The endocannabinoid system's genetic polymorphisms in sickle cell anemia patients

Sci Rep. 2024 Dec 30;14(1):31562. doi: 10.1038/s41598-024-76480-0.

Abstract

Sickle cell anemia (SCA) is a monogenic blood disease with complex and multifactorial pathophysiology. The endocannabinoid system (ECS) could be a candidate for modulating SCA complications, such as priapism, as it has demonstrated an essential role in hematopoiesis, platelet aggregation, and immune responses. We evaluated the association of ECS-related single nucleotide polymorphisms (SNP) (FAAH rs324420, MAGL rs604300, CNR1 rs7766029, and CNR2 rs35761398) with priapism in a Brazilian SCA cohort. The study involved 138 SCA patients (n = 80 with priapism and n = 58 without priapism). SCA was detected with HPLC, and the Hb SS genotype was confirmed with PCR-RE. Alpha thalassemia mutations were detected with Multiplex-PCR, and SNP genotyping was performed using TaqMan genotyping assays. We observed a lower frequency of -α3.7kb-thalassemia mutation in patients with priapism than in patients without this complication (p < 0.001), and in adjusted multivariate analyses TT-CC genotype of CNR2 rs35761398 was associated with a lower chance of developing priapism (OR = 0.386 [0.175-0.854], p = 0.019) and a lower risk of it over time (HR = 0.634 [0.402-0.987], p = 0.049). The SCA ischemic priapism is related to unbalanced vasodilation/vasoconstriction pathways, such as decreased RhoA/Rho-kinase (ROCK) signaling. Since activating the type 2 cannabinoid receptor (CB2) decreases RhoA activation, we suggest a novel approach to SCA priapism involving CB2.

Keywords: Endocannabinoids; Hemolysis; Priapism; Prognostic.

MeSH terms

  • Adolescent
  • Adult
  • Anemia, Sickle Cell* / complications
  • Anemia, Sickle Cell* / genetics
  • Brazil
  • Endocannabinoids* / genetics
  • Endocannabinoids* / metabolism
  • Female
  • Genetic Predisposition to Disease
  • Genotype
  • Humans
  • Male
  • Polymorphism, Single Nucleotide*
  • Priapism / etiology
  • Priapism / genetics
  • Receptor, Cannabinoid, CB2 / genetics
  • Young Adult

Substances

  • Endocannabinoids
  • Receptor, Cannabinoid, CB2
  • CNR2 protein, human