Browsing by keyword "Sarcoma, Experimental"
Now showing items 1-2 of 2
-
Reticulum cell sarcomas of SJL mice have rearranged immunoglobulin heavy and light chain genesThe immunoglobulin (Ig) heavy (H) and light (L) chain gene rearrangements of the high incidence SJL lymphomas (reticulum cell sarcoma, RCS) have been analyzed. Both primary and transplanted RCS show rearrangements of H and kappa L chains, demonstrating that these tumors are of B cell origin. These data are consistent with previous results indicating that these tumors are a mouse model for follicular lymphoma. A long-term transplanted line and the in vitro line derived from it, cRCS-X, have a single rearranged JH-C gamma 2a fragment and one rearranged C alpha gene fragment which does not hybridize with a probe for the JH gene segments. These cell lines also have two rearranged J kappa-C kappa fragments. Primary tumors and early passages are more heterogeneous with respect to Ig gene rearrangements, possibly because more than one B cell clone is present. Although no synthesis of IgG2a, or of any Ig, could be detected by the in vitro cRCS-X cells, these cells contain abundant poly(A)+ RNA that hybridize with gamma 2a and kappa probes as well as lesser amounts of alpha and epsilon RNA. None of these H chain RNA hybridized with probes for the JH gene segments. The epsilon and alpha RNA are the same size as transcripts of germ-line CH genes which have been identified in other systems. However, the gamma 2a RNA are smaller than previously described germ-line C gamma 2a RNA and appear to be transcribed from aberrantly rearranged JH-C gamma 2a genes.
-
Thyroid hormone regulates the extracellular organization of laminin on astrocytesAstrocytes produce laminin, a key extracellular matrix guidance molecule in the developing brain. Laminin is bound to transmembrane receptors on the surface of astrocytes known as integrins, which are, in turn, bound to the microfilament meshwork inside the astrocyte. Previous studies have shown that T4 regulates the pattern of integrin distribution in astrocytes by modulating the organization of the microfilaments. In this study, the effect of thyroid hormone on the secretion and topology of laminin in astrocytes was examined. Linear arrays of secreted laminin were observed on the surface of the T4-treated astrocytes within 10 h after seeding the cells onto poly-D-lysine-coated coverslips and became an organized meshwork by 24 h. In contrast, little if any laminin was identified on the surface of either hormone-deficient or T3-treated cells until 36 h after seeding and then was restricted to punctate deposits. Secretion of laminin into the medium by hormone-deficient and T3-treated cells was significantly greater than that by T4-treated cells. Conversely, deposition of laminin into the extracellular matrix was significantly greater in T4-treated cells than in hormone-deficient and T3-treated cells. Thyroid hormone had no effect on the production of laminin by astrocytes. These data show that T4 regulates the extracellular deposition and organization of laminin on the surface of astrocytes and provide a mechanism by which this morphogenic hormone can influence neuronal migration and axonal projection in the developing brain.