ArticleBioengineered2022
Leucine rich alpha-2-glycoprotein 1 (Lrg1) silencing protects against sepsis-mediated brain injury by inhibiting transforming growth factor beta1 (TGFβ1)/SMAD signaling pathway.
Article in Bioengineered, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 2 of them syntheses that pooled it.
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Who cites it
14 citing papers in PubMed, 2 syntheses or guidelines pooled it, 21 citations in OpenAlex.
- Dissecting the genetic and proteomic risk factors for delirium.Nature aging · 2026Pooled it
- The Key Drivers of Brain Injury by Systemic Inflammatory Responses after Sepsis: Microglia and Neuroinflammation.Molecular neurobiology · 2023Pooled it
- Research Advances in the Pathogenesis of Sepsis-Associated Encephalopathy.International journal of molecular sciences · 2026Review
- Plasma Proteomic Signatures of Pediatric Sepsis Reveal Persistent Inflammation and Phase-Specific Biomarkers.FASEB bioAdvances · 2026Article
- Hydrocephalus: Molecular and Neuroimaging Biomarkers in Diagnosis and Management.Biomedicines · 2025Review
- ADAMTS18 deficiency leads to abnormal brain methylation metabolism, dysregulated neuroinflammatory response, and unsound blood-brain barrier structure in mice.Metabolic brain disease · 2025Article
- DNMT3a Deficiency Contributes to Anesthesia/Surgery-Induced Synaptic Dysfunction and Cognitive Impairment in Aged Mice.Aging cell · 2025Article
- lncRNA CASC7 contributes to the progression of LPS-induced liver injury by targeting miRNA-217/TLR4 axis.Biomolecules & biomedicine · 2025Article
- Predicting microRNAs and their Target Genes Involved in Sepsis Pathogenesis by using Bioinformatics Methods.Current pharmaceutical design · 2025Article
- Detection ofFood and waterborne parasitology · 2024Article
- Review
- Deciphering Proteomic Expression in Inflammatory Disorders: A Mass Spectrometry Exploration Comparing Infectious, Noninfectious, and Traumatic Brain Injuries in Human Cerebrospinal Fluid.Neurotrauma reports · 2024Article
- LRG1 Promotes ECM Integrity by Activating the TGF-β Signaling Pathway in Fibroblasts.International journal of molecular sciences · 2023Article
- Improvement of Spatial Memory and Cognitive Function in Mice via the Intervention of Milk Fat Globule Membrane.Nutrients · 2023Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sepsis-associated encephalopathy (SAE) is key manifestation of sepsis which is responsible for increased morbidity and mortality. Leucine rich alpha-2-glycoprotein 1 (Lrg1) is a secreted protein implicated in a variety of diseases. We aimed to explore the effects and potential mechanism of Lrg1 on sepsis-mediated brain injury. A sepsis-induced brain damage mice model was established. Then, ELISA was utilized to detect the levels of inflammatory factors in brain tissues. Behavioral performance, spatial learning and memory of mice were evaluated by open field test and Morris water maze test. The number of neurons was tested by H&E staining. Lrg1 expression was evaluated by RT-qPCR and western blot. In vitro, mouse hippocampal neuronal cell line (HT22) was stimulated by lipopolysaccharide (LPS). After Lrg1 silencing, cell viability was determined using CCK-8 and cell apoptosis was assessed by TUNEL. The levels of inflammatory factors were detected by ELISA. Moreover, western blot was applied to analyze the expression of proteins in transforming growth factor beta1 (TGFβ1)/SMAD signaling. Results revealed that mice in the model group showed obvious behavioral changes. Lrg1 was highly expressed in the brain tissues of model mice. Besides, Lrg1 knockdown suppressed the inflammation and apoptosis of LPS-induced HT22 cells. Moreover, Lrg1 silencing caused the inactivation of TGFβ1/SMAD signaling. Rescue assays confirmed that TGFβ1 overexpression reversed the impacts of Lrg1 deletion on the inflammation and apoptosis in LPS-induced HT22 cells. Collectively, Lrg1 silencing alleviates brain injury in SAE via inhibiting TGFβ1/SMAD signaling, implying that Lrg1 might serve as a promising target for SAE treatment.
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