Network analysis of the progranulin-deficient mouse brain proteome reveals pathogenic mechanisms shared in human frontotemporal dementia caused by GRN mutations.
Results from conditional progranulin-knockout mice that lack progranulin in nestin-expressing cells (Nes-cKO mice) which include most neurons as well as astrocytes suggest that increased lipofuscinosis and gliosis in Grn-null animals are not caused by intrinsic progranulin deficiency in neurons and that microglia-derived progranulin may be sufficient to maintain neuronal health and homeostasis in the brain.
In progranulin knockout mice there was no estrogen receptor alpha immunoreactivity in astrocytes in males or females at various ages. These results suggest that PGRN plays a crucial role in the expression of ERalpha in astrocytes regardless of the estrous cycle stage sex and maturity.
The results suggest that PGRN may affect the differentiation of retinal precursor cells to photoreceptor cells through the HGF receptor signaling pathway.
Data show that progranulin is upregulated in neuroendocrine tumors (NETs) and islets of the multiple endocrine neoplasia 1 protein (MEN1) mouse as well as in the serum of patients with pancreatic NETs associated with glucagonoma syndrome.
Results suggest that PGRN is involved in the development and/or maturation of neuronal networks comprising Purkinje cells in the cerebellum which may be a prerequisite to normal motor function
Progranulin overproduction due to Fli-1 deficiency may contribute to the constitutive activation of SSc dermal fibroblasts by antagonizing the antifibrotic effect of TNF.
physiological role for PGRN in hypothalamic glucose-sensing and appetite regulation. Alterations in hypothalamic PGRN production or action may be linked to appetite dysregulation in obesity
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