Loss of β1-integrin-deficient cells during the development of endoderm-derived epithelia

Berger, T. M.; Hirsch, E.; Djonov, V.; Schittny, J. C. (2003). Loss of β1-integrin-deficient cells during the development of endoderm-derived epithelia. Anatomy and embryology, 207(4-5), pp. 283-288. Springer-Verlag 10.1007/s00429-003-0354-1

[img] Text
art%3A10.1007%2Fs00429-003-0354-1.pdf - Published Version
Restricted to registered users only
Available under License Publisher holds Copyright.

Download (350kB) | Request a copy
[img]
Preview
Text
429_2003_Article_354.pdf - Other
Available under License Publisher holds Copyright.

Download (350kB) | Preview

Beta1-integrins (beta1) represent cell surface receptors which mediate cell-matrix and cell-cell interactions. Fässler and Meyer described chimeric mice containing transgenic cells that express the LacZ gene instead of the beta1 gene. They observed beta1-negative cells in all germ layers at embryonic day E 8.5. Later in development, using a glucose phosphate isomerase assay of homogenized tissue samples, high levels of transgenic cells were found in skeletal muscle and gut, low levels in lung, heart, and kidney and none in the liver and spleen (Fässler and Meyer 1995). In order to study which cell types require beta1 during development of the primitive gut including its derivatives, chimeric fetuses containing 15 to 25% transgenic cells were obtained at days E 14.5 and E 15.5. They were LacZ (beta-galactosidase) stained "en bloc" and cross-sectioned head to tail. In esophagus, trachea, lung, stomach, hindgut, and the future urinary bladder, we observed various mesoderm-derived beta1-negative cells (e.g. fibroblasts, chondrocytes, endothelial cells, and smooth muscle cells) but no beta1-negative epithelial cells. Since the epithelia of lung, esophagus, trachea, stomach, hindgut, and urinary bladder are derived from the endodermal gut tube, we hypothesize that beta1 is essential for the development and/or survival of the epithelia of the fore- and hindgut and its derivatives.

Item Type:

Journal Article (Original Article)

Division/Institute:

04 Faculty of Medicine > Pre-clinic Human Medicine > Institute of Anatomy
04 Faculty of Medicine > Pre-clinic Human Medicine > Institute of Anatomy > Functional Anatomy

UniBE Contributor:

Berger, Thomas M.; Djonov, Valentin and Schittny, Johannes

Subjects:

600 Technology > 610 Medicine & health

ISSN:

0340-2061

Publisher:

Springer-Verlag

Language:

English

Submitter:

Johannes Schittny

Date Deposited:

01 Sep 2014 12:03

Last Modified:

26 Nov 2019 06:53

Publisher DOI:

10.1007/s00429-003-0354-1

PubMed ID:

14648219

Uncontrolled Keywords:

Fetal development, Cell migration, Cell differentiation, Transgenic mice, Lung

BORIS DOI:

10.7892/boris.50150

URI:

https://boris.unibe.ch/id/eprint/50150

Actions (login required)

Edit item Edit item
Provide Feedback