JQL
Alkaline Phosphatase
Alpha-Glucosidases
Androgens
Bacterial Proteins
Cdkn1a protein, rat
Cdkn1b protein, rat
Cell Cycle Proteins
Cyclin-Dependent Kinase Inhibitor p21
Cyclin-Dependent Kinase Inhibitor p27
Cyclins
Dexamethasone
EC 3.1.3.1
EC 3.2.1.-
EC 3.2.1.20
Glucocorticoids
Hydrocortisone
Journal Article
Microtubule-Associated Proteins
Progesterone
Receptors, Steroid
Research Support, U.S. Gov't, P.H.S.
Sucrase-Isomaltase Complex
Sucrase-isomaltase-maltase
Tritium
Tumor Suppressor Proteins
WI4X0X7BPJ

Anmerkungen:

Date Completed 14.12.1999

Date Revised 25.09.2018

published: Print

Citation Status MEDLINE

doi:

10.1152/ajpgi.1999.277.5.G1027

funding:

Förderinstitution / Projekttitel:

PPN (Katalog-ID):

NLM104941189