Albumin is a major plasma protein that has become ubiquitous in regenerative medicine research. As such, many studies have examined its structure and advantageous properties. However, a systematic and comprehensive understanding of albumin's role, capabilities and therapeutic potential still eludes the field. In the present work, we review how albumin is applied in tissue engineering, including cell culture and storage, in vitro fertilization and transplantation. Furthermore, we discuss how albumin's physiological role extends beyond a carrier for metal ions, fatty acids, pharmacons and growth factors. Albumin acts as a bacteriostatic coating that simultaneously promotes attachment and proliferation of eukaryotic cells. These properties with the combination of free radical scavenging, neutrophil activation and as a buffer molecule already make the albumin protein beneficial in healing processes supporting functional tissue remodeling. Nevertheless, recent data revealed that albumin can be synthesized by osteoblasts and its local concentration is raised after bone trauma. Interestingly, by increasing the local albumin concentration in vivo, faster bone healing is achieved, possibly because albumin recruits endogenous stem cells and promotes the growth of new bone. These data also suggest an active role of albumin, even though a specific receptor has not yet been identified. Together, this discussion sheds light on why the extravascular use of the albumin molecule is in the scope of scientific investigations and why it should be considered as a local therapeutic agent in regenerative medicine. © 2016 BioFactors, 43(3):315-330, 2017.

Transcription of Brain-derived neurotrophic factor (Bdnf) is induced in response to a wide variety of extracellular stimuli via the activation of a complex array of transcription factors. However, to what degree individual transcription factors confer specificity upon the regulation of Bdnf is poorly understood. Previous studies have shown that members of the Myocyte Enhancer Factor 2 (MEF2) transcription factor family bind a regulatory element upstream of Bdnf promoter I and associate with an unknown binding site in Bdnf promoter IV. Here we identify the calcium-response element CaRE1 as the MEF2 binding site in promoter IV of the Bdnf gene and determine the requirements for individual MEF2 family members in Bdnf regulation. MEF2A, C, and D are all highly expressed in embryonic rat cortical neurons, however only the Mef2c gene encodes a MEF2 splice variant that lacks the γ repressor domain. We find that MEF2C variants lacking the γ-domain are particularly sensitive to activation by membrane depolarization, raising the possibility that the MEF2s may differentially contribute to activity-regulated gene expression. We find that only knockdown of MEF2C significantly impairs membrane depolarization-induced expression of Bdnf exon IV. By contrast, knockdown of MEF2D significantly enhanced depolarization-induced expression of Bdnf exon I. Taken together, these data show that individual members of the MEF2 family of transcription factors differentially regulate the expression of Bdnf, revealing a new mechanism that may confer specificity on the induction of this biologically important gene.

Results from the present study indicate that donor site pain, a disturbing long-term side effect of bone-patellar tendon-bone surgery, is significantly reduced if bone buildup in the patella and the tibia is augmented by serum albumin-coated bone allografts.