Phenotypic characteristics of adipocytes generated from Meckel's chondrocytes in response to chick serum in vitro.
When present in the culture medium, chick serum (CKS) modulated the phenotypic change from chondrocytes of Meckel's cartilage to adipocytes in vitro, as revealed by light and electron microscopy, the incorporation of BrdU, and immunocytochemistry. CKS inhibited DNA synthesis in chondrocytes and the proliferation of these cells, while it facilitated the differentiation to adipocytes. CKS contributed to phenotypic changes in undifferentiated chondrocytes, but did not affect the characteristics of differentiated chondrocytes. Electron microscopy revealed that the lipid droplets in adipocytes were enclosed by limiting membranes that fused to yield larger lipid droplets. Immunocytochemical staining of adipocytes with stage-specific antibodies revealed the presence of immunoreactive uncoupling protein (UCP-1) and peroxisome proliferator-activated receptor (PPARgamma) in immature adipocytes, and leptin and glucose transporter (Glut-4) in mature adipocytes. The adipocytes that were formed in the present study were multilocular adipocytes that contained many small lipid droplets, but in many ways they resembled white adipocytes. CKS contains a high level of estrogen, compared with fetal bovine serum, and it is possible that estrogen might have induced the differentiation to adipocytes.
Ishizeki
Kiyoto
K
Department of Oral Anatomy, School of Dentistry, Iwate Medical University, Chuo-dori 1-3-27, Morioka 020-8505, Japan. ishizeki@iwate-med.ac.jp
Takahashi
Noriaki
N
Nawa
Tokio
T
D017667:Adipocytes / Q000166:cytology* / Q000378:metabolism* / Q000648:ultrastructure; D000818:Animals; D002352:Carrier Proteins / Q000378:metabolism; D002356:Cartilage / Q000166:cytology / Q000187:drug effects / Q000196:embryology / Q000378:metabolism* / Q000648:ultrastructure; D002454:Cell Differentiation; D002455:Cell Division; D002478:Cells, Cultured; D002645:Chickens / Q000097:blood*; D019902:Chondrocytes / Q000166:cytology / Q000378:metabolism* / Q000648:ultrastructure; D003470:Culture Media; D051275:Glucose Transporter Type 4; D066298:In Vitro Techniques; D007473:Ion Channels; D020738:Leptin / Q000378:metabolism; D008565:Membrane Proteins / Q000378:metabolism; D051379:Mice; D008815:Mice, Inbred Strains; D024101:Mitochondrial Proteins; D009004:Monosaccharide Transport Proteins / Q000378:metabolism; D009124:Muscle Proteins; D010641:Phenotype; D018160:Receptors, Cytoplasmic and Nuclear / Q000378:metabolism; D014157:Transcription Factors / Q000378:metabolism; D000071256:Uncoupling Protein 1
D002352:Carrier Proteins; D003470:Culture Media; D051275:Glucose Transporter Type 4; D007473:Ion Channels; D020738:Leptin; D008565:Membrane Proteins; D024101:Mitochondrial Proteins; D009004:Monosaccharide Transport Proteins; D009124:Muscle Proteins; D018160:Receptors, Cytoplasmic and Nuclear; C495693:Slc2a4 protein, mouse; D014157:Transcription Factors; C000604372:Ucp1 protein, mouse; D000071256:Uncoupling Protein 1