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The in situ non-isotopic hybridization carried out in the present study clearly identifies α- and β-tanycytes as the main hypothalamic cells positive for GK expression; however, a reduced hybridization signal in neuronal soma (arcuate nucleus) was also detected.
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Experimental evidences show that Klf10 is a positive regulator of Trh promoter activity in primary cultures of fetal hypothalamic cells and that its expression coincides with the establishment of the hypothalamic TRH neurons in vivo [ 38].
Indeed, treatment of cultured hypothalamic cells and primary hypothalamic neurons to oleic acid increased interactions between phagosomes/lysosomes and neuronal lipids, demonstrating that as we observed in liver, hypothalamic autophagy functions to deliver neuronal lipid droplets to lysosomes [ 36].
To investigate the proliferative potential of embryonic hypothalamic cells and evaluate the expression of feeding-related neuropeptides, we generated neurospheres from embryonic rat hypothalamic cells.
Immortalized hypothalamic cells transfected with GRIA1Asn release less GnRH than do cells with GRIA1Ser.
Possibly, 3rd ventricle precursor cells give rise to hypothalamic cells [12], [13], [14].
To test this hypothesis, we evaluated MCT1 and MCT4 expression and function in hypothalamic cells.
Quantitative RT-PCR analysis showed that MCT1 expression in hypothalamic cells is 20 times higher than MCT4 (Fig. 1B).
Initially, we evaluated the effect of the HF diet on the induction of apoptosis in hypothalamic cells.
Altogether, this further supported our demonstration of a preferential activation of STAT3 in IL-7-responsive hypothalamic cells.
Furthermore, UCP-2 has been described to protect hypothalamic cells from inflammation damage induced by TNF alpha [31].
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