Expression of Prostaglandin Genes and β-Catenin in Whole Blood as Potential Markers of Muscle Degeneration

Prostaglandin signaling pathways are closely related to inflammation, but also muscle regeneration and processes associated with frailty and sarcopenia, whereas β-catenin (CTNNB1 gene) as a part of Wnt signaling is also involved in the differentiation of muscle cells and fibrosis. The present study analyzed the association between selected prostaglandin pathway genes and clinical parameters in patients with sarcopenia and frailty syndrome. The present study was conducted on patients with sarcopenia, frailty syndrome, and control older patients (N = 25). Additionally, two healthy controls at the age of 25–30 years (N = 51) and above 50 years old (N = 42) were included. The expression of the PTRGER4, PTGES2 (COX2), PTGS2, and CTNNB1 genes in whole blood was checked by the qPCR method. The serum cytokine levels (IL-10, TNFα, IFN-y, IL-1α, IL-1β) in patients and controls were checked by the Q-Plex Human Cytokine Panel. The results showed a significant effect of age on PTGER4 gene expression (p = 0.01). A negative trend between the appendicular skeletal muscle mass parameter (ASSM) and the expression of PTGER4 has been noted (r = −0.224, p = 0.484). PTGES2 and PTGS2 expressions negatively correlated with creatine phosphokinase (r = −0.71, p = 0.009; r = −0.58, p = 0.047) and positively with the functional mobility test timed up and go scale (TUG) (r = 0.61, p = 0.04; r = 0.63, p = 0.032). In the older control group, a negative association between iron levels and the expression of PTGS2 (r = −0.47, p = 0.017) was observed. A similar tendency was noted in patients with sarcopenia (r = −0.112, p = 0.729). A negative trend between appendicular skeletal muscle mass (ASMM) and PTGER4 seems to confirm the impairment of muscle regeneration associated with sarcopenia. The expression of the studied genes revealed a trend in associations with the clinical picture of muscular dystrophy and weakening patients. Perhaps PTGS2 and PTGES2 is in opposition to the role of the PTGER4 receptor in muscle physiology. Nevertheless, further, including functional studies is needed.