Apolipoprotein A-II, a Player in Multiple Processes and Diseases.

Apolipoprotein A-II (apoA-II) is the second most abundant apolipoprotein in high-density lipoprotein (HDL) particles, playing an important role in lipid metabolism. Human and murine apoA-II proteins have dissimilar properties, partially because human apoA-II is dimeric whereas the murine homolog is a monomer, suggesting that the role of apoA-II may be quite different in humans and mice. As a component of HDL, apoA-II influences lipid metabolism, being directly or indirectly involved in vascular diseases. Clinical and epidemiological studies resulted in conflicting findings regarding the proatherogenic or atheroprotective role of apoA-II. Human apoA-II deficiency has little influence on lipoprotein levels with no obvious clinical consequences, while murine apoA-II deficiency causes HDL deficit in mice. In humans, an increased plasma apoA-II concentration causes hypertriglyceridemia and lowers HDL levels. This dyslipidemia leads to glucose intolerance, and the ensuing high blood glucose enhances apoA-II transcription, generating a vicious circle that may cause type 2 diabetes (T2D). ApoA-II is also used as a biomarker in various diseases, such as pancreatic cancer. Herein, we provide a review of the most recent findings regarding the roles of apoA-II and its functions in various physiological processes and disease states, such as cardiovascular disease, cancer, amyloidosis, hepatitis, insulin resistance, obesity, and T2D.

Heterogeneity of human fibroblasts isolated from hypertrophic scar.

Pathological wound healing states, such as hypertrophic scarring and keloids, represent a huge clinical and financial burden on healthcare system. The complex biological mechanisms occurring in hypertrophic scarring are still barely understood. To date, there is no satisfactory description of hypertrophic fibroblasts. Therefore, in the present study we focused on the comparatively characterization of the fibroblasts residing in different regions of hypertrophic scars. To achieve this aim, fibroblasts were isolated from normal skin samples (n=4) and hypertrophic scars (n=4). These cell populations were further were used for the evaluation of proliferation and migration capacity, for the gene and protein expression of extracellular matrix protein type I collagen and fibronectin and for the presence of myofibroblasts. Our results demonstrated that perilesional and intralesional fibroblasts isolated from hypertrophic scars could be considered as distinct populations, having different properties. Thus, the intralesional fibroblasts had an increased proliferation capacity and increased gene and protein expression of collagen I and fibronectin. However, the perilesional fibroblasts had augmented mobility as revealed by in vitro scratch test and contained a higher percentage of myofibroblasts [alpha-smooth muscle actin (α-SMA)high cells], in comparison to the intralesional population. In conclusion, our data could provide an explanation regarding the inconsistent efficacy of topic therapies for hypertrophic scars.