ABSTRACT
Proteoglycans are considered integral structural components of tendon and ligament and have been implicated in the resistance of compressive forces, collagen fibrillogenesis, matrix remodelling and cell signalling. Several sequence variants within genes encoding proteoglycans were recently implicated in modulating anterior cruciate ligament ruptures (ACLR). This study aimed to test the previously implicated variants in proteoglycan and vascular epithelial growth factor encoding genes with risk of ACLR in a population from Poland. A case control genetic association study was conducted using DNA samples from 143 healthy participants without a history of ACL injuries (99 male and 44 females) (CON group) and 229 surgically diagnosed ACLR participants (158 males and 71 females). All samples were genotyped for the ACAN: rs1516797, BGN: rs1042103, rs1126499, DCN: rs516115 and VEGFA: rs699947 variants. Main findings included the (i) ACAN rs1516797 G/T genotype which was underrepresented in the CON group (CON: 36%, n=52, ACLR: 49%, n=112, p=0.017, OR=1.68, 95% CI 1.09 to 2.57) when all participants were investigated and (ii) the BGN rs1042103 A allele was significantly under-represented in the male CON group compared to the male ACLR group (CON: 39%, n=78, ACLR: 49%, n=156, p=0.029, OR=1.5, 95% CI 1.05 to 2.15). Furthermore, BGN inferred haplotypes were highlighted with altered ACLR susceptibility. Although the study implicated the ACAN and BGN genes (combination of genotype, allele and haplotype) in modulating ACLR susceptibility, several differences were noted with previous published findings.
ABSTRACT
BACKGROUND: Aging is a multifactorial process defined by an accumulation of damage in all tissues and organs, including the skin, throughout the lifespan of an individual. The reduction of both cellular and extracellular matrix components of the dermis during the aging process is followed by the alteration of the morphology of the skin tissue. This study was conducted to assess skin morphology in men before and 3 months after the intradermal injection of autologous fibroblastic cells. METHODS: Tissue biopsies were surgically obtained before and 3 months after the treatment with autogenously harvested fibroblasts expanded in vitro, as well as after injection of phosphate-buffered saline. The thickness of collagen fiber bundles and number of fibroblasts in the dermis were analyzed in morphometric studies. The morphologic evaluation, using different methods of staining has been performed to analyze of extracellular matrix proteins, including collagen and reticular fibers, fibrillin-1-rich microfibrils, elastic fibers, and hyaluronic acid. RESULTS: After administration of the cells, we found a noticeable increase in the number of fibroblasts within the dermis, a significant enlargement in diameter of the collagen fiber bundles, and an improvement in the density of reticular fibers, fibrillin-1-rich microfibrils, and elastic fibers compared with the initial, steady-state condition. CONCLUSIONS: The administration of autogenous fibroblasts could be an effective and safe adjunctive therapy to conventional health care treatment to prevent and reduce the age-related accumulation of dermal tissue damage.
