<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Aghanoori MR</submitter><funding>Research Manitoba Postdoctoral Fellowship</funding><funding>University of Manitoba Graduate Fellowship</funding><funding>Bank of Montreal (BMO) Financial Group</funding><funding>Canadian Institute of Health Research</funding><pagination>193</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8930798</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>79(4)</volume><pubmed_abstract>Aberrant insulin-like growth factor 1 (IGF-1) signaling has been proposed as a contributing factor to the development of neurodegenerative disorders including diabetic neuropathy, and delivery of exogenous IGF-1 has been explored as a treatment for Alzheimer's disease and amyotrophic lateral sclerosis. However, the role of autocrine/paracrine IGF-1 in neuroprotection has not been well established. We therefore used in vitro cell culture systems and animal models of diabetic neuropathy to characterize endogenous IGF-1 in sensory neurons and determine the factors regulating IGF-1 expression and/or affecting neuronal health. Single-cell RNA sequencing (scRNA-Seq) and in situ hybridization analyses revealed high expression of endogenous IGF-1 in non-peptidergic neurons and satellite glial cell</pubmed_abstract><journal>Cellular and molecular life sciences : CMLS</journal><pubmed_title>CEBPβ regulation of endogenous IGF-1 in adult sensory neurons can be mobilized to overcome diabetes-induced deficits in bioenergetics and axonal outgrowth.</pubmed_title><pmcid>PMC8930798</pmcid><funding_grant_id>MOP-130282</funding_grant_id><pubmed_authors>Lee S</pubmed_authors><pubmed_authors>Gauvin E</pubmed_authors><pubmed_authors>Agarwal P</pubmed_authors><pubmed_authors>Smith DR</pubmed_authors><pubmed_authors>Jones MJ</pubmed_authors><pubmed_authors>Aghanoori MR</pubmed_authors><pubmed_authors>Bonomo R</pubmed_authors><pubmed_authors>Miller DW</pubmed_authors><pubmed_authors>Fernyhough P</pubmed_authors><pubmed_authors>Hai Y</pubmed_authors><pubmed_authors>Dolinsky VW</pubmed_authors><pubmed_authors>Czubryt MP</pubmed_authors><pubmed_authors>Mansuy-Aubert V</pubmed_authors><pubmed_authors>Nagalingam RS</pubmed_authors><pubmed_authors>Jolivalt CG</pubmed_authors><pubmed_authors>Yathindranath V</pubmed_authors><pubmed_authors>Calcutt NA</pubmed_authors></additional><is_claimable>false</is_claimable><name>CEBPβ regulation of endogenous IGF-1 in adult sensory neurons can be mobilized to overcome diabetes-induced deficits in bioenergetics and axonal outgrowth.</name><description>Aberrant insulin-like growth factor 1 (IGF-1) signaling has been proposed as a contributing factor to the development of neurodegenerative disorders including diabetic neuropathy, and delivery of exogenous IGF-1 has been explored as a treatment for Alzheimer's disease and amyotrophic lateral sclerosis. However, the role of autocrine/paracrine IGF-1 in neuroprotection has not been well established. We therefore used in vitro cell culture systems and animal models of diabetic neuropathy to characterize endogenous IGF-1 in sensory neurons and determine the factors regulating IGF-1 expression and/or affecting neuronal health. Single-cell RNA sequencing (scRNA-Seq) and in situ hybridization analyses revealed high expression of endogenous IGF-1 in non-peptidergic neurons and satellite glial cell</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Mar</publication><modification>2026-03-31T11:40:50.641Z</modification><creation>2024-11-09T21:42:51.372Z</creation></dates><accession>S-EPMC8930798</accession><cross_references><pubmed>35298717</pubmed><doi>10.1007/s00018-022-04201-9</doi></cross_references></HashMap>