ArticleInflammation2025
p62 Binding to Protein Kinase C Regulates HIV-1 gp120 V3 Loop Induced Microglial Inflammation.
Article in Inflammation, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed.
- Rosiglitazone alleviates white matter injury by inhibiting NLRP3/capspase-1 mediated microglial pyroptosis via downregulating KLF4.Experimental brain research · 2026Article
- Neuroinflammation and NeuroHIV: understanding the role of HIV-1 related factors in microglial activation.Translational psychiatry · 2026Review
- Phosphodiesterase 4B (PDE4B) inhibitors and their applications in recent years (2014 to early 2025).Molecular diversity · 2026Review
- LncRNA SNHG1 Knockdown Ameliorates HIV-1 gp120V3 Loop-Induced Microglial Neuroinflammation by Regulating the Autophagy Process.Inflammation · 2026Article
- Crosstalk Between Allergic Inflammation and Autophagy.International journal of molecular sciences · 2025Review
- Revealing the Oxidative Stress-Related Molecular Characteristics and Potential Therapeutic Targets of Schizophrenia through Integrated Gene Expression Data Analysis.Molecular neurobiology · 2025Article
- CircZNF418 alleviates oxidative stress-induced cartilage endplate degeneration by stabilizing Sox9 through HuR.Journal of molecular histology · 2025Article
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- Photoaging: UV radiation-induced cGAS-STING signaling promotes the aging process in skin by remodeling the immune network.Biogerontology · 2025Review
- Inhibition of TRPM3 channels in the medial prefrontal cortex mitigates OCD symptoms following traumatic brain injury.Inflammopharmacology · 2025Article
- MAFF alleviates hepatic ischemia-reperfusion injury by regulating the CLCF1/STAT3 signaling pathway.Cellular & molecular biology letters · 2025Article
- Quercetin alleviates neonatal hypoxic-ischaemic brain injury by rebalancing microglial M1/M2 polarization through silent information regulator 1/ high mobility group box-1 signalling.Inflammopharmacology · 2025Article
- Therapeutic potential of plant polyphenols in acute pancreatitis.Inflammopharmacology · 2025Review
- ACE2 alleviates sepsis-induced cardiomyopathy through inhibiting M1 macrophage via NF-κB/STAT1 signals.Cell biology and toxicology · 2024Article
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Authors and funding
9 authors.
Funding
Abstract
The main pathogenic mechanism of HIV-associated neurocognitive disorders (HAND) is neuronal apoptosis induced by inflammatory mediators, in which microglial inflammation plays a crucial role. However, the exact pathogenic mechanism remains unclear. Previous studies have shown that the HIV-1 gp120 V3 loop can trigger inflammation in CHME-5 microglia. p62 is a post-translational modified multidomain protein that is involved in the regulation of autophagy and is closely related to neuroinflammation. In this study, we found that p62 knockout down-regulated the expression of MCP-1, IL-6 and COX-2, and improved the inflammation of HIV-1 gp120 V3 loop induced microglia, while overexpression of p62 up-regulated the expression of MCP-1, IL-6 and COX-2, and promoted the inflammation of microglia. In addition, protein kinase C (PKC) knockout down-regulated the expression of MCP-1, IL-6 and COX-2 and inhibited the activation of IKK/ NF-κ B pathway, while tumor necrosis factor receptor-associated factor 6 (TRAF6) knockout had no significant effect on the expression of MCP-1, IL-6 and COX-2. Co-immunoprecipitation showed that p62 was bound and interacted with PKC. Inhibition of IKK/ NF-κ B pathway can down-regulate the expression of MCP-1, IL-6 and COX-2, and improve the inflammatory response of microglia. Our research further found that inhibition of IKK/ NF-κ B can decrease the expression of Caspase-3 and reduce the apoptosis of neurons in the co-culture of CHME-5 microglia and primary mouse neurons. The results of this study suggest that HIV-1 gp120 V3 loop induced CHME-5 microglial inflammation may be activated by the direct binding of p62 and PKC through the IKK/ NF-κ B signaling pathway, and these findings provide an important reference for the prevention and treatment of HAND.
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