C57bl 6j

Eight-week-old male MPTP-induced Parkinson model mice (on a C57BL/6J background, MPTP-PD) and recommended control (C57BL/6J, CN) were purchased from the Shanghai Model Organisms Center, Inc, Shanghai, China. The animals were anesthetized with 500 mg/kg tribromoethanol (Sigma, Saint Louis, MO, USA) and were killed by cervical dislocation. After the animals were sacrificed, brain tissues (cerebral cortex, hippocampus, striatum and cerebellum) were isolated, quickly frozen in liquid nitrogen and stored in liquid nitrogen (n = 1). Four brain regions were pooled for nuclei isolated according to the ‘Nuclear Isolation by Single-cell RNA Sequencing’ protocol of 10X Genomics^®. In brief, the tissue was lysed in a chilled lysis buffer (10 mM Tris-HCl, 10 mM NaCl, 3 mM MgCl2, 0.1% NP-40). Then, the suspension was filtered and nuclei were pelleted by centrifugation. Nuclei pellets were then washed in ‘nuclei wash and resuspension buffer’ (1× PBS, 1% BSA, 0.2 U/μL RNase inhibitor, 2 mM DTT), filtered and pelleted again. Cell count was then performed to calculate the concentration of nuclear suspension.

Male Yod1 knockout mice on the C57BL/6J background were purchased from Shanghai Model Organisms (Shanghai, China). Wild-type (WT) C57BL/6J mice were purchased from Sipeifu (Beijing, China). To establish an in vivo model of sepsis-induced DIC, mice were randomly assigned to experimental groups. Adult male mice (8 weeks old) were injected with MRSA (1 × 10⁸ colony-forming units/mouse) through a caudal vein. The control group was injected with an equal volume of phosphate buffer solution (PBS). Yod1^−/− mice and their matched WT mice were sacrificed and subjected to coagulation analysis at 12 h after injection of MRSA. All mice were housed in the SPF animal room with free access to water and food.

C57BL/6N mice of 6–8 weeks of age were purchased from Charles River (Beijing, China). C57BL/6J Cd19^Cre, C57BL/6J Ppard^flox, C57BL/6J IL-10^flox mice were purchased from Shanghai Model Organisms, and Cd19^Cre/CrePpard^f/f and Cd19^Cre/CreIL-10^f/f mice were generated by breeding C57BL/6J Cd19^Cre mice with C57BL/6J Ppard^flox mice or with C57BL/6J IL-10^flox mice, respectively. Protocols involving the use of animals were reviewed and approved by the Institutional Animal Care and Use Committee of the First Hospital of Jilin University and all experiments were performed in accordance with the protocols.

All procedures were performed in adherence to the Fourth Military Medical University’s Guidelines on the Care and Use of Laboratory Animals and were approved by the Ethics Committee on Animal Care. Adipose tissue-specific Adipsin transgenic mice (Adipsin-Tg) and adipose tissue-specific deletion of Adipsin mice (Adipsin-KO) were generated on C57BL/6J background provided by Shanghai Model Organisms Center (Shanghai, China). Male littermates (6–8 weeks, 20–25 g) were utilized in all animal experiments.

C57BL/6 J (B6) (#000664), B6.SJL (#002014), OT-I (#003831), OT-II (#004194), β2m^−/− (#002087), CD11c-Cre (#008068) mice were originally from the Jackson Laboratory. The strain of C57BL/6J-Zeb1^{tm1(flox-Neo)Smoc}, in which exon 4 was flanked by LoxP and FRT sites on a C57BL/6 N background, was generated using a standard gene-targeting strategy by Shanghai Model Organisms Center, Inc, and then were crossed with FLP deleter strain (#009086, the Jackson Laboratory) to remove Neo cassette to generate the floxed Zeb1 mice (Zeb1^fl/fl). All mice (both genders) were littermates and were 8–12 weeks old, unless otherwise indicated in the text. The mice were housed in specific pathogen-free facilities of Xiamen University Laboratory Animal Center with a 12 h day/night cycle, at a temperature about 22 °C, a relative humidity about 50%, and were fed with a standard mouse chow diet. All animal protocols were approved by members of the Institutional Animal Care and Use Committee of Xiamen University.

All animal procedures described in this study were performed using 8- to 16-week-old mice and were approved by the Institutional Animal Care and Use Committee of Soochow University (20140431). For platelet specific deletion of CLEC-2 expression, Clec2^fl/fl; Pf4-Cre mice were created by crossing Clec2^fl/flmice with Pf4-Cre mice (stock number 008535; C57BL/6J and Sv129 background; Jackson Laboratory). For hematopoietic deletion of PDPN expression, PDPN^fl/fl; LysM-Cre mice (Mye Pdpn^-/-) were created by crossing PDPN^fl/fl mice with LysM-Cre mice (stock number 004781; C57BL/6J and Sv129 background; Jackson Laboratory). Selplg^-/- mice were obtained from the Jackson Laboratory (stock number 004201, C57BL/6J background). ApoE^-/- mice (stock number T001782, C57BL/6J background), Ldlr^-/- mice (stock number T001464, C57BL/6J background), C57BL/6J mice (stock number N000013) and EGFP (stock number NM-TG-00005, C57BL/6J background) mice were purchased from Shanghai Model Organisms Center. All mice were housed in a pathogen-free facility at an ambient temperature of 22 °C to 25 °C, humidity and light cycle (12:12 h light: dark), and free access to water and food. All mice were backcrossed on C57BL/6J or Sv129 for > 10 generations.