title: Mannose-binding dietary lectins induce adipogenic differentiation of the marrow-derived mesenchymal cells via an active insulin-like signaling mechanism.
abstract: We have recently demonstrated that the mannose-binding lectins, namely banana lectin (BL) and garlic lectin (GL), interacted with the insulin receptors on M210B4 cells--an established mesenchymal cell line of murine marrow origin--and initiate mitogen-activated protein kinase kinase (MEK)-dependent extracellular signal-regulated kinase (ERK) signaling in them. In this study, we show that this lectin-mediated active ERK signaling culminates into an adipogenic differentiation of these cells. Gene expression studies indicate that the effect takes place at the transcriptional level. Experiments carried out with pharmacological inhibitors show that MEK-dependent ERK and phosphatidylinositol 3-kinase-dependent AKT pathways are positive regulators of the lectin- and insulin-mediated adipogenic differentiation, while stress-activated kinase/c-jun N-terminal kinase pathway acts as a negative one. Since both lectins could efficiently substitute for insulin in the standard adipogenic induction medium, they may perhaps serve as molecular tools to study the mechanistic aspects of the adipogenic process that are independent of cell proliferation. Our study clearly demonstrates the ability of BL and GL to activate insulin-like signaling in the mesenchymal cells in vitro leading to their adipocytic differentiation. The dietary origin of these lectins underscores an urgent need to examine their in vivo effects on tissue homeostasis.
authors.affiliation: National Center for Cell Science, NCCS Complex, University of Pune Campus, Pune 411007, India.
authors.forename: Manmohan
authors.initials: M
authors.lastname: Bajaj
authors.forename: Ashwini
authors.initials: A
authors.lastname: Hinge
authors.forename: Lalita S
authors.initials: LS
authors.lastname: Limaye
authors.forename: Rajesh Kumar
authors.initials: RK
authors.lastname: Gupta
authors.forename: Avadhesha
authors.initials: A
authors.lastname: Surolia
authors.forename: Vaijayanti P
authors.initials: VP
authors.lastname: Kale
mesh_terms: D041721:3T3-L1 Cells; D050156:Adipogenesis / Q000187:drug effects; D000818:Animals; D000943:Antigens, Differentiation / Q000378:metabolism; D001854:Bone Marrow Cells / Q000166:cytology / Q000187:drug effects*; D022762:CCAAT-Enhancer-Binding Proteins / Q000235:genetics; D002454:Cell Differentiation / Q000187:drug effects*; D048049:Extracellular Signal-Regulated MAP Kinases / Q000378:metabolism; D050556:Fatty Acid-Binding Proteins / Q000235:genetics; D005737:Garlic; D005993:Glycerolphosphate Dehydrogenase / Q000235:genetics; D006801:Humans; D007328:Insulin / Q000494:pharmacology; D020930:MAP Kinase Kinase Kinases / Q000378:metabolism; D059630:Mesenchymal Stem Cells / Q000166:cytology / Q000187:drug effects*; D051379:Mice; D028521:Musa; D047493:PPAR alpha / Q000235:genetics; D047495:PPAR gamma / Q000235:genetics; D037121:Plant Lectins / Q000494:pharmacology*; D015398:Signal Transduction / Q000187:drug effects; D014158:Transcription, Genetic / Q000187:drug effects; D015854:Up-Regulation / Q000187:drug effects
chemical_list: D000943:Antigens, Differentiation; D022762:CCAAT-Enhancer-Binding Proteins; C493411:Fabp4 protein, mouse; D050556:Fatty Acid-Binding Proteins; D007328:Insulin; D047493:PPAR alpha; D047495:PPAR gamma; D037121:Plant Lectins; D005993:Glycerolphosphate Dehydrogenase; D048049:Extracellular Signal-Regulated MAP Kinases; D020930:MAP Kinase Kinase Kinases