ArticleOxidative medicine and cellular longevity2020
Rh-CSF1 Attenuates Oxidative Stress and Neuronal Apoptosis via the CSF1R/PLCG2/PKA/UCP2 Signaling Pathway in a Rat Model of Neonatal HIE.
Article in Oxidative medicine and cellular longevity, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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22 citing papers in PubMed, 44 citations in OpenAlex.
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- Novel GLP-1/GIP Dual Receptor Agonist Alleviates Neonatal Hypoxic-Ischemic Encephalopathy by Inhibiting TLR2/NF-κB/NLRP3 Mediated-Neuroinflammation : The role of DA5-CH in neonatal hypoxic-ischemic encephalopathy.Neurochemical research · 2025Article
- hUC-MSC extracellular vesicles protect against hypoxic-ischemic brain injury by promoting NLRP3 ubiquitination.Biomolecules & biomedicine · 2025Article
- Overexpression of PLCG2 and TMEM38A inhibit tumor progression in clear cell renal cell carcinoma.Scientific reports · 2025Article
- Flavonoids in Brain Ischemia-Reperfusion and their Effect on Kinases as Signaling Pathway Activity.CNS & neurological disorders drug targets · 2025Article
- EPO modified MSCs protects SH-SY5Y cells against ischemia/hypoxia-induced apoptosis via REST-dependent epigenetic remodeling.Scientific reports · 2024Article
- Patients with restless legs syndrome exhibit reduced serum colony-stimulating factor-1, humanin-like 3 and 10 levels.Acta neurologica Belgica · 2024Article
- Bone marrow mesenchymal stem cell-derived exosomes shuttle microRNAs to endometrial stromal fibroblasts that promote tissue proliferation /regeneration/ and inhibit differentiation.Stem cell research & therapy · 2024Article
- Treadmill training improves lung function and inhibits alveolar cell apoptosis in spinal cord injured rats.Scientific reports · 2024Article
- Overexpression of TRPV6 Inhibits Coronary Atherosclerosis-Related Inflammatory Response and Cell Apoptosis via the PKA/UCP2 Pathway.Cardiovascular therapeutics · 2024Article
- Increased expression of CSF1 in patients with eosinophilic asthma.Immunity, inflammation and disease · 2023Article
- Macrophage subsets and their role: co-relation with colony-stimulating factor-1 receptor and clinical relevance.Immunologic research · 2023Review
- Bioinformatics analysis of the common targets of miR-223-3p, miR-122-5p, and miR-93-5p in polycystic ovarian syndrome.Frontiers in genetics · 2023Article
- Inhibitory effect of PDE2 on inflammation and apoptosis in cerebral ischemia‑reperfusion injury.International journal of molecular medicine · 2022Article
- Chlorogenic acid exerts neuroprotective effect against hypoxia-ischemia brain injury in neonatal rats by activating Sirt1 to regulate the Nrf2-NF-κB signaling pathway.Cell communication and signaling : CCS · 2022Article
- Ki20227 aggravates apoptosis, inflammatory response, and oxidative stress after focal cerebral ischemia injury.Neural regeneration research · 2022Article
- Neuroprotective Mechanism of Icariin on Hypoxic Ischemic Brain Damage in Neonatal Mice.Oxidative medicine and cellular longevity · 2022Article
- Activation of LRP6 with HLY78 Attenuates Oxidative Stress and Neuronal Apoptosis via GSK3Oxidative medicine and cellular longevity · 2022Article
- Differential Regulation of Microglial Activation in Response to Different Degree of Ischemia.Frontiers in immunology · 2022Article
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Authors and funding
11 authors at 2 institutions in 2 countries.
Funding
Abstract
Oxidative stress (OS) and neuronal apoptosis are major pathological processes after hypoxic-ischemic encephalopathy (HIE). Colony stimulating factor 1 (CSF1), binding to CSF1 receptor (CSF1R), has been shown to reduce neuronal loss after hypoxic-ischemia- (HI-) induced brain injury. In the present study, we hypothesized that CSF1 could alleviate OS-induced neuronal degeneration and apoptosis through the CSF1R/PLCG2/PKA/UCP2 signaling pathway in a rat model of HI. A total of 127 ten-day old Sprague Dawley rat pups were used. HI was induced by right common carotid artery ligation with subsequent exposure to hypoxia for 2.5 h. Exogenous recombinant human CSF1 (rh-CSF1) was administered intranasally at 1 h and 24 h after HI. The CSF1R inhibitor, BLZ945, or phospholipase C-gamma 2 (PLCG2) inhibitor, U73122, was injected intraperitoneally at 1 h before HI induction. Brain infarct volume measurement, cliff avoidance test, righting reflex test, double immunofluorescence staining, western blot assessment, 8-OHdG and MitoSOX staining, Fluoro-Jade C staining, and TUNEL staining were used. Our results indicated that the expressions of endogenous CSF1, CSF1R, p-CSF1R, p-PLCG2, p-PKA, and uncoupling protein2 (UCP2) were increased after HI. CSF1 and CSF1R were expressed in neurons and astrocytes. Rh-CSF1 treatment significantly attenuated neurological deficits, infarct volume, OS, neuronal apoptosis, and degeneration at 48 h after HI. Moreover, activation of CSF1R by rh-CSF1 significantly increased the brain tissue expressions of p-PLCG2, p-PKA, UCP2, and Bcl2/Bax ratio, but reduced the expression of cleaved caspase-3. The neuroprotective effects of rh-CSF1 were abolished by BLZ945 or U73122. These results suggested that rh-CSF1 treatment attenuated OS-induced neuronal degeneration and apoptosis after HI, at least in part, through the CSF1R/PLCG2/PKA/UCP2 signaling pathway. Rh-CSF1 may serve as therapeutic strategy against brain damage in patients with HIE.
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