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T F Clawson

Publications and source records attributed to T F Clawson.

2 recordsLinked to original sources

Differential expression of insulin-like growth factor binding proteins in murine hematopoietic stromal cell lines.

The expression of the insulin-like growth factor (IGF) system in the hematopoietic microenvironment during ontogeny was studied utilizing immortalized murine cell lines established from several sites of hematopoiesis. Conditioned media was obtained from tissue cultures of murine yolk sac endoderm and mesoderm, fetal liver and adult bone marrow stromal cell lines. IGF-I and -II were quantified by radioimmunoassay and RT-PCR. The presence of insulin-like growth factor binding proteins (IGFBPs) in conditioned media was determined by Western ligand blot and Western immunoblot. IGF-I and IGF-II were present in conditioned media from every stromal cell line and differential expression of the IGFBPs was found among the hematopoietic sites. Stimulation of the cell lines with interleukin-1 alpha altered the IGFBPs in yolk sac endoderm and bone marrow conditioned media. We report that IGF-I and -II are expressed in stromal cell lines obtained from different ontogenic sites of hematopoiesis and IGFBPs are differentially expressed by these sites. The expression of IGFBPs, but not IGFs, is in part regulated by interleukin-1 alpha.

Animals↗

Hypoxia-ischemia-induced apoptotic cell death correlates with IGF-I mRNA decrease in neonatal rat brain.

Hypoxia-ischemia induces apoptotic and necrotic cell death, which results partially from persistent alterations in cellular energy homeostasis. Insulin-like growth factor I (IGF-I) is an anabolic pleiotrophic factor required by developing neurons for their optimal proliferation, differentiation, and survival. To determine how cell death and changes in IGF-I gene expression relate to the extent of hypoxia-ischemia, we evaluated the time course of apoptosis in a neonatal hypoxia-ischemia model in relation to the cellular distribution of IGF-I and IGFBP5 mRNA. Severe hypoxia-ischemia results in an immediate decrease in neuronal IGF-I and IGFBP5 mRNA. The decrease in neuronal IGF-I mRNA was concurrent with an increase in the number of apoptotic cells. It is conceivable that the immediate decrease in IGF-I gene expression may contribute to the impending neuronal death and selective vulnerability of myelinogenesis during the perinatal period.

Animals↗