{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Ivy ZK"],"funding":["NHLBI NIH HHS","NCI NIH HHS"],"pagination":["1918-1927"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC10731576"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["142(22)"],"pubmed_abstract":["Vaso-occlusive pain episodes (VOE) cause severe pain in patients with sickle cell disease (SCD). Vaso-occlusive events promote ischemia/reperfusion pathobiology that activates complement. We hypothesized that complement activation is linked to VOE. We used cold to induce VOE in the Townes sickle homozygous for hemoglobin S (HbSS) mouse model and complement inhibitors to determine whether anaphylatoxin C5a mediates VOE. We used a dorsal skinfold chamber to measure microvascular stasis (vaso-occlusion) and von Frey filaments applied to the plantar surface of the hind paw to assess mechanical hyperalgesia in HbSS and control Townes mice homozygous for hemoglobin A (HbAA) mice after cold exposure at 10°C/50°F for 1 hour. Cold exposure induced more vaso-occlusion in nonhyperalgesic HbSS mice (3"],"journal":["Blood"],"pubmed_title":["Cold exposure induces vaso-occlusion and pain in sickle mice that depend on complement activation."],"pmcid":["PMC10731576"],"funding_grant_id":["T32 HL007062","R01 HL114567","R01 CA241627","R01 HL147562","R01 CA263777"],"pubmed_authors":["Khasabova IA","Juliette JP","Khasabov SG","Chen C","Beckman JD","Ivy ZK","Belcher JD","Nguyen J","Rogness VM","Taylor RP","Allen K","Simone DA","Vercellotti GM","Abdulla F","Ruan C","Gupta K"],"additional_accession":[]},"is_claimable":false,"name":"Cold exposure induces vaso-occlusion and pain in sickle mice that depend on complement activation.","description":"Vaso-occlusive pain episodes (VOE) cause severe pain in patients with sickle cell disease (SCD). Vaso-occlusive events promote ischemia/reperfusion pathobiology that activates complement. We hypothesized that complement activation is linked to VOE. We used cold to induce VOE in the Townes sickle homozygous for hemoglobin S (HbSS) mouse model and complement inhibitors to determine whether anaphylatoxin C5a mediates VOE. We used a dorsal skinfold chamber to measure microvascular stasis (vaso-occlusion) and von Frey filaments applied to the plantar surface of the hind paw to assess mechanical hyperalgesia in HbSS and control Townes mice homozygous for hemoglobin A (HbAA) mice after cold exposure at 10°C/50°F for 1 hour. Cold exposure induced more vaso-occlusion in nonhyperalgesic HbSS mice (3","dates":{"release":"2023-01-01T00:00:00Z","publication":"2023 Nov","modification":"2025-04-18T16:02:20.893Z","creation":"2025-04-07T03:02:46.469Z"},"accession":"S-EPMC10731576","cross_references":{"pubmed":["37774369"],"doi":["10.1182/blood.2022019282"]}}