In situ localization of thrombospondin-1 and thrombospondin-3 transcripts in the avian embryo

Abstract

Two novel cDNA probes to chicken thrombospondin‐1 (TSP‐1) and TSP‐3 were used to determine by in situ hybridization the origins of these extracellular matrix proteins during embryogenesis. Both TSP‐1 and TSP‐3 are expressed in embryonic cartilage. TSP‐1 expression is limited to early chondrocytes, in contrast to TSP‐3 mRNAs that are found in older proliferative and hypertrophic chondrocytes. TSP‐1 and TSP‐3 are expressed consecutively during neurogenesis as well, with the TSP‐1 probe hybridizing in proliferating neuroblasts, and TSP‐3 expressed by neurons as they are actively extending processes. A TSP‐1 hybridization signal reappears in subpopulations of neurons in the spinal cord and brain after the periods of active neurite extension and programmed cell death are complete. TSP‐1 is also expressed in the spinal cord floor plate, in mesenchyme surrounding the developing paramesonephric duct, at the tips of growing lung bronchioles, in lens, and in corneal endothelium. These observations indicate that there is little overlap in the expression patterns of TSP‐1 and TSP‐3 and that they are expressed consecutively during the development of cartilage and neurons. The pattern of TSP‐1 expression in avascular tissues and in the floor plate is consistent with possible roles for this glycoprotein in regulating angiogenesis and establishing morphogenetic gradients. Dev. Dyn. 208:326–337, 1997. © 1997 Wiley‐Liss, Inc.

Tenascin-C: Form versus function

“…46 In contrast, lower Mr isoforms (Tn190/200) are observed to be expressed more stably in dense connective tissue in areas such as gizzard tendons, intramuscular connective tissue, aortic mesenchyme, articular cartilage, inner layer of perichondrium and zones of active chondrocyte proliferation, where cell condensation and differentiation are more prevalent. 22,39,41,[44][45][46][47][50][51][52] Similar patterns of tenascin-C expression are observed in mice and rats, although significantly less is known about the presence of alternatively spliced tenascin-C during human fetal development. WB and real-time PCR (RT-PCR) techniques revealed that smaller Mr tenascin-C variants are the predominant isoforms expressed in E14 mouse gut mesenchyme, 53 and in the developing thymus and skin from E17 to P6 respectively.…”

“…38,39 High Mr variants (Tn230/200) were associated with regions of active tissue remodeling, cell migration and cell division; evidenced by their presence in epithelial substratum for migrating neurons, embryonic skin fibroblasts, whole brain, cerebellum, chord glia, Bergmann glia, endoderm-derived epithelium at developing lung bronchioles, growing wing bud tips, base of feather buds, major blood vessel endothelium, kidney, lung, osteoblasts and regions of osteogenesis; where the expression of tenascin-C is only required transiently. 22,34,[40][41][42][43][44][45][46][47][48][49] In these regions, large Mr tenascin-C is expressed by migrating glia and Bergmann glia in the developing chick spinal chord and cerebellum respectively; expression in the latter of which facilitates granule cell migration. 46 In contrast, lower Mr isoforms (Tn190/200) are observed to be expressed more stably in dense connective tissue in areas such as gizzard tendons, intramuscular connective tissue, aortic mesenchyme, articular cartilage, inner layer of perichondrium and zones of active chondrocyte proliferation, where cell condensation and differentiation are more prevalent.…”

“…22,34,[40][41][42][43][44][45][46][47][48][49] In these regions, large Mr tenascin-C is expressed by migrating glia and Bergmann glia in the developing chick spinal chord and cerebellum respectively; expression in the latter of which facilitates granule cell migration. 46 In contrast, lower Mr isoforms (Tn190/200) are observed to be expressed more stably in dense connective tissue in areas such as gizzard tendons, intramuscular connective tissue, aortic mesenchyme, articular cartilage, inner layer of perichondrium and zones of active chondrocyte proliferation, where cell condensation and differentiation are more prevalent. 22,39,41,[44][45][46][47][50][51][52] Similar patterns of tenascin-C expression are observed in mice and rats, although significantly less is known about the presence of alternatively spliced tenascin-C during human fetal development.…”

Neurite Outgrowth by the Alternatively Spliced Region of Human Tenascin-C Is Mediated by Neuronal α7β1 Integrin

“…1 A). Periods of increased axonal growth in the developing CNS have been closely correlated with expression of large but not small tenascin-C (Crossin et al, 1989;Tucker, 1993), suggesting that fnA-D might stimulate neuronal growth during embryogenesis.…”

Human tenascin-C: Identification of a novel type III repeat in oral cancer and of novel splice variants in normal, malignant and reactive oral mucosae

“…A diverse but restricted spatio-temporal distribution, that it is different from that described for any other extracellular matrix protein, has been reported for tenascin-C in soft and mineralised tissues (Carter et al, 1991;Tucker, 1993). Increased tenascin-C expression has been observed in many examples of tissue morphogenesis and cell migration (Luomanen and Virtanen, 1993;Julian et al, 1994;Shrestha et al, 1995).…”