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Loss of Serpin E2 alters antimicrobial gene expression by microglia but not astrocytes

ABSTRACT: To investigate the influence of Serpin E2 (aka PN-1) on glia in the brain, we purified microglia and astrocytes and performed RNA sequencing from Serpine2-/- mice

ORGANISM(S): Mus musculus

PROVIDER: GSE226269 | GEO | 2026/02/02

REPOSITORIES: GEO

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Loss of Serpin E2 alters antimicrobial gene expression by microglia but not astrocytes

Project description:Loss of Serpin E2 alters antimicrobial gene expression by microglia but not astrocytes

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Loss of Serpin E2 alters antimicrobial gene expression by microglia but not astrocytes.

Project description:Microglia are the brain-resident immune cells responsible for surveilling and protecting the central nervous system. These cells can express a wide array of immune genes, and that expression can become highly dynamic in response to changes in the environment, such as traumatic injury or neurological disease. Though microglial immune responses are well studied, we still do not know many mechanisms and regulators underlying all the varied microglial responses. Serpin E2 is a serine protease inhibitor that acts on a wide variety of serine proteases, with particularly potent affinity for the blood clotting enzyme thrombin. In the brain, Serpin E2 is highly expressed by many cell types, especially glia, and loss of Serpin E2 leads to behavioral changes as well as deficits in synaptic plasticity. To determine whether Serpin E2 is important for maintaining homeostasis in glia, we performed RNA sequencing of microglia and astrocytes from Serpin E2-deficient mice in a healthy state or under immune activation due to lipopolysaccharide (LPS) injection. We found that microglia in Serpin E2-deficient mice had higher expression of antimicrobial genes, while astrocytes did not display any robust changes in transcription. Furthermore, the lack of Serpin E2 did not affect transcriptional responses to LPS in either microglia or astrocytes. Overall, we find that Serpin E2 is a regulator of antimicrobial genes in microglia.

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Project description:One of important insect defense mechanisms is melanization, which are mediated by clip domain serine protease (cSP) cascades and regulated by Serpins. In vitro, activation of melanization can efficiently kill Nucleopolyhedrovirus (NPV). However, quantitative proteomics revealed that the infection of NPV in cotton bollworm Helicoverpa armigera suppressed protein levels of melanization components in the host hemolymph. It also reduced the prophenoloxidase (PPO) activity. In contrast, Serpin-9 and -5 were sequentially up-regulated. Serpin-5 and -9 induced by NPV infection play important roles in regulate host melanization by directly inhibiting their target proteases cSP4 and cSP6 respectively. Furthermore, Serpin-5 or -9 depleted insects exhibited high PO activities and show resistance to NPV infection. Together, our results characterized melanization cascade in H. armigera, and suggests that natural insect virus NPV has evolved a distinct strategy to suppress host immune system. This finding may be exploited to design more potent viruses against agricultural pests.

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