Bax inhibitor-1 overexpression reduces the suppressive effect of calcium mobilizing agent on adipogenesis.
Bax inhibitor-1 is a conserved protein which suppresses endoplasmic reticulum stress-induced apoptosis and regulates calcium release from the endoplasmic reticulum. Recent studies have revealed that adipogenesis, the process of adipocyte differentiation, is influenced by a change of intracellular calcium concentration. Here, we examined the effect of endoplasmic reticulum calcium regulation by Bax inhibitor-1 on adipogenesis using 3T3-L1 preadipocytes stably transfected with a pcDNA3-BI-1-HA plasmid. Bax inhibitor-1 functionality was confirmed by inhibiting the thapsigargin-induced increase of endoplasmic reticulum stress markers. Bax inhibitor-1 overexpression did not alter normal process of adipogenesis. Thapsigargin treatment inhibited adipogenesis in control cells, but Bax inhibitor-1 overexpressing 3T3-L1 cells retained their adipogenesis function. Endoplasmic reticulum stress did not seem to be involved in thapsigargin-reduced adipogenesis, since other endoplasmic reticulum stress inducers, such as tunicamycin and dithiothreitol, did not suppress the differentiation of 3T3-L1 cells. Bax inhibitor-1 might affect adipogenesis through regulating cytosolic calcium, because the thapsigargin-induced robust intracellular calcium rise was not observed in Bax inhibitor-1 overexpressing 3T3-L1 cells. A23187, a calcium ionophore, showed the same effect on adipogenesis as thapsigargin. Taken together, Bax inhibitor-1 overexpression in 3T3-L1 preadipocytes inhibits calcium mobilizing agent-induced suppression of adipogenesis. As adipogenesis is dependent on a change of intracellular calcium concentration, endoplasmic reticulum calcium regulation by Bax inhibitor-1 may play an important role in adipogenesis process.
Department of Biochemistry, Medical School and Diabetes Research Center, Chonbuk National University, Jeonju, Jeonbuk, Republic of Korea.
Jiahua
J
Yu
Kang-Beom
KB
Kwon
Jin-Woo
JW
Park
Han-Jung
HJ
Chae
Byung-Hyun
BH
Park
D041721:3T3-L1 Cells; D050156:Adipogenesis / Q000187:drug effects*; D000818:Animals; D000001:Calcimycin / Q000494:pharmacology; D002118:Calcium / Q000378:metabolism; D020013:Calcium Signaling / Q000187:drug effects*; D004721:Endoplasmic Reticulum / Q000187:drug effects / Q000473:pathology; D005786:Gene Expression Regulation / Q000187:drug effects; D007476:Ionophores / Q000494:pharmacology; D008565:Membrane Proteins / Q000235:genetics / Q000378:metabolism*; D051379:Mice; D013312:Stress, Physiological / Q000187:drug effects; D019284:Thapsigargin / Q000494:pharmacology*
D007476:Ionophores; D008565:Membrane Proteins; C490015:Tmbim6 protein, mouse; D000001:Calcimycin; D019284:Thapsigargin; D002118:Calcium