Cord lining progenitor cells: potential in vitro adipogenesis model.

OBJECTIVE: To investigate the effect of glucose and insulin concentrations on differentiation of umbilical cord lining progenitor cells to adipocyte-like cells (ALCs). METHODS: Cord lining mesenchymal cells (CLMCs) were isolated from the explant of human umbilical cord amniotic membrane. CLMCs were subjected to differentiation under various culture conditions for 20 days. Lipid droplets were confirmed with Oil Red O staining. Gene expressions of adipsin and peroxisome proliferator-activated receptor gamma (PPARγ) were analyzed using reverse transcription-PCR. Leptin and adiponectin secretions were detected using enzyme-linked immunosorbent assay kit. RESULTS: CLMCs became irregular, cuboidal-shaped cells that resemble adipocytes, and Oil Red O staining showed the presence of lipid droplets. The gene expressions of PPARγ and adipsin were upregulated. Leptin and adiponectin secretions by naive CLMCs were below the limits of detection. Matured ALCs cultured in low-glucose medium significantly secreted leptin and adiponectin, whereas those in high-glucose medium significantly secreted only leptin. Insulin concentration affects leptin but not adiponectin secretion. CONCLUSIONS: Under different culture conditions, CLMCs can differentiate into ALCs that resemble adipocytes in either normal-weight or obese individuals. Hence, these ALCs have the potential to be used as an in vitro model to study adipogenesis and obesity, and possibly as a drug discovery model for metabolic disorders.

Targeting of Sp1 transcription factor: a novel therapeutic approach for keloids, an in vitro analysis.

Keloid scars are fibroproliferative disorders characterized by the accumulation of extracellular matrix (ECM) components resulting in a fibrotic condition. Several ECM promoters are regulated by Sp1. Thus, our aim was to investigate the role of Sp1 in keloid pathogenesis and investigate the antiproliferative and antifibrotic effects of Wp631 and mitoxantrone, potent inhibitors of Sp1-activated transcription. An elevated level of Sp1 was observed in tissue extracts obtained from keloid tissue. Serum stimulation elevated Sp1 levels in keloid fibroblasts (KF). Under coculture conditions Sp1 seemed to be downregulated. Wp631 and mitoxanthrone in serum growth factors resulted in a reduced expression of ECM components in KF. Both Wp631 and mitoxanthrone were also able to inhibit the proliferation of normal and keloid keratinocytes and fibroblasts significantly. As Wp631 seems to be potent in downregulating the ECM components in KF and also inhibiting the proliferation of these cells it could be explored as a possible therapeutic agent in the treatment of keloids.