Regulation of human thyroid follicular cell function by inhibition of vascular endothelial growth factor receptor signalling.

The potential autocrine role of human thyroid vascular endothelial growth factors (VEGFs) was examined using the VEGF receptor (VEGFR) inhibitor, ZM306416HCl. ZM306416HCl reduced VEGFR2 phosphorylation and inhibited endogenous, steady-state levels of p42/44 MAPK phosphorylation. It potently inhibited the secretion of plasminogen activators (PA) and increased (125)I uptake.

Taurine reduces nitrosative stress and nitric oxide synthase expression in high glucose-exposed human Schwann cells.

The role of taurine in regulating glucose-induced nitrosative stress has been examined in human Schwann cells, a model for understanding the pathogenesis of diabetic neuropathy. Exposure to high glucose increased nitrated proteins (1.56 fold p<0.

Expression of receptors for VEGFs on normal human thyroid follicular cells and their role in follicle formation.

Human thyroid follicular cells in culture expressed the mRNAs for the receptors for vascular endothelial growth factors (VEGFRs). The relative expression was neuropilin1 = neuropilin2 = VEGFR2 > VEGFR1 > VEGFR3. Western blotting for VEGFR2 showed labeling of proteins ~200-230 kDa.

Molecular regulation of thyroid gland function.

Purpose Of Review: For de-novo thyroid hormone synthesis ex vivo, thyroid follicular cells require a serum-free medium supplying nutrients, iodide, thyroid-stimulating hormone and insulin-like growth factor I (IGF-I) (or insulin). Under these conditions, T3 and T4 are secreted but so are other factors such as growth factors, plasminogen activators, their inhibitors known as serpins, and so on. What is the function of these factors? Do thyroid cells respond to them or are these paracrine/endocrine factors? The purpose of this review is to highlight the current developments in the identification and role of the signalling pathways that regulate thyroid growth and function and the putative role of endogenous thyroid proteases in regulating this.